2012 Science Of Supplements: Winter Issue

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The Science of Supplements section of Nutrition Industry Executive has been offered for a decade to help manufacturers gain a better understanding of the ingredients available that can make their products stand out.

This second installment for the year gives advertisers an opportunity to describe in some detail the research that substantiates their branded ingredients, products and company services.

These companies have responded to this opportunity with background information about the health concerns their products are intended to address, histories of nutrients behind their ingredients and details of research that has been carried out. We’ve also provided company addresses, phone numbers, email and website addresses to make obtaining additional information as easy as possible.

Following is an index of companies participating in this year’s Nutrition Industry Executive’s Science of Supplements Winter Issue section:

Albion

Anderson Global Group, LLC

Bioenergy Life Science, Inc.

Cyvex Nutrition, Inc.

Deerland Enzymes

Embria Health Sciences

Gencor Nutrients, Inc.

Healthco

InterHealth Nutraceuticals

Lallemand Health Solutions

Nutrition 21, LLC.

OmniActive Health Technologies

P.L. Thomas

Sabinsa Corporation

Specialty Enzymes & Biotechnologies

Stratum Nutrition

VDF FutureCeuticals, Inc.

Verdure Sciences

Albion

Human Nutrition Division 100 Maple Park Blvd., Ste. 110 Saint Clair Shores, MI 48081 Phone: (801) 825-9877; (800) 222-0733 Email: mmotyka@albionminerals.com Website: www.albionminerals.com

Oral Magnesium Supplementation in Children With Cystic Fibrosis

This article is an abstract of Cle´sio Gontijo-Amaral, Elizabet V. Guimara˜es and Paulo Camargos. “Oral Magnesium Supplementation in Children With Cystic Fibrosis Improves Clinical and Functional Variables: A Double-Blind, Randomized, Placebo-Controlled Crossover Trial.” AJCN; First published ahead of print May 30, 2012 as doi: 10.3945/ajcn.112.034207. The magnesium was Albion’s Magnesium Glycinate Chelate Taste Free.

Introduction

Patients with cystic fibrosis (CF) may have magnesium deficiency1,2, even though a previous study did not find any reduction in serum magnesium concentrations in these patients.3 A promising new strategy in CF patients could be increasing the magnesium concentration in the airway surface liquid by aerolization of magnesium solutions or by oral intake of magnesium supplements, which may facilitate the removal of highly viscous mucus in chronic lung disease by activating endogenous DNase activity.4,5

We hypothesized that CF patients have low body magnesium storage and that magnesium supplementation could improve respiratory muscle strength.

Subjects & Methods

After an initial screening, 44 patients were randomly assigned to the study treatments.6 Each participant received 300 mg oral magnesium bisglycinate chelate (n = 22) or a placebo control (n = 22) once daily for eight weeks, with a washout period of four weeks between trials.8 Magnesium bisglycinate chelate (taste free; lot number 251755) from Albion Human Nutrition was used. The magnesium dose used for each participant ranged from 5 to 12 mg _ kg21 _ d21 according to the RDA. We evaluated the average weight of the group to perform a stratified randomization. Thus, we arbitrarily chose the dose of 300 mg/d on the basis of the median weight of the children and adolescents included in the study (40 kg · 7.5 mg/kg = 300 mg/d).2,5,7

All patients were undergoing conventional treatment for CF. This included clinical evaluation, assessment of urinary concentration of magnesium, and manuvacuometric measurements maximal inspiratory pressure (MIP) and maximal expiratory pressure (MEP). MIP was the primary outcome.2,7

The urinary concentration of magnesium was assessed in all patients before and after each study period. Concentrations were determined by using the VITROS magnesium slide method with the Mg Slides and Chemistry Products Calibrator Kit 1 in VITROS 250/350/950/5, the 1 FS (shading coefficient) and 4600 Chemistry Systems, and the 5600 Integrated System (Johnson & Johnson).

Results

Forty-four patients screened for participation in this study met the study criteria. There were no dropouts. After the intervention period MIP showed an 11 +/- 7.8% predicted increase (from 98.3 +/- 29.7% to 109.3 +/- 31.8% predicted) in the magnesium group, with a slight 0.5 +/- 6.3% predicted increase (from 99.2 +/- 28.6 to 99.7 +/- 29.3% predicted) in the placebo group. MEP also showed an 11.9 +/- 7.7% predicted increase (from 97.5 +/- 27.8 to 109.4 +/- 27.3% predicted) after magnesium administration and a slight 0.8 +/- 6.5% predicted increase (from 97.4 +/- 26.6% to 98.2 +/- 27.3% predicted) after placebo administration. The differences between the intervention and placebo periods were significant.8

In conclusion, our double-blind, randomized, crossover study showed that children and adolescents with CF who receive conventional treatment in combination with oral magnesium bisglycinate chelate supplementation achieve significant improvement in functional status of the respiratory musculature and better clinical results.

References:

1 Staab D. Cystic fibrosis—therapeutic challenge in cystic fibrosis children. Eur J Endocrinol 2004;151:S77–80.

2 Flume PA, O’Sullivan BP, Robinson KA, Goss CH, Mogayzel PJ, Willey-Courand DB, Bujan J, Finder J, Lester M, Quittell L, et al. Cystic fibrosis pulmonary guidelines: chronic medications for maintenance of lung health. Am J Respir Crit Care Med 2007;176: 957–69.

3 Foucard T, Gebre-Medhin M, Gustavson KH, Lindh U. Low concentrations of sodium and magnesium in erythrocytes from cystic fibrosis heterozygotes. Acta Paediatr Scand 1991;80:57–61.

4 Arnaud MJ. Update on the assessment of magnesium status. Br J Nutr 2008;99:S24–36.

5 Sanders NN, Franckx H, De Boeck K, Haustraete J, De Smedt SC, Demeester J. Role of magnesium in the failure of rhDNase therapy in patients with cystic fibrosis. Thorax 2006;61:962–8.

6 Gontijo-Amaral C, Ribeiro MAGO, Gontijo LSC, Condino-Neto A, Ribeiro JD. Oral magnesium supplementation in asthmatic children: a double-blind randomized placebo-controlled trial. Eur J Clin Nutr 2007;61:54–60.

7 Sinaasappel M, Stern M, Littlewood J,Wolfe S, Steinkamp G, Heijerman G, Robberecht E, Do¨ring G. Nutrition in patients with cystic fibrosis: a European Consensus. J Cyst Fibros 2002;1:51–75.

8 Turner RM, White IR, Croudace T. Analysis of cluster randomized cross-over trial data: a comparison of methods. Stat Med 2007;26: 274–89.

Anderson Global Group, LLC

2030 Main St., Ste. 560 Irvine, CA 92614 Phone: (949) 502-4773 Website: www.andersongg.com

Polycan: The Future of Natural Bone Health

Americans tend to deal with medical issues by getting something prescribed by a doctor and then assume we’re effectively dealing with the problem. The multi-billion dollars spent on advertising by Big Pharma may have something to do with this, but isn’t it more logical to assume that naturally occurring health concerns can be more effectively dealt with through naturally occurring compounds?

The bone health (nearly $10 billion dollars) segment of the pharmaceutical market, for example, is growing at a steady clip. Yet more information continues to come out regarding the ineffectiveness of these drugs, not to mention the incredible side effects that are associated with them. Ineffectiveness plus significant side effects equals a losing equation.

It’s no wonder why the dietary supplement industry is also providing more natural solutions to bone health. There is a thoroughly researched new product on the market that demonstrates excellent efficacy without side effects associated with their drug counterparts—Polycan™.

Polycan is an innovative compound new to the North American marketplace offering significant benefits in the areas of bone health and mobility. Formul-ated and heavily researched in Korea, Polycan is a patented soluble compound fermented from a novel strain of black yeast clinically proven to support bone health, mobility and a healthy immune system. Polycan’s unique composition of multiple polysaccharides has been granted a U.S. patent and GRAS status by the FDA. It has been the feature of seven completed clinical studies targeting the areas of bone health, inflammation and immunity.

After seven intriguing animal studies indicating strong benefits in the arenas of immunity and bone health,3-5 Polycan research was accelerated in 2009 with a 12-week, randomized, 60-person double-blind clinical study.1 This critical study indicated significant gains in the activation of key bone formation biomarker osteoblast and the suppression of key bone resorption biomarker osteoclast. No other ingredient in the marketplace has been shown to target both of these biomarkers simultaneously.

Bone Resportion

Osteoclast (bone resorption) occurs in many circumstances. One of which is when cytokines, such as TGF-beta, TNF-alpha, IL-1 and IL-2, are increased by inflammation, which in turn causes an increase of iNO (inducible nitric oxide). The increase of iNO is known for one of the causes of osteoporosis. Polycan has been shown to decrease TNF-alpha, IL1 and iNOS resulting in the suppression of osteoclast.1,2

Bone Formation

One of the circumstances that cause osteoblast activity is when a substrate called endothelial nitric oxide (eNO), or constitutive NO, activates osteoblast with its naturally made substance. The generation of eNO is one of the known mechanisms to prevent osteoporosis. It is also known that the existence of iNO by inflammation prevents the generation of eNO. In the osteoblast activity, Polycan is hypothesized to have a similar mechanism to estrogen—inhibiting the generation of iNO and promoting the generation of eNo at the same time, resulting in the activation of osteoblast.1,2

A second human clinical trial2 featuring 90 test subjects was recently completed and is expected to be published in the coming months. Results from this subsequent study solidify the Polycan results from 2009.

Polycan offers a new alternative for brands and consumers looking for additional efficacious options in the bone, immunity and mobility categories. This emerging ingredient is starting to make its way into a growing number of bone health supplements as it naturally aids bones for long-term health—and with no side effects.

Polycan is synergistic with other natural compounds and actually improves bone health by improving natural bone metabolism.

References:

1 Effects of Polycan on Bone Metabolism Improvement – Results from a Randomized, Double-Blind Human Clinical Trial. DS Kim, HJ Chae, December Kor. J. Clin. Pharm., Vol. 21, No.4, 2011297-304.

2 Effects of Polycan and Polycalcium on Bone Metabolism & Joint Health Improvement – Results from a Randomized, Double-Blind Human Clinical Trial. DS Jong-Dae Kim, Mi-Yeon Park Daegu Haany University 2011, May.

3 Immunomodulatory Effects of Aureobasidium Pullulans SM-2001 Exopolymers on Cyclophosphamide-Treated Mice Yoon. Hyun Soo, Joo-Wan Kim, Hyung-Rae Cho, Seung-Bae Moon, Hyun-Dong Shin, Kun-Ju Yang, Young-Sam Kwon, and Sae-Kwang Ku. Korea J. of Microbiology & Biotechnology, (2010), 20(2), 438-445.

4 Effect of Exopolymers from Aureobasidium {pullulans on Formalin Induced Chronic Paw Inflammation in Mice. Kim,Hyuong-Dong, Hyung-Rae Cho, Seung-Bae Moon, Hyun-Dong Shin, Kun-Juyang, Bok-Ryeon Park, Hee-Heong Jang, Lin-Su Kim, Hyeung-Sik Lee, and Sae-Kwang Ku. Korea J. of Microbiology & Biotechnology, 2006, 16(12), 1954-1960.

5 Effect of Beta Glucan from Aureobasidium Pullulans on Acute Inflammation in Mice. Hyeon-Dong Kim, Hyung-Rae Cho, Seung-bae Moon, Hyun-Dong Shin, Kun-Ju Yang, Bok-ryeon Park, Hee-Jeong Jang, Lin-Su Km, Hyeung-Sik Lee, and Sae-Kwang Ku. Arch Pharm Res, Vol 30, No 3, 323-38, 2007.

Bioenergy Life Science, Inc.

13840 Johnson St. N.E. Minneapolis, MN 55304 Phone: (877)-4RIBOSE (474-2673) Website: www.bioenergyribose.com

The Science Behind the Powerful Energy Ingredient

Bioenergy Ribose® is a bioactive ingredient that energizes functional foods, beverages and nutraceuticals. It is natural, safe and clinically proven.

Ribose is the vital structural backbone of critical cellular compounds called purines and pyrimidines. Our bodies must have an adequate supply of purines and pyrimidines to form major cellular constituents such as our genetic material (DNA and RNA), numerous cofactors and certain vitamins. Most importantly, ribose regulates the production of adenosine triphosphate (ATP)—the source for all cellular energy and tissue repair. Ribose is the starting point for the synthesis of these fundamental cellular compounds, and the availability of ribose determines the rate at which they can be made by our cells and tissues.

Bioenergy Ribose is unique in this metabolic role. No other compound—whether bioactive ingredient or ethical drug—can replace ribose in the important job of regulating the metabolic processes involved in synthesizing purines and pyrimidines. And, without these vital structural components, our bodies would quickly run out of energy, could not make proteins and our cells would lose the ability to replicate. Energy recovery and tissue repair are slower in heart and muscle cells, especially after overwork or exercise. Ribose stimulates the process that replenishes ATP and other energy components in these cells.

Ribose is made in our bodies’ cells from glucose, in the pentose phosphate pathway, which is slow in heart and skeletal muscle tissue. Although ribose is present in all living matter, only a small amount can be ingested through the diet. In many U.S. and European clinical studies, supplemental Bioenergy Ribose has been shown to significantly improve endurance during strenuous exercise, shorten recovery time, reduce cramping and soreness, and reduce fatigue in people suffering from energy depletion.

Bioenergy Ribose is GRAS (generally recognized as safe) and is affirmed by the U.S. Food and Drug Administration by the issuance of a “no questions letter.” It is certified kosher and halal and has an extensive portfolio of patents, backing its claims with clinical research.

References:

Hellsten Y, L Skadhauge, J Bangsbo. Effect of ribose supplementation on resynthesis of adenine nucleotides after intense intermittent training in humans. Am J Physiol Regul Integr Comp Physiol, 2004;286:R182-R188.

Tullson PC, RL Terjung. Adenine nucleotide synthesis in exercising and endurance-trained skeletal muscle. Am J Physiol, 1991;261(Cell Physiol 30):C342-C347.

Hancock CR, JJ Brault, RW Wiseman, RL Terjung, RA Meyer. 31P-NMR observation of free ADP during fatiguing, repetitive contractions of murine skeletal muscle lacking AK1. Am J Physiol Cell Physiol, 2005;288:C1298-C1304.

Brault JJ, RL Terjung. Purine salvage to adenine nucleotides in different skeletal muscle fiber types. J Appl Physiol, 2001;91: 231-238.

Zarzeczny R, JJ Brault, KA Abraham, CR Hancock, RL Terjung. Influence of ribose on adenine salvage after intense muscle contractions. J Appl Physiol, 2001;91:1775-1781.

Gumaa KA, P McLean. The pentose phosphate pathway of glucose metabolism. Biochem J, 1969;115:1009-1029.

Hellsten-Westing Y, PD Balsom, B Norman, B Sjodin. The effect of high-intensity training on purine metabolism in man. Acta Physiol Scand, 1993;149:405-412.

Hellsten-Westing Y, B Norman, PD Balsom, B Sjodin. Decreased resting levels of adenine nucleotides in human skeletal muscle after high-intensity training. J Appl Physiol, 1993;74(5):25232528.

Cyvex Nutrition, Inc.

(A Subsidiary of Omega Protein Corporation) 1851 Kaiser Ave. Irvine, CA 92614 Phone: (949) 622-9030 • Fax: (949) 622-9033 Email: sales@cyvex.com Website: www.cyvex.com

Using the Synergies of Proteins and PI-2 to Manage Weight

One of the most profound health challenges is the growing obesity epidemic in the Western world. A brief look at the statistics tells us why: complications relating to obesity are now the second leading cause of preventable death in the United States; 60 million Americans are grossly overweight; an additional nine million children and teens are obese; and obesity has been linked to breast cancer, coronary heart disease, diabetes, sleep apnea, hypertension and even osteoarthritis.

To combat this growing epidemic, scientists and physicians are looking at potential substances that can help combat the deadly combination of the modern high calorie-rich diet and sedentary lifestyle. Traditionally, potential supplements have fallen into three broad categories: first, those that increase metabolism; second, those that decrease appetite and hence decrease consumption of food; and finally, those that decrease the amount absorbed by the body through the gastronintestinal (GI) tract.

Yet increasingly, studies have shown supplements that increase metabolism come with great risk. That’s because these compounds increase heart rate and muscle work, in addition to increasing reactive oxygen species (ROS), causing potentially damaging health effects in both the immediate and long term. Additionally, any substance that decreases absorption usually comes with the unwanted side effects of diarrhea and gas, with the potential to cause serious harm by affecting fluid balances in the body.

This has lead most experts to consider supplements that decrease consumption of food as a safer alternative for managing the proper weight. It is with this in mind that Cyvex Nutrition has recently launched SOLATHIN®, a potent appetite suppression agent that is derived from a mixture of potato proteins and backed by nearly 20 years of animal and human clinical studies, with no known side effects. SOLATHIN is a potent mixture of potato proteins that naturally contain the powerful appetite-suppressing agent known as protease inhibitor II or PI-2.

Numerous scientific studies over the last 10 years have shown that proteins are potent appetite suppressing agents. Recently, a groundbreaking paper published in Journal Cell reported appetite suppression occurs when proteins bind to select receptors in the GI track, which in turn relay information back to the brain to communicate satiety. SOLATHIN works by a different but equally powerful mechanism.

SOLATHIN’s PI-2 properties prevent the breakdown of a hormone called cholecystokinin (CCK), which acts as a neurotransmitter in the brain to suppress appetite. When food levels are low, CCK is degraded rapidly by trypsin and protease enzymes, resulting in lower amounts of CCK in the system. Hence CCK is no longer binding to the brain, signaling it is full. PI-2 blocks protease enzymes from degrading CCK, leading to higher levels of CCK in the blood, resulting in appetite suppression. The effects of PI-2 have been demonstrated in numerous studies over the years in both animal and human studies. Overall, the studies have revealed that consuming PI-2, naturally derived from potato proteins, leads to increased circulating levels of CCK and also slower reductions in CCK following meals. Additionally, this results in slowed gastric emptying, thereby further suppressing appetite in addition to lower glucose peak levels and lower insulin responses—two powerful mechanisms leading to overall better glucose health.

Human studies have shown that PI-2 ingestion does lead to weight loss in double-blind, controlled studies. SOLATHIN is one of the most powerful natural supplements on the market for maintaining proper weight and glucose health. SOLATHIN naturally suppresses appetite by the synergistic mechanisms of proteins and PI-2 without any adverse side effects and represents a potential revolution in the weight management nutritional industry.

© 2012 Cyvex Nutrition, Inc. SOLATHIN® is a registered trademark of Cyvex Nutrition, Inc.

References: Liddle RA. Regulation of cholecystokinin secretion in humans. J Gastroenterol, 2000; 35: 181–187.

Peikin SR. Role of cholecystokinin in the control of food intake. Gastroenterol Clin North America, 1989; 18: 757–775.

Hill AJ, Peikin SR, Ryan CA, Blundell JE. Oral-administration of proteinase inhibitor-ii from potatoes reduces energy-intake in man. Physiol Behav 1990; 48: 241–246.

Vasselli JR, Greenfield D, Schwartz L, Heymsfield SB. Protease inhibitor from potatoes decreases hunger and increases fullness in overweight subjects following a meal. Obesity Res, 1989; 7.

Schwartz JG, Guan D, Green GM, Phillips WT. Treatment with an oral proteinase-inhibitor slows gastric-emptying and acutely reduces glucose and insulin levels after a liquid meal in type-2 diabetic-patients. Diab Care, 1994; 17: 255–262.

Peikin SR, Springer CJ, Dockray GJ, Calam J. Oral-administration of the protease inhibitor potato-2 stimulates release of cholecystokinin in man. Gastroenterology 1987; 92: 1570.

Van Strien T, Frijters JER, Bergers GPA, Defares PB. The Dutch eating behavior questionnaire (Debq) for assessment of restrained, emotional, and external eating behavior. Int J Eating Disorders, 1986; 5: 295–315.

Fear G, Komarnytsky S, Raskin I. Protease inhibitors and their peptidomimetic derivatives as potential drugs. Pharmacol Therapeutics, 2007; 113: 354–368.

Little TJ, Horowitz M, Feinle-Bisset C. Role of cholecystokinin in appetite control and body weight regulation. Obesity Rev, 2005; 6: 297–306.

Deerland Enzymes

3800 Cobb International Blvd. Kennesaw, GA 30152 Phone: (800) 697-8179 Email: info@deerland-enzymes.com Website: www.deerlandenzymes.com

Small Bowel Bacterial Overgrowth and the Effect of Natural Antimicrobial Compounds on the Growth of Colonic Bacteria

The entire gastrointestinal tract naturally contains a certain amount of bacteria. The number of bacteria is greatest in the colon (at least one billion bacteria per ml of fluid), and much lower in the small intestine (less than 10,000 bacteria per ml of fluid).1 The bacterial composition within the small intestine is different than the colon.1,2

Proximal SIBO

Small intestinal bacterial overgrowth (SIBO) refers to a condition in which abnormally large numbers of bacteria (at least 100,000 bacteria per ml of fluid) are present in the small intestine, and the bacteria resemble the type usually found in the colon.3,4

The symptoms of SIBO include:

• Excess gas

• Abdominal bloating and distension

• Diarrhea

• Abdominal pain

• Malabsorption

• Malnutrition/weight loss

A typical patient with SIBO can experience symptoms that fluctuate in intensity over long periods of time before the diagnosis is established.5 For example, a small number of patients with SIBO may experience chronic constipation rather than diarrhea. Some may even experience symptoms that are unrelated to the gastrointestinal tract, such as body aches or fatigue. In any case, the symptoms of SIBO tend to be chronic.

Recent studies have shown that many patients with irritable bowel syndrome also suffer from SIBO, and may benefit from eradication of the offending organism to maintain normal bacterial populations in the gut.4

Bacteria Defense Mechanisms The bacterial stability of the small bowel is accomplished by several bodily functions:

• Stomach acid kills bacteria that are present in foods or drinks.

• Motility of the small intestine moves bacteria along preventing colonization and avoiding overgrowth.

• Pancreatic enzymes digest and allow nutrients to be absorbed by the body.

• Mucosal immune response through IgA secretion constitutes a first line of defense responsible for neutralizing antigens and pathogens.

• The ileo-cecal valve prevents reflux of colonic contents back into the small intestines.

When one or more of these natural defenses are compromised, bacteria overgrowth in the small intestine may result; this overgrowth is difficult to correct. The bacteria bind to the lining of the small intestine and mount their own defense mechanism, preventing the body from removing it.

Natural Antimicrobial Formula Testing

A number of natural compounds from enzymes, essential oils, peptides and chelators possess anti-microbial properties and are safe for human consumption. Research has shown that these compounds alone or in combination may reduce and suppress the growth of bacteria in patients with SIBO.6,7

Deerland Enzymes conducted a study to test these various natural ingredients alone and in combination for their efficacy in reducing and/or inhibiting the growth of the two most common offending bacterial species, E. coli and Bacteroides. In addition, because it is important to replace these SIBO-causing micro-organisms with beneficial bacteria (probiotics), the company tested a number of lactobacilli for their compatibility in such a composition. All tests were performed under the physiological conditions of the small intestine.

After more than 50 studies using single or combinations of test ingredients, a final formula was selected for further testing. The results showed that this formula was effective in the reduction and suppression of the growth of the E. coli population, and did not interfere with the B. subtilis population.

Deerland Enzymes has developed ThioZyme™GI, a formula that includes enzymes, essential oils, peptides and chelators plus the probiotic Bacillis subtilis, and is designed to support normal populations of bacteria in the small intestine.

For details on the studies described in this article, or for more information on ThioZymeGI, contact Deerland Enzymes at (800) 697-8179.

References:

1 Hersh T, et al, Disturbance of the Jejunal and Colonic Bacterial Flora in Immunglobulins Deficiencies, American Journal of Clinical Nutrition, 1970; 23;1595-1601.

2 Lee, KJ, et al, Altered Intestinal Microbiota in Irritable Bowel Syndrome, Neurogastroenterology Motility, 2010; 22: 493-498.

3 Ford A et al, Small Intestinal Bacterial Overgrowth in Irritable Bowel Syndrome, systematic review and meta-analysis, Clinical Gastroenterology & Hepatology, 2009; (12):1279-86.

4 Sing VV, Toskes, Philip PP, Small Bowel Bacterial Overgrowth: Presentation, diagnosis & treatment, Current Gastroenterology Reports, 2003; 5:365-72.

5 Zhao, J, et al, Lactose Intolerance in Patients with Chronic Functional Diarrhea, the Role of Small Intestinal Bacterial Overgrowth, Alimentary Pharmacology & Therapeutics, 2010; (8):892-900.

6 Dorman, H.J.D, and Deans SG (2000). Antimicrobial agents from plants: antibacterial activity of plant volatile oils. Journal of Applied Microbiology, 88, 308-316; Kirsch M. Bacterial overgrowth. Am J Gastroenterol, 1990;85: 231-237.

7 Marino M, Bersani C, Comi G (2001) Impedance measurements to study the antimicrobial activity of essential oils from Lamiacea and Compositae. International Journal of Food Microbiology, 67, 187-195.

Embria Health Sciences

2105 S.E. Creekview Dr. Ankeny, IA 50021 Phone: (877) 362-7421 (EMBRIA1) Fax: (515) 964-9004 Email: info@embriahealth.com Website: www.embriahealth.com

Iowa City Renews Award-winning Corporate Wellness Program With EpiCor

EpiCor®, an all natural immune balancing dietary supplement, is continuing to change the face of employee wellness in its hometown of Ankeny, IA, by helping local municipal employees and their families stay well through the cold and flu season.

After a successful trial launch in 2011, the City of Ankeny has reinstated the award-winning Corporate Wellness Initiative1 this year by implementing a new online ordering system for employees to continue using the product for improved overall wellness and decreased health care costs.

Embria Health Sciences, makers of EpiCor, spearheaded the initial trial program by partnering with ProActive Health Products to distribute supplements of EpiCor to City of Ankeny employees who elected to participate. The City paid half of the cost for a six-month supply for employees who participated. The initial trial group consisted of approximately 100 participants, both employees and family members. The study process began in October 2010 and continued through completion in early 2011.

The City’s human resource department noted a 28 percent decrease in employee doctor visits for cold, flu and upper respiratory illnesses in 2011, for those employees taking EpiCor versus the prior year for those same employees not taking EpiCor. This decrease paralleled two previously published scientific studies on the ingredient EpiCor, both of which noted a 26 percent decrease in the incidence and duration of cold and flu symptoms among adults who took the supplement versus placebo.2,3

“We feel like the initial trial was a success,” said Dawn Gean, City of Ankeny human resources officer. “Many employees felt better knowing they were taking EpiCor to improve their immune systems, and the majority of participants felt like it helped them stay healthy through the tough Midwestern cold and flu season.”

Because of the program’s success, ProActive Health Products, an Iowa-based dietary supplement marketer, worked with the City to offer its employees the entire line of EpiCor supplements via ProActive Health’s website (www.4greathealth.com).

The Corporate Wellness Program is also getting attention in the food and nutrition industry for its efforts to promote health and wellness in the workforce. In addition to receiving the Scientific Excellence Award from SupplySide West in 2010, Embria’s EpiCor was also honored with the Investment in the Future Award from the Nutrition Business Journal.1

“We are very pleased with the results of our first Corporate Wellness Initiative study with the City of Ankeny,” said Paul Faganel, president of Embria Health Sciences. “We believe in the quality and efficacy of EpiCor, and we hope to expand this program because we truly believe it can help organizations decrease health care costs while helping employees stay happy, healthy and productive.”

After the first trial of the program was complete and the data collected, the results were positive. Gean said the City benefited from the program because its employees were healthier, which represents significant cost savings for the organization. The City of Ankeny has implemented the Corporate Wellness Initiative permanently, and officials are confident the new online ordering system will promote easier access for participants while reducing the burden of administrative costs for the City.

To learn more about Embria Health Sciences and EpiCor, and its all natural health ingredient designed to support a strong balanced immune system, visit www.epicorimmune.com.

References:

1 Embria Health Sciences Wins the 2011 NBJ Investment in the Future Award…An economic impact study in its Iowa hometown puts Embria on the vanguard of immune support, Nutrition Business Journal, Jan. 20, 2012.

2 Moyad MA, et al., Immunogenic Yeast-Based Fermentate for Cold/Flu-like Symptoms in Nonvaccinated Individuals; The Journal of Alternative and Complementary Medicine, Vol. 16, No. 2, 2010, pp. 213-218.

3 Moyad, MA, et al., Effects of a Modified Yeast Supplement on Cold/Flu Symptoms; Urologic Nursing, Vol. 28; No. 1, 2008, pp. 50-55.

Gencor Nutrients, Inc.

920 E. Orangethorpe Ave., Ste. B Anaheim, CA 92801 Phone: (714) 870-8723 Fax: (732) 875-0306 Email: info@gencorpacific.com Website: www.gencorpacific.com

Overweight and Obesity: The Case for Caralluma

Under normal (evolutionary) conditions, the peptide hormone leptin transmits a satiety signal to the hypothalamus as a negative feedback loop of the “lipostat” with other mediators such as ghrelin acting as counter-inducers of hunger. Under modern conditions, these feedback loops are prone to malfunction.

Leptin’s effects on food intake and neuroendocrine functions involve intermediate neuropeptides such as pro-opiomelanocortin (POMC) and neuropeptide-Y (NPY) in the hypothalamus, which regulate appetite, energy expenditure and sympathetic nervous system outflow. In obesity, however, high leptin levels are no longer associated with appetite suppression, giving rise to the concept of central leptin resistance. This resistance can be caused by mutations affecting leptin transport, receptor affinity or signal transduction. Most cases, however, reflect physiological desensitisation caused by excessive adiposity and leptin levels. Restoring leptin sensitivity and appetite control presents an exciting new strategy in appetite and obesity management.

Pregnane glycosides in Hoodia gordonii exert appetite suppressant effects via enhanced hypothalamic signaling. This plant is near extinction, but the food plant Caralluma fimbriata contains near-identical compounds. This plant is still used by hunters in Northern India who, unable to carry large amounts of food with them on their hunting expeditions, take portions of Caralluma with them to prevent hunger pangs. Seeing these hunters return after a fortnight on the trail, healthy and vigorous and having experienced little or no hunger, stimulated research into this plant.

Background & Science

Caralluma fimbriata, an edible succulent of the family Asclepiadaceae, grows wild in India, Africa and Europe. It is a traditional food plant in the Mediterranean countries, and was cultivated in Britain as far back as 1830. Listed by the Indian Health Ministry as a vegetable and famine food, it is widely consumed as a food, appetite suppressant and treatment for diabetes. There are no reports of adverse effects; an acute oral rat toxicity study showed no toxicity at doses up to 5 g/kg.

A proprietary extract of C. fimbriata containing standardized levels of pregnane and metastigmane glycosides was developed by Gencor Pacific, and is marketed as a supplement for weight loss under the name Slimaluma®.

The evidence shows that Slimaluma is a safe and effective tool for weight and appetite control. Two further double-blind, randomized, placebo-controlled trials substantiated its weight reducing properties, and a recent study showed its ability to prevent the hyperphagia, adiposity and atherogenesis otherwise induced in CFO rats by the cafeteria diet. In CFO, increased body weight is largely due to increased fat mass as a result of pre-adipocyte proliferation and differentiation. Slimaluma demonstrated pronounced and dose-dependent appetite suppressant and anti-obesogenic effects in this model, plus complete prevention of aortic atherogenesis. The appetite suppressant effects were reflected in the feed intake, body weight, liver weight, fat pad mass and serum lipid profiles of the rats. Hyperleptinaemia and leptin resistance were also abolished.

Subsequent investigation found that Slimaluma also prevented pre-adipocyte differentiation by inhibiting the import of cyclin-D1 into pre-adipocyte nuclei. This novel mechanism prevents hypertrophic (and therefore hyperblastic) adipogenesis, and the proliferation of adipose tissue, as shown in the CFO study.

Slimaluma’s effectiveness and excellent safety profile allow it to be used not only for long-term weight control, but also as a prophylactic in those who do not wish to gain weight. Clinical experience in Australia, where Slimaluma is being used to treat notoriously refractory Prader-Willi patients, suggests that ghrelin amplification may also be involved. A clinical trial is planned shortly.

Slimaluma has not been tested to pharmaceutical standards, and the absence of pharma standards of proof has been used to attack this and other natural products. A healthy degree of skepticism is always warranted, but in this case the convergence of ethnobotany, in vitro mechanistic data, pre-clinical and clinical trial results indicate that Slimaluma is a genuinely useful therapeutic tool.

References:

Rohner-Jeanrenaud F, Jeanrenaud B, “Obesity, leptin, and the brain,” New England Journal of Medicine, vol. 334, no. 5, pp.324–325, 1996.

Sahu, A. “Evidence suggesting that galanin (GAL), melaninconcentrating hormone (MCH), neurotensin (NT), proopiomelanocortin (POMC) and neuropeptide Y (NPY) are targets of leptin signaling in the hypothalamus,” Endocrinology, vol. 139, no. 2, pp. 795–798, 1998.

Sahu, A. “Leptin signaling in the hypothalamus: emphasis on energy homeostasis and leptin resistance,” Frontiers in Neuroendocrinology, vol. 24, no. 4, pp. 225–253, 2003.

Plut C, Ribi`ere C, Giudicelli Y, Dausse J-P, “Hypothalamic leptin receptor and signaling molecule expressions in cafeteria diet-fed rats,” Journal of Pharmacology and Experimental Therapeutics, vol. 307, no. 2, pp. 544–549, 2003.

Ren D, Li M, Duan C, Rui L, “Identification of SH2- B as a key regulator of leptin sensitivity, energy balance, and body weight in mice,” Cell Metabolism, vol. 2, no. 2, pp. 95–104, 2005.

Soos S, Balasko M, Jech-Mihalffy A, Szekely M, Petervari E, “Anorexic vs. metabolic effects of central leptin infusion in rats of various ages and nutritional states,” Journal of Molecular Neuroscience, vol. 41, no. 1, pp. 97–104, 2010.

Shukla YJ, Pawar RS, Ding Y, Li X-C, Ferreira D, Khan A, “Pregnane glycosides from Hoodia gordonii,” Phytochemistry, vol. 70, no. 5, pp. 675–683, 2009.

MacLean DB, LuoL-G, “Increased ATP content/ production in the hypothalamus may be a signal for energy-sensing of satiety: studies of the anorectic mechanism of a plant steroidal glycoside,” Brain Research, vol. 1020, no. 1-2, pp. 1–11, 2004.

Kunert O, Rao VG, Babu GS et al., “Pregnane glycosides from Caralluma adscendens var. fimbriata,” Chemistry and Biodiversity, vol. 5, no. 2, pp. 239–250, 2008.

Wealth of India (1992) A Dictionary of Indian Raw Materials and Industrial Products.

Rivera D, Obon C, Heinrich M, Inocencia C, Verde A, Fajardo J. “Gathered Mediterranean Food  Plants – Ethnobotanical Investigations and Historical Development”. In Heinrich M, Müller WE, Galli C (eds): Local Mediterranean Food Plants and Nutraceuticals. Forum Nutr. Basel, Karger, 2006, vol 59, pp 18–74.

Loudon, J.C. (1830) Loudon’s Hortus Britannicus. A catalogue of all the plants, indigenous, cultivated in, or introduced to Britain, London, Longman, Rees, Orme, Brown, and Green.

Preuss, H. (2004) Report on the safety of Caralluma Fimbriata and its extract, Hong Kong.

Kurpad AV et al; unpublished.

Abdel-Sattar, E., Meselhy, M.R. and Al-Yahya, M.A. “New oxypregnane glycosides from Caralluma penicillata”, Planta Medica, vol. 68, no. 5, May 2002, pp. 430-434.

Kuriyan R, Raj T, Srinivas SK, Vaz M, Rajendran R, Kurpad AV, “Effect of Caralluma Fimbriata extract on appetite, food intake and anthropometry in adult Indian men and women,” Appetite, vol. 48, no. 3, pp. 338–344, 2007.

Lawrence RM, Choudhary S, “Caralluma Fimbriata in the treatment of obesity,” in Proceedings of the 12th Annual World Congress of Anti-Aging Medicine, Las Vegas, Nev, USA, 2004.

Kamalakannan S, Rajendran R, Venkatesh R, Clayton P, Akbarsha AK. ‘Anti-Obesegenic and Anti-Atherosclerotic Properties of Caralluma fimbriata Extract’. J Nut Metabolism (2011a), Article ID 285301, 6 pages.

Harris RB, “The impact of high- or low-fat cafeteria foods on nutrient intake and growth of rats consuming a diet containing 30% energy as fat,” International Journal of Obesity, vol. 17, no. 6, pp. 307–315, 1993.

Roca P, Rodriguez AM, Oliver P et al., “Brown adipose tissue response to cafeteria diet-feeding involves induction of the UCP2 gene and is impaired in female rats as compared to males,” Pflugers Archiv European Journal of Physiology, vol. 438, no. 5, pp. 628–634, 1999.

Llado I, Estrany ME, Rodriguez E, Amengual B, Roca P, Palou A, “Effects of cafeteria diet feeding on β3-adrenoceptor expression and lipolytic activity in white adipose tissue of male and female rats,” International Journal of Obesity, vol. 24, no. 11, pp. 1396–1404, 2000.

22 Kamalakkanan S, Rajendran R, Venkatesh V, Clayton P, Akbarsha AK, ‘Effects of Caralluma fimbriata Extract on 3T3-L1 pre-adipocyte cell division.’ 2011b, Food & Nutrition Sciences 2:329-336.

Dutt HC, Singh S, Avula B, Khan IA, Bedi YS. Pharmacological review of Caralluma R.Br. with special reference to appetite suppression and anti-obesity. J Med Food. 2012 Feb;15(2):108-19.

Healthco

395 S. Glen Ellyn Rd. Bloomingdale, IL 60108 Phone: (630) 545-9095 Email: info@healthco-intl.com

Resolving Vitamin B12 Deficiency Using Oral Supplementation With NOW Foods Methyl B-12 5,000 mcg Lozenges

By: L.G. Ber, MD, and R.L. Sharpee, PhD

Vitamin B12 (often referred to as cobalamin) is an essential nutrient that can only be obtained from diet or supplements. Cobalamin, in conjunction with folate, plays a critical role in DNA synthesis and neurological function. Cobalamin deficiency can therefore lead to a wide spectrum of blood related (e.g., macrocytic anemia) and neurologic symptoms (e.g., depression, memory loss, confusion and tingling in the extremities) that can be easily reversed by early diagnosis and treatment.

The true prevalence of vitamin B12 deficiency is unknown; however, the incidence appears to increase with age, with an estimated 15 percent of people over 65 having low serum cobalamin.1 Because the normal body stores of cobalamin are significant (2,000 to 5,000 mcg, mostly in the liver), it takes years to develop symptoms of deficiency. The signs are often non-specific and might be hard to recognize unless B12 levels are measured directly in the blood.2

Because cobalamin absorption requires robust digestion and intact production of Intrinsic Factor (IF) in the stomach, the elderly are more likely to develop deficiency due to dwindling digestive function combined with limited consumption of meat (the main dietary source). Gastric juices enable extraction of cobalamin from food and IF binds with extracted cobalamin for further absorption in the small intestine. Eventually, body reserves of cobalamin are depleted and symptoms of deficiency emerge. Because dietary vitamin B12 is found almost exclusively in food of animal origin, vegetarians also have a significant risk of becoming cobalamin-depleted.

After B12 Deficiency Diagnosis

Traditionally, physicians have administered vitamin B12 injections to bypass the digestive tract, but current clinical research conducted with high-dose oral vitamin B12 supplementation challenges the traditional practice of injections.

Since the discovery of its critical role in cobalamin absorption, the IF-dependent pathway has been understood to be the sole mechanism by which vitamin B12 can cross the gastrointestinal (GI) cell membrane. It is important to understand that IF allows for absorption of only up to 3 mcg of vitamin B12 from a single meal or supplement administration.3 Since the typical multivitamin contains only about 6 mcg, and absorption from this low dose has to rely on intact IF production, oral supplementation with a typical multivitamin is not an effective way to address vitamin B12 deficiency. In contrast, a single injection can deliver 1,000 mcg of vitamin B12, which is administered once a week at first, followed by a once a month regimen for the rest of the patient’s life.

Fortunately, research has shown that vitamin B12 can be absorbed by “passive diffusion” without IF participation when administered in high doses.3 Although only about one percent of orally administered cobalamin crosses the GI cell membrane by this mechanism, the amount absorbed becomes significant as the dose of vitamin B12 increases. Because vitamin B12 has no known toxicity, very high doses can be given orally without safety concerns. Research shows that after administration of 10,000 mcg of cobalamin, about 100 mcg of vitamin B12 can be absorbed. A series of recent human bioavailability studies with 10,000 mcg vitamin B12 supports this conclusion (Unpublished, NOW Foods®, 2011-2012).

Injections or Supplementation?

The latest clinical confirmation of the effectiveness of oral vitamin B12 in the form of methylcobalamin lozenges, comes from a study conducted at ABC Wellness Clinic (Sterling Heights, MI) in collaboration with NOW Foods.4 In this clinical trial, 10 patients with newly diagnosed cobalamin deficiency were randomly assigned to receive either once a week B12 injections or daily high-dose 10,000 mcg methylcobalamin lozenge (NOW Methyl B-12, 5,000 mcg) for eight weeks. The study demonstrated that vitamin B12 lozenges were as effective as injections (see chart). All patients’ cobalamin and homocysteine levels returned to normal and their symptoms improved independent of the treatment group to which they belonged. The results strongly suggest that a high-dose daily lozenge regimen is a viable and convenient option to injections and should be used more often.

Additionally, lozenge supplementation offered a significant cost advantage as compared to injections ($35 for eight-week supplementation vs. $800 for eight-weeks of office-visit injections).

References:

1 Clarke R, Grimley Evans J, Schneede J, et al. Vitamin B12 and folate deficiency in later life. Age and Ageing. Jan 2004;33(1):334-41.

2 Spence JD, Stampfer MJ. Understanding the complexity of homocysteine lowering with vitamins: the potential role of subgroup analyses. JAMA. Dec 21 2011;306(23):2610-2611.

3 Andres E, Dali-Youcef N, Vogel T, Serraj K, Zimmer J. Oral cobalamin (vitamin B12) treatment. An update. Int J Lab Hemotal. Feb 2008;31(1):1-8.

4 Culik DA BL, Sharpee RL, Pacholok SM. Effect of Daily High-Dose Methylcobalamin Lozenge Regimen or Weekly Injections in Patients with Cobalamin Deficiency. A Single-Center Prospective Randomized Open-Label Trial. AANP 2012 Conference: ABC Wellness; NOW Foods; 2012.

InterHealth Nutraceuticals

5451 Industrial Way Benicia, CA 94510 Phone: (707) 751-2800 Fax: (707) 751-2801 Email: info@interhealthusa.com Website: www.interhealthusa.com

UC-II Offers Joint-Health Efficacy at 40 mg a Day

UC-II® for joint health is a patented undenatured type II collagen that is derived from chicken sternum cartilage. This ingredient is prepared by a patented, low-temperature, non-enzymatic manufacturing process, which ensures that the collagen remains in its native form. As such, UC-II offers a unique mechanism of action for joint health support. UC-II is an FDA-notified and published new dietary ingredient. Peer-reviewed clinical research, published in a major journal, shows that 40 mg of UC-II per day supports joint comfort, mobility and flexibility twice as effectively as 1,500 mg glucosamine plus 1,200 mg chondroitin.

Mechanism of Action

The unique functional activity of UC-II derives from the presence of natural epitopes of type II collagen fibers in the product. These epitopes are central in helping the body to modulate the breakdown of collagen. Products marketed and sold as denatured or hydrolyzed type II collagen cannot modulate the biology of collagen breakdown the way an undenatured type II collagen product can. That’s because the epitopes in UC-II remain immune-reactive, which means that they are recognized by the immune system.

Dose- and time-dependent studies conducted in simulated human gastric fluid suggest that the “active” epitopes in UC-II remain immune-reactive during their passage through the gut, thereby arriving at the small intestine in their native form where the product is taken up by Peyer’s Patches, a type of lymphoid tissue similar to the lymph node.1 Once there, UC-II goes to work with the immune system to modulate the breakdown of joint cartilage. This unique mechanism of action allows UC-II to address joint mobility and flexibility at its source. UC-II’s small serving size and once-per-day dosing regimen makes it the ideal ingredient for joint health when used singularly or synergistically with other joint-health ingredients.

Published Research

A daily dose of 40 mg of UC-II was more than twice as effective as 1,500 mg of glucosamine + 1,200 mg of chondroitin in promoting joint health. The randomized, double-blind, clinical study was conducted in North America on 52 people with osteoarthritis of the knee. UC-II significantly promoted joint comfort and mobility compared to baseline and outperformed glucosamine + chondroitin using three different assessment tools: WOMAC, VAS and Lequesne functional index.

• Reduced WOMAC score by 33 percent compared to 14 percent with glucosamine + chondroitin

• Reduced VAS score by 40 percent compared to 15 percent with glucosamine + chondroitin

• Reduced Lequesne score by 20 percent compared to six percent with glucosamine + chondroitin

UC-II significantly decreased pain during certain daily activities, including walking on flat surface, performing heavy domestic duties, walking up and down stairs and while resting in bed compared to glucosamine + chondroitin.2

Safe, Regulatory Friendly Ingredient

UC-II is an FDA-notified and published new dietary ingredient (NDI) and is a non-novel food in the E.U. A comprehensive safety profile on UC-II has been established demonstrating a wide margin of safety for human consumption based on an array of toxicological studies.3 UC-II has been determined GRAS by one of the nation’s leading toxicology groups.

Dependable Quality

UC-II is made using a patented, low-temperature, non-enzymatic manufacturing process. A highly specific, proprietary and sensitive immunological “ELISA” assay is used to measure the presence of native type II collagen epitopes in UC-II. This extra testing ensures that this revolutionary product is bioactive. UC-II is sourced and manufactured in the U.S. in a GMP-certified facility.

To learn more about UC-II, e-mail info@interhealthusa.com or call (800) 783-4636.

* These statements have not been evaluated by the Food and Drug Administration. This product is not intended to diagnose, treat, cure or prevent any disease.

References:

1 Bagchi D, Misner B, Bagchi M, et al. Effects of orally administered undenatured type II collagen against arthritic inflammatory diseases: a mechanistic exploration. Int J Clin Pharm Res., 2002;22:101-110.

2 Crowley DC, Lau FC, Sharma P, et al. Safety and efficacy of undenatured type II collagen in the treatment of osteoarthritis of the knee: a clinical trial. Int J Med Sci., 2009;6:312-321.

3 Marone PA, Lau FC, Gupta RC, Bagchi M, Bagchi D. Safety and toxicological evaluation of undenatured type II collagen. Toxicol Mech Meth. 2010;20:175-189.

Lallemand Health Solutions

19 rue des Briquetiers BP59 31702 Blagnac Cedex, France Phone : +33 5 62 74 55 55 • Fax: +33 5 62 74 55 00 Email: healthsolutions@lallemand.com Website: www.lallemand-health-solutions.com

Designer’s Probiotic Supplements

Due to their very nature (live microorganisms), probiotic yeast and bacteria are not like any other ingredients and their formulation requires specific technological and microbiological know-how to ensure their viability, hence optimal efficacy when delivered to the consumer. This is why probiotic formulation is an art and science, and the selection of the strain(s), even though a key step, is not sufficient to ensure quality and stability of the finished supplements: manufacturing processes—from fermentation to freeze-drying and blending, as well as the interaction with other ingredients of the formula—should all be taken into account.

When Choosing a Probiotic Strain

The first point to consider when developing new probiotic formula is the choice of the manufacturer and the strain(s) according to the desired positioning. Attention should be drawn to the documentation provided by the manufacturer about its strains properties and ingredients.

A probiotic strain product should be:

• Characterized. At Lallemand, for example, microscopic procedures, metabolic profiling and advanced genetic techniques are systematically performed to determine strain identity.

• Safe. Safety for the consumer and the environment: absence of antibiotic resistance gene or transposable genetic material, for example.

• Alive. It should survive processing, storage and digestion. Not all strains are equal with regard to gastric acidity survival (Fig. 1). In case of poor acidic resistance of a strain, enteric coating can be suggested. For example, the STAR® technology protects the probiotic against gastric acidity. Another technological aid that can be considered, in particular for drastic processing conditions or to allow for versatile formulations, is probiotic specific microencapsulation technology (e.g. Probiocap®).

• Effective. Specific health benefits and modes of action should be documented.

Moreover, it is important to select the product from a reputable provider with high quality standard assurance. The purity (absence of chemical and microbiological contaminants) is particularly important.

Single or Multiple Strains Formula?

Beyond the trends, there are some pros and cons to consider for both single- or multiple-strain products. The arguments are numerous for a multi-strain option:

• The intestinal microflora contains 1,000 different bacterial species and numerous stains.

• Different microbes reside in different intestinal tract niches, thus the association of several species can have an effect at various levels along the gut, while a single strain cannot reside in all niches (e.g. lactobacilli and bifidobacteria).

• Probiotic strains exert multiple modes of action; the association of various strains can have a synergistic effect.

However, all strains are not always compatible with each other, and some even exert contradictory effects; some strains are more stable than others. Moreover, too many strains used in the same formulation can make it difficult for the bacteria to stabilize. Thus, it is crucial to find the right balance when formulating a multiple-strain product and to rely on the manufacturers know-how to ensure the stability of the finished product.

Which Health Benefits?

Then, when selecting probiotic strain(s) for a target indication, pre-clinical and clinical data, when available, should be carefully compared. Certain strains show complementary modes of action or effects and their combination can help offer optimal efficacy for one specific indication or even multiple benefits for a more generic indication (e.g. ‘digestive health’). Table 1 summarizes the documented health benefits demonstrated for some of Lallemand registered strains. It is important to note that all these strains are compatible with one another.

Compatible Health Ingredients for Added Benefits

For optimal health benefits or for marketing purposes, certain manufacturers can choose to add other health ingredients to their probiotic formula, (ex. prebiotics, vitamins or minerals).

However, when probiotic strains are combined with other ingredients, it is necessary to ensure that these ingredients will not affect the viability of the probiotic and the product stability over time. Lallemand conducts research programs to verify the compatibility of its strains with several ingredients. Most of the companies’ strains have been tested for compatibility with many vitamins and minerals from the Lalmin® range of yeast based bioavailable mineral and vitamins (selenium, vitamin D, etc.) as well as some other key ingredients: cranberry, inulin, omega-3. In several cases, real-time stability studies are also conducted at room temperature to verify this compatibility over time.

References:

Bisson J.F., Hidalgo S., Rozan P., Messaoudi M. Preventive Effects of Different Probiotic Formulations on Travelers’ Diarrhea Model in Wistar Rats. Dig Dis Sci, 2009.

Cazzola M, Pham-Thi N, Kerihuel JC, Durand H, Bohbot S. Efficacy of a synbiotic supplementation in the prevention of common winter diseases in children: a randomized, double-blind, placebo-controlled pilot study. Ther Adv Respir Dis. 2010 Oct;4(5):271-8.

Cazzola M, Tompkins TA, Matera MG. Immunomodulatory impact of a synbiotic in T(h)1 and T(h)2 models of infection. Ther Adv Respir Dis. 2010 Oct;4(5):259-70.

Foster, L.M., Tompkins,T.A. and Dahl, W.J. A comprehensive post-market review of studies on a probiotic product containing Lactobacillus helveticus R0052 and Lactobacillus rhamnosus R0011. Beneficial Microbes, December 2011; 2(4): 319-334

P. Tláskal, A. Kokešová, J. Schramlová, H. Tlaskalová-Hogenová, J. Adamus, D. Bubáková, N. Kocnarová, K. Kopecký, M. Mucková, J. Pacovská, E. Sládková. Probiotics and Metabolites of Intestinal Bacteria in Treatment of Diarrheal Disease of Viral Etiology in Children. 2005.

P. Tláskal, J. Schramlová, A. Kokesová, J.  Adamus, D. Bubáková, N. Kocnarová, K. Kopecka, M. Mucková, J. Pacovská, E. Sládková. Probiotics in the treatment of diarrhoael disease of children. NAFAS, December 2005. VOL 3, N°6.

R L Clancy, M Gleeson, A Cox, R Callister, M Dorrington, C D’Este, G Pang, D Pyne, P Fricker, A Henriksson. Reversal in fatigued athletes of a defect in interferon secretion after administration of Lactobacillus acidophilus. Br J Sports Med 2006;000:1–5.

S. Elahi, G. Pang, R. Ashman and R. Clancy. Enhanced clearance of Candida albicans from the oral cavities of mice following oral administration of Lactobacillus acidophilus. British Society for Immunology, Clinical and Experimental Immunology, 2005, 29–36.

T. A. Tompkinsa, X. Xub, J. Ahmarani. A Comprehensive Review of Post-Market Clinical Studies Performed in Adults with an Asian Probiotic Formulation. Beneficial Microbes, 2010; 1(1): 93-106.

Nutrition 21, LLC.

3 Manhattanville Rd. Purchase, NY 10577 Phone: (914) 701-4500 Fax: (914) 696-0860 Email: info@nutrition21.com Website: www.nutrition21.com

The Proven Benefits of Chromax Chromium Picolinate

Nutrition 21’s Chromax® chromium picolinate is a high-purity, cGMP-grade chromium picolinate, available for use within the U.S., E.U., Canada, China and other global markets. Chromax chromium picolinate uses and combinations are covered by more than 20 active and pending patents. Fifty-three human clinical studies involving more than 2,300 subjects make Chromax chromium picolinate the most extensively studied chromium compound commercially available. Forty of the studies were conducted using double-blind, placebo-controlled design to ensure the quality and reliability of the results. These studies provide a comprehensive body of data that empirically evidences the many ways Chromax supplementation can safely support health.

For more than a decade, Chromax chromium picolinate has been affirmed as generally recognized as safe (GRAS) for use in nutritional bars and beverage products. It is one of only a handful of marketed ingredients to have secured this. Chromax is easy to use in food and beverage products. It is used in very low dosages and doesn’t require formulation rebalancing. It is extremely stable and is resistant to breaking down when exposed to common, high temperature processing methods. Chromax does not impart off-flavors, nor does it react with other ingredients.

Years of study have revealed that chromium is a potentiator of the insulin receptor.1 Primarily, insulin acts to regulate uptake of glucose from the blood2; thus Chromax clinical studies with 707 study subjects with diabetes demonstrate its beneficial effects on glucose. Studies that look at individuals whose blood glucose is in the normal range, showed healthy blood glucose levels remain healthy. The ability of Chromax to maintain healthy blood glucose levels is an advantage over other products that can lower normal level blood sugar to harmful hypoglycemic levels.3

Chromax has also shown positive results in body composition as losses in fat mass are accompanied by gains in lean body mass.4 In a double-blind, placebo-controlled study published in 2008, obese subjects on Chromax supplementation reported lowered cravings for fat and carbohydrates as they reduced caloric intake.5 This is especially valuable for dieters, as reduction in caloric intake generally results in intense cravings that make it difficult to continue the reduced diet, often stifling or reversing weight loss.5

The brain is a large consumer of glucose, supporting neurological activity. Single-blind case reports were published detailing the effects of chromium picolinate on mood.6,7 These patients also reported improvements in energy level and attention.

Studies have examined the link between diabetes and insulin resistance to Alzheimer’s and cognitive decline.8 In 2010, Krikorian et al. published a study on the effects of Chromax in subjects with age-related mild cognitive impairment. The Chromax subjects experienced higher accuracy in learning and recall tasks. In addition to enhanced cognitive inhibitory control, a subset of subjects was evaluated by functional magnetic resonance imaging. Interestingly, the Chromax group showed significant increases in cerebral activation during memory tasks compared to no changes in the placebo group, which corroborates the results of enhanced inhibitory control from the memory assessments.8

Chromax has proven to provide benefits for many different aspects of human health. Nutrition 21 supplies Chromax to leading manufacturers marketing products designed to help support consumer’s dietary and nutritional needs. With a commitment to high-quality research, Nutrition 21 continues to ask and answer the questions of uses, mechanisms and applications of Chromax chromium picolinate.

To learn more about Nutrition 21 and its Chromax chromium picolinate, visit www.nutrition21.com.

References:

1 Albarracin et al., Diab Metab Res Rev, (24) 2008, 41-51.

2 Juturu et al., Trace Elem and Electrol, 23 (1) 2006, 66-72.

3 Singer and Geohas, Diab Tech & Ther, 8(6) 2006, 636-43.

4 Trent and Thieding-Cancel, J Sports Med Phys Fit, (35) 1995, 273-80.

5 Anton et al, Diab Technol Ther, 10 (5) 2008, 405-12.

6 McLeod et al., J Clin Psych, (60) 1999, 237-40.

7 McLeod and Golden, Int J Neuro, (3) 2000, 311-14.

8 Krikorian et al., Nutr Neurosci, 13 (3) 2010, 116-22.

OmniActive Health Technologies

67 East Park Pl., Ste. 500 Morristown, NJ 07960 Phone: (866) LUTEMAX (588-3629) Fax: (877) LUTEMAX (588-3629) Email: info@omniactives.com Website: www.omniactives.com

Focus on Lutemax 2020

To preserve healthy vision for a lifetime and prevent the loss of vision in the elderly, it is important to start caring about eye health at a younger age.

Vision loss contributes to daily living difficulties: risk of falling, serious accidents, premature death, nursing home admissions and depression.1 By 2030, serious ocular disease may affect most seniors and consume approximately 50 percent of the health care budget for the elderly.2 Quality of life drops dramatically with poor vision, coupled with mounting dependencies on others.

Fortunately, most visual impairment is preventable, according to the World Health Organization.3 One well recognized intervention is lutein and zeaxanthin, which are yellow carotenoids abundant in fruits and vegetables. The ratio of lutein to zeaxanthin is approximately 5:1 in the diet4-8 and in blood.9 Lutein and zeaxanthin isomers are actively transported to the retina10 to form the macular pigment. As the only carotenoids present in the retina and lens, they help protect the eyes from oxidative stress.11,12 The macular pigment works like internal sunglasses to filter out solar radiation13 and neutralize free radicals.14

A wealth of research supports the role of lutein and zeaxanthin in protecting vision.15,16 The macular pigment protects against photo-oxidation from ultraviolet (UV) radiation and high-energy blue light.17-20 Supplementation with lutein- and zeaxanthin can enrich the macular pigment, whereas high doses of standard lutein oil suspension may not.21-26 A staggering 70 percent of adults do not eat the lutein and zeaxanthin-rich vegetables, fruits and other carotenoid-packed foods needed to maintain healthy vision, and may benefit from supplementation.26

Macular pigment is associated with clear vision, and helps prevent age-related macular degeneration (AMD), a disease characterized by progressive loss of central vision. AMD is the leading cause of blindness in the U.S., affecting approximately 15 million people.27 One study conducted in 1994 showed a significantly reduced risk of AMD at intakes of ~6 mg lutein daily.28 Many studies have since supported the role of lutein and zeaxanthin for eye health.16,29,30 Low levels of lutein and zeaxanthin in the macula are associated with AMD risk.31 Conversely, higher intake is linked to improved visual function in AMD.32 Lutein and zeaxanthin supplementation increased macular pigment and helped improve visual function in AMD patients.33-35 Reduced cataract risk was also linked to lutein and zeaxanthin intakes in studies involving nearly 100,000 subjects.36-44 A National Eye Institute review concluded that lutein and zeaxanthin supplementation prevents vision loss, and could help over 300,000 people at risk in the next five years, with a health care savings of several billion.45,46 The Age-Related Eye Disease Study, a multi-center clinical trial sponsored by the National Eye Institute, is now focused on lutein and zeaxanthin and omega-3 fatty acids.47

Lutein and zeaxanthin can also improve vision.48 Supplementation in humans showed improvements in visual performance and acuity33,49 reduced glare sensitivity50, enhanced contrast sensitivity51, improved vision in dim light52 and reduced chromatic blur.53 Elderly veterans who took zeaxanthin for 12 months showed greater recognition of fine detail, improvement on the eye chart, disappearance of blind spots, and improved night driving ability.21

Regarding daily intake, the recommended lutein dose is 6-40 mg/day. While 6 mg can reduce the risk of age-related disease, higher dosages (20-40 mg) may be ideal for visual health.16 Optimal zeaxanthin intake of 2-4 mg/day requires numerous servings of fruits and vegetables. Meso-zeaxanthin is hard to obtain from food, and recommended intakes have not been established. However, many could benefit from supplementation, particularly the elderly and those prone to severe AMD.25,26,32,54,55 It may be conditionally essential under these circumstances.56

Regarding mechanism of action, lutein and zeaxanthin function by preventing peroxidation of membrane fats57 and blocking oxygen penetration into membranes.58 They can neutralize most free radicals, including singlet oxygen, superoxide, hydroxyl and peroxynitrite radicals59-61, and can increase the activity of antioxidant enzymes.12 They are even more potent than a-tocopherol for protecting the lens against UVB insult.62

Lutemax 2020® from OmniActive Health Technologies is a nutritional supplement derived from marigold flowers, and provides optimal amounts of lutein with enhanced levels of zeaxanthin. Zeaxanthin levels in Lutemax 2020 are higher than in most commercial forms. This carotenoid combination is provided due to their differential and synergistic effects on vision.16,26,34,57,58,60 Carotenoids are unstable, but OmniActive’s technologies preserve them and enhance their delivery. Lutemax 2020 has recently attained FDA-notified GRAS status, and no adverse effects were reported for lutein and zeaxanthin at very high levels for long time periods.63-65 The antioxidant combination in Lutemax 2020 may be ideal for maintaining healthy vision for the world’s population.

References:

1  AMD Alliance International. The Global economic cost of visual impairment: summary report. April 2010. http://www.amdalliance.org/cost-of-blindness.html.

2  Eichenbaum JW. Geriatric vision loss due to cataracts, macular degeneration, and glaucoma. Mt Sinai J Med 2012;79:276-94.

3  World Health Organization. Visual impairment and blindness. Fact Sheet N°282. October 2011. http://www.who.int/mediacentre/factsheets/fs282/en/.

4  Le Marchand L, Hankin JH, Bach F, et al. “An ecological study of diet and lung cancer in the South Pacific.” Int J Cancer 63 (1995): 18-23.

5  Nebeling LC, Forman MR, Graubard BI, Snyder RA. “Changes in carotenoid intake in the United States: the 1987 and 1992 National Health Interview Surveys.” J Am Diet Assoc 97 (1997): 991-6.

6  Sommerburg O, Keunen JE, Bird AC, van Kuijk FJ. “Fruits and vegetables that are sources for lutein and zeaxanthin: the macular pigment in human eyes.” Br J Ophthalmol 82 (1998): 907-10.

7  Mohamedshah F, Douglas JS, Amann MM, Heimbach JM. “Dietary intakes of lutein + zeaxanthin and total carotenoids among Americans age 50 and above.” FASEB J. [1999]: A554.

8  Thürmann PA, Schalch W, Aebischer J-C, Tenter U, Cohn W. “Plasma kinetics of lutein, zeaxanthin, and 3-dehydro-lutein after multiple oral doses of a lutein supplement.” Am J Clin Nutr 82 (2005): 88-97.

9  Chew EW, SanGiovanni JP. “Lutein.” In Encyclopedia of Dietary Supplements, by et al Coates P. New York: Marcel Dekker, Inc., 2005.

10  Britton, G. “Structure and properties of carotenoids in relation to function.” FASEB J 9 (1995): 1551-8.

11  Khachik F, Beecher GR, Smith JC. “Lutein lycopene and their oxidative metabolites in chemoprevention of cancer.” J Cell Biochem 22 (1995): 236.

12  Sindhu ER, Preethi KC, Kuttan R. “Antioxidant activity of carotenoid lutein in vitro and in vivo.” Ind J Exp Biol 48 (2010): 843-8.

13  Khachik F, Bernstein PS, Garland DL. “Identification of lutein and zeaxanthin oxidation products in human and monkey retinas.” Invest Ophthalmol Vis Sci 38 (1997): 1802-11.

14  Landrum JT, Bone RA. “Lutein, zeaxanthin, and the macular pigment.” Arch Biochem Biophys 385 (2001): 28-40.

15 Morganti P, Bruno C, Guarneri F, et al. “Role of topical and nutritional supplement to modify the oxidative stress.” Int J Cosmet Sci 24 (2002): 331-9.

16 Ma L, Dou HL, Wu YQ, et al. “Lutein and zeaxanthin intake and the risk of age-related macular degeneration: a systematic review and meta-analysis.” Br J Nutr 107 (2011): 350-9.

17 Landrum JT, Bone RA, Kilburn MD. “The macular pigment: a possible role in protection from age-related macular degeneration.” Adv Pharmacol 38 (1997): 537-56.

18  Beatty S, Boulton M, Henson D, et al. “Macular pigment and age related macular degeneration.” Br J Ophthalmol 83 (1999): 867-77.

19  Zuclich JA, Previc FH, Novar BJ, et al. “Near-UV/blue light-induced fluorescence in the human lens: potential interference with visual function.” J Biomed Opt 10 (2005): 44021.

20  Wang M, Lin X. “Protective role of lutein on light-damage of retina.” Wei Sheng Yan Jiu 37 (2008): 115-7.

21  Richer SP, Stiles W, Graham-Hoffman K, et al. “Randomized, double-blind, placebo-controlled study of zeaxanthin and visual function in patients with atrophic age-related macular degeneration: the Zeaxanthin and Visual Function Study.” Optometry 82 (2011): 667-80.

22  Trieschmann M, Beatty S, Nolan JM, et al. “Changes in macular pigment optical density and serum concentrations of its constituent carotenoids following supplemental lutein and zeaxanthin: the LUNA study.” Exp Eye Res 84 (2007): 718-28.

23  Bernstein PS, Delori FC, Richer S. “The value of measurement of macular carotenoid pigment optical densities and distributions in age-related macular degeneration and other retinal disorders.” Vision Res 50 (2010): 716–28.

24  Bone RA, Landrum JT, Cao Y, et al. “Macular pigment response to a supplement containing meso-zeaxanthin, lutein and zeaxanthin.” Nutr Metab 4 (2007): 12.

25  Connolly EE, Beatty S, Loughman J, et al. “Supplementation with all three macular carotenoids: response, stability, and safety.” Invest Ophthalmol Vis Sci 52 (2011): 9207-17.

26  Nolan JM, Akkalia MC, Loughman J. “Macular carotenoid supplementation in subjects with atypical spatial profiles of macular pigment.” Expt Eye Research, June 2012.

27  Friedman DS, O’Colmain BJ, Munoz B, et al. “Prevalence of age-related macular degeneration in the United States.” Arch Opthalmol 122 (2004): 564-72.

28  Seddon JM, Ajani UA, Sperduto RD, et al. “Dietary carotenoids, vitamins A, C, and E, and advanced age-related macular degeneration. Eye Disease Case-Control Study Group.” JAMA 272 (1994): 1413-20.

29  Guymer RH, Chong EW. “Modifiable risk factors for age-related macular degeneration.” MJA 184 (2006): 455–8.

30  Tan JS, Wang JJ, Flood V, et al. “Dietary antioxidants and the long-term incidence of age-related macular degeneration: the Blue Mountains Eye Study.” Ophthalmology 115 (2008): 334-41.

31  Snellen EL, Verbeek AL, Van den Hoogen GW, et al. “Neovascular age-related macular degeneration and its relationship to antioxidant intake.” Acta Ophthalmol Scand 80 (2002): 368-71.

32  Krinsky NI, Landrum JT, Bone RA. “Biological mechanisms of the protective role of lutein and zeaxanthin in the eye.” Annu Rev Nutr 23 (2003): 171–201.

33  Richer S, Stiles W, Statkute L, et al. “Double-masked, placebo-controlled, randomized trial of lutein and antioxidant supplementation in the intervention of atrophic age-related macular degeneration: The Veterans LAST study (Lutein Antioxidant Supplementation Trial).” Optometry 75 (2004): 216-30.

34  Richer S, Devenport J, Lang JC. “LAST II: Differential temporal responses of macular pigment optical density in patients with atrophic age-related macular degeneration to dietary supplementation with xanthophylls.” Optometry 78 (2007): 213-9.

35  Parisi V, Tedeschi M, Gallinaro G, et al. “Carotenoids and antioxidants in age-related maculopathy Italian study: Multifocal electroretinogram modifications after 1 year.” Ophthalmol 115 (2008): 324-33.

36  Brown L, Rimm EB, Seddon JM, et al. “A prospective study of carotenoid intake and risk of cataract extraction in US men.” Am J Clin Nutr 70 (1999): 517-24.

37  Chasan-Taber L, Willett WC, Seddon JM, et al. “A prospective study of carotenoid and vitamin A intakes and risk of cataract extraction in US women.” Am J Clin Nutr 70 (1999): 509-16.

38  Delcourt C, Carrière I, Delage M, et al. “Plasma lutein and zeaxanthin and other carotenoids as modifiable risk factors for age-related maculopathy and cataract: the POLA Study.” Invest Ophthalmol Vis Sci 47 (2006): 2329-35.

39  Javitt JC, Wang F, West SK. “Blindness due to cataract: epidemiology and prevention.” Ann Rev Public Health 17 (1996): 159-77.

40  Lyle BJ, Mares-Perlman JA, Klein BE, et al. “Antioxidant intake and risk of incident age-related nuclear cataracts in the Beaver Dam Eye Study.” Am J Epidemiol 149 (1999): 801-9.

41  Vu HT, Robman L, McCarty CA, et al. “Does dietary lutein and zeaxanthin increase the risk of age related macular degeneration? The Melbourne Visual Impairment Project.” Br J Ophthalmol 90 (2006): 389-90.

42  Moeller SM, Voland R, Tinker L, et al. “Associations between age-related nuclear cataract and lutein and zeaxanthin in the diet and serum in the carotenoids in the Age-Related Eye Disease Study (CAREDS), an ancillary study of the Women’s Health Initiative.” Arch Ophthalmol 126 (2008): 354-64.

43  Christen WG, Liu S, Glynn RJ, et al. “Dietary carotenoids, vitamin C and E, and risk of cataract in women.” Arch Ophthalmol 126 (2008): 102-9.

44  Karppi J, Laukkanen JA, Kurl S. “Plasma lutein and zeaxanthin and the risk of age-related nuclear cataract among the elderly Finnish population.” Br J Nutr Oct 18 (2011): 1-7.

45  Dietary Supplement Education Alliance. New Study Shows Dietary Supplement Usage Could Save $24+ Billion in Healthcare Costs . Jan 2007. http://www.nutraceuticalsworld.com/issues/2007-06/view_industry-news/.

46  National Eye Institute. Age-Related Macular Degeneration. 2006. http://www.nei.nih.gov/ health/ maculardegen/armd_facts.asp#2b (accessed March 2012).

47  Age-Related Eye Disease Study 2. The Lutein/Zeaxanthin and Omega-3 Supplementation Trial. 2009. http://www.areds2.org/ (accessed March 19, 2012).

48  Bartlett H, Eperjesi F. “Dietary analysis and patterns of nutritional supplement use in normal and age-related macular disease affected subjects: A prospective cross-sectional study.” Nutr J 3 (2004): 16.

49  Olmedilla B, Granado F, Blanco I, et al. “Lutein, but not alpha-tocopherol, supplementation improves visual function in patients with age-related cataracts: a 2-y double-blind, placebo-controlled pilot study.” Nutr 19 (2003): 21-4.

50  Stringham JM, Hammond BR. “Macular pigment and visual performance under glare conditions.” Optom Vis Sci 85 (2008): 82-8.

51  Renzi LM, Hammond BR. “The effect of macular pigment on heterochromatic luminance contrast.” Exp Eye Res 91 (2010): 896-900.

52  Kvansakul J, Rodriguez-Carmona M, Edgar DF, et al. “Supplementation with the carotenoids lutein or zeaxanthin improves human visual performance.” Ophthalmic Physiol Opt 26 (2006): 362-71.

53  Rodriguez-Carmona M, Kvansakul J, Harlow JA, et al. “The effects of supplementation with lutein and/or zeaxanthin on human macular pigment density and colour vision.” Ophthalmic Physiol Opt 26 (2006): 137-47.

54  Bone RA, Landrum JT, Dixon Z, et al. “Lutein and zeaxanthin in the eyes, serum, and diet of human subjects.” Exp Eye Res 71 (2000): 239-45.

55  Sabour-Pickett S, Nolan JM, Loughman J. “A review of the evidence germane to the putative protective role of the macular carotenoids for age-related macular degeneration.” Mol Nutr Food Res, Nov 2011.

56  Semba RD, Dagnelie G. “Are lutein and zeaxanthin conditionally essential nutrients for eye health?” Med Hypotheses 61 (2003): 465-72.

57  Sujak A, Gabrielska J, Grudziński W, et al. “Lutein and zeaxanthin as protectors of lipid membranes against oxidative damage: the structural aspects.” Arch Biochem Biophys 371 (1999): 301-7.

58  Subczynski WK, Markowska E, Sielewiesiuk J. “Effect of polar carotenoids on the oxygen diffusion-concentration product in lipid bilayers. An EPR spin label study.” Biochim Biophys Acta 1068 (1991): 68-72.

59  Boileau TWM, Moore AC, Erdman JW. “Carotenoids and vitamin A in human health.” In Antioxidant status, diet, nutrition, and health, by Papas AM, 133-58. Boca Raton, FL: CRC Press, 1999.

60  Trevithick-Sutton CC, Foote CS, Collins M, et al. “The retinal carotenoids zeaxanthin and lutein scavenge superoxide and hydroxyl radicals: A chemiluminescence and ESR study.” Mol Vis 12 (2006): 1127-35.

61  Li B, Ahmed F, Bernstein PS. “Studies on the singlet oxygen scavenging mechanism of human macular pigment.” Arch Biochem Biophys 504 (2010): 56-60.

62  Chitchumroonchokchai C, Bomser JA, Glamm JE, Failla ML. “Xanthophylls and a-tocopherol decrease UVB-induced lipid peroxidation and stress signaling in human lens epithelial cells.” J Nutr 134 (2004): 3225-32.

63  JECFA. “Joint FAO/WHO Expert Committee on Food Additives.” Sixty-third meeting. Geneva, 2004.

64  Harikumar KB, Nimita CV, Preethi KC, et al. “Toxicity profile of lutein and lutein ester isolated from marigold flowers (Tagetes erecta).” Int J Toxicol 27 (2008 ): 1-9.

65  Ravikrishnan R, Rusia S, Ilamurugan G, et al. “Safety assessment of lutein and zeaxanthin (Lutemax 2020): subchronic toxicity and mutagenicity studies.” Food Chem Toxicol 49 (2011): 2841-8.

P.L. Thomas

119 Headquarters Plaza Morristown, NJ 07960 Phone: (973) 984-0900 Fax: (973) 984-5666 Email: info@plthomas.com Website: www.plthomas.com

Zembrin for Improved Cognitive Flexibility, Executive Function, Mood and Quality of Sleep

Zembrin is the trade name for the proprietary standardized plant extract of Sceletium tortuosum, one of the most important functional food plants utilized by South African Nama nomads, the descendants of original “hunters and gatherers” the San people, also known as the Bushmen.

Sceletium tortuosum, a succulent, is endemic to the arid Namaqualand and Karoo areas of South Africa, and has been successfully selected and cultivated as a new commercial crop for the production of Zembrin by HG&H Pharmaceuticals with the full backing of the South African government, who awarded HG&H Pharmaceuticals South Africa’s first ever export and bioprospecting permit. The contribution of the San’s ancient indigenous knowledge to the research and development of Zembrin has been recognized through Africa’s first prior informed consent benefit-sharing agreement.1

Recently published scientific research2 indicates that traditional benefits of Zembrin may be due to one of the most sought after mechanisms of action in neuropharmacology: phosphodiesterase inhibition (PDE-4 inhibition). PDE-4 inhibitors like Zembrin augment intracellular secondary messenger signaling in brain cells. PDE-4 inhibitors prevent the breakdown of the key intracellular secondary messenger, cyclic AMP (cAMP), which is intimately involved in modulating multiple molecular processes involved in cognitive function, mood, and in inflammation.3

To date, the clinical application of synthetic pharmaceutical PDE-4 inhibitors in mood and neurodegenerative disorders have met with limited success because of unwanted side effects, most notably nausea and vomiting. Zembrin, however, has been shown in a clinical safety and tolerability study in 36 healthy adults for three months to be very well tolerated.4

Zembrin has been clinically studied for efficacy in healthy people in a sophisticated double-blind, placebo-controlled, cross-over clinical study. The principal investigator was Dr. Simon Chiu at the Department of Psychiatry at the University of Western Ontario in London, ON, Canada. The objective of the study was to evaluate 25 mg Zembrin taken daily as a putative PDE-4 inhibitor using the CNS Vital Signs computerized testing of cognitive function domains, and effect on mood using the Hamilton Depression score (HAM-D). The 20 healthy adults (mean age of 54.6 +/-6.0 years) were give either placebo or 25 mg Zembrin once a day for three weeks, then given a three-week washout period, which was followed by a switch with a further three weeks of either Zembrin or placebo. The 20 healthy subjects tolerated Zembrin very well with no nausea or vomiting. Compared to placebo, Zembrin at 25 mg per day selectively and significantly improved two key cognitive function domains: cognitive set flexibility (CNS VitalSign score improved from 44.7 to 57.0 p<0.003) and executive function (CNS VitalSign score improved from 45.9 to 57.5 p<0.002). Both of these functions are compromised by stress. Cognitive flexibility is the ability to shift attention between two or more tasks, and the ability to adapt to rapidly changing directions. This ability is necessary in decision-making, impulse control and strategy formation. Executive function is the ability to exercise initiative, sound judgement, discipline and to work in favor of an abstract reward. In practical terms, executive function is the ability to exercise goal-directed behavior and to take action.

Despite the fact that the baseline HAM-D score was small since the study was performed on non-depressed healthy subjects, the change in HAM-D was greater for the 25 mg Zembrin group compared with the change in the placebo group. The quality of sleep of the 25 mg Zembrin group also improved compared to that of the placebo group.

The findings of statistically significant changes in healthy mature subjects in cognitive flexibility and executive function provide the first supporting clinical evidence of PDE-4 modulation for Zembrin, a compelling finding with multiple potential applications, including in enhancing cognitive function during stress in healthy people, improving cognitive decline in the elderly, and treating neurodegenerative disorders and mood-related conditions.

The clinical study has been presented by Chiu at the Natural Bioactives International Conference July 9-12, 2012 in London, ON, Canada. The abstract of the study has been accepted for the World Psychiatric Association International Congress, Prague Congress Center, Czech Republic, October 17-21, 2012, and the full study is currently being written up for publication in a peer-reviewed journal.

References:

1 Harvey, A.L. & Gericke, N. 2011. Bioprospecting: Creating a Value for Biodiverity. In: Pavlinov, I.Y. (Ed.) 2011. Research in Biodiversity – Models and Applications. InTech.

2 Harvey, et al. 2011. Pharmacological actions of the South African medicinal and functional food plant Sceletium tortuosum and its principal alkaloids. Journal of Ethnopharmacology, 137: 1124-1129.

3 Schmidt, C.J. 2010. Phosphodiesterase inhibitors as potential cognition enhancing agents. Current Topics in Medicinal Chemistry,Vol. 12 No.2. pp. 222-230.

4 Nel, H. et al.2012. A randomised double-blind, parallel group, placebo-controlled trial of extract Sceletium tortuosum (Zembrin) in healthy adults. Submitted for publication to Journal of Alternative and Complementary Medicine.

Sabinsa Corporation

20 Lake Dr. East Windsor, NJ 08520 Phone: (732) 777-1111 Fax: (732) 777-1443 Email: info@sabinsa.com Website: www.sabinsa.com

Curcumin’s Powerful Proven Capabilities

Turmeric is one the most revered plants in ayurveda. It is well documented in ayurveda for its protective activity against various health ailments. With growing scientific evidences, the interest in health benefits of turmeric has grown several folds. It will not be wrong to say that in recent past, turmeric has been one of the most researched herbs. Numerous health benefits of curcuminoids, the active molecules present in turmeric rhizomes, have caught the interest of researchers and clinicians likewise.

Curcumin is naturally present along with two other compounds in the turmeric rhizomes—demethoxycurcumin and bisdemethoxycurcumin. These two minor components of turmeric rhizome play a very important role by exerting the stabilizing effect on curcumin.1 An optimized composition containing all the three curcuminoids has been described in U.S. patent 5861,415 assigned to Sabinsa for its brand Curcumin C3 Complex®.2

Curcumin is known to be a strong antioxidant and liver protectant compound, but with the role of curcumin so evident in reducing the inflammation, its use is now explored in various health conditions such as Alzheimer’s disease, arthritis, diabetes, rhinitis, gingivitis, bronchitis and various cancers.

Clinical evidences have shown a wide range of health benefits from curcumin. A recent study in Iran3 shows benefits of curcumin in obese patients. The study, which was carried out with a dosage of 1 g curcumin, showed significant reduction in serum triglyceride concentrations in obese patients in the study period of 30 days. This antihypertriglyceridemic activity of curcumin can be helpful for obese and diabetic people alike. The curcumin brand Curcumin C3 Complex used in this study was from Sabinsa Corporation. Curcumin C3 Complex is self-affirmed GRAS (generally recognized as safe) product, which can be also added in functional food.

A majority of curcumin research today has been focused on its anti-inflammatory activity, which can play an extremely important role in reducing the growth of cancer and even reversing it. Studies on the anti-cancer effects of curcumin are being carried out around the world in prestigious institutions such as MD Anderson Cancer Center. In one such study on pancreatic cancer patients done at MD Anderson Cancer Center4, the researchers found that curcuminoids were well tolerated in pancreatic cancer patients and also showed biological efficacy in some patients. Results reported in the study showed curcumin significantly lowered expression of disease biomarkers NF-Kappa B and COX-2. Pancreatic cancer remains one of the most fatal and short prognosis cancers, with few available treatments for the disease. Sabinsa’s Curcumin C3 Complex was used in this study.

Curcumin is not known to be a very bioavailable product and several attempts have been made to enhance its bioavailability. BioPerine, a piperine extract from Sabinsa, has been clinically studied to enhance the bioavailability of curcuminoids. BioPerine is a self-affirmed GRAS ingredient from Sabinsa Corporation. In a clinical study recently conducted by Tuft University School of Medicine, Boston, MA5, found that the combination of piperine and curcumin is unlikely to cause a clinically significant interaction with drugs such as acetaminophen, Flurbiprofen and Midazolam. Thus, bioavailability of curcumin can be safely enhanced by use of piperine.

References:

1 Han G, et al. Zhongguo Zhong Yao Za Zhi, 2008. 33(22): 2611-4.

2 U.S. Patent 5,861,415 Bioprotectant composition, method of use and extraction process of curcuminoids.

3 A. Mohammadi, et al. (2012) Phytother Res, (epub ahead of print).

4 N. Dhillon, et al. Clin Cancer Res, 2008; 14(14); 4491-99.

5 LP Volak, et al. Br J Clin Pharmacol, 2012 (Epub ahead of print).
Specialty Enzymes & Biotechnologies

13591 Yorba Ave. Chino, CA 91710 Phone: (909) 613-1660 • Fax: (909) 613-1663 Email: adm@specialtyenzymes.com Website: www.specialtyenzymes.com

Peptizyme SP (aka Serratiopeptidase, Serrapeptase & Serrapeptidase)

Peptizyme® SP is a proteolytic enzyme variously called serrapeptase, serrapeptidase, serratiopeptidase and serratia peptidase. It is isolated from the microorganism Serratia marcescens, which originally came from the intestine of silkworms. This enzyme enables the emerging moth to dissolve its fibrous cocoon. Today, of course, it is grown in the laboratory. Peptizyme SP is also available as Peptizyme® SP EN, the enterically coated version and preferred form of this remarkable proteolytic enzyme.

In human nutrition, Peptizyme SP is classified as a systemic enzyme. That is, one absorbed directly from intestine into the blood stream. Research confirms that orally administered serrapeptase is absorbed into the circulation in its enzymatically active form.1 Serra-peptase has numerous beneficial properties, and by reviewing the scientific literature, we can gain an appreciation for some of them.

Fibrinolytic Activity

Like other proteases, serrapeptase has potent anti-inflammatory activity as well as several other beneficial properties. However, probably the most important aspect of serrapeptase is its fibrinolytic activity. It is this fibrinolytic activity that is of particular interest to clinicians and nutritionists. To understand fibrinolytic activity, first one must understand the basic process of coagulation or clotting of blood. In damaged tissue, the broken blood vessel releases a compound called thromboplastin. At the same time platelets adhere to the broken edges of the vessel and disintegrate, releasing platelet factor 3. Both of these react with protein factors and calcium ions to form prothrombin activator. Once the prothrombin activator is formed, the process goes from prothrombin to fibrin and finally a clot follows.2

Blood clots (thrombi) form when strands of fibrin accumulate in the circulatory system. These clots can cause blockage of blood flow. If blood flow is blocked, the oxygen supply to that tissue is cut off and it eventually dies. In the heart, this can result in myocardial infarction (heart attack). In the brain, it can result in strokes or mini-strokes. Deep vein thrombosis can result in pulmonary emboli. All these events can be life threatening. Of course, clotting forms an important function in tissue repair. However, improper buildup of fibrin in the circulatory system becomes a significant risk factor for cardiovascular disease.

Diverse Anti-Inflammatory and/or Pain Research

Researchers conducted a study to assess the response of serrapeptase in patients with carpal tunnel syndrome (CTS) with very good results. They wanted to determine if a conservative, non-surgical approach would be beneficial.3

Another study was conducted comparing the efficacy of two proteolytic enzymes in the treatment of venous inflammatory disease serrapeptase was shown along with another enzyme to be statistically effective.4

A clinical evaluation of serrapeptase was conducted to determine its efficacy in reducing inflammation in patients with breast engorgement. Serrapeptase was noted to be superior for improvement of breast pain, breast swelling. No adverse reactions were reported with the use of serrapeptase.5

A prospective study was conducted on the effect of serrapeptase on post-operative swelling and pain of the ankle. In the serrapeptase group, the swelling decreased by 50 percent on the third post-operative day, while in the control groups (no treatment and treatment with ice) no reduction in swelling occurred.6 A clinical evaluation was conducted in men with amicrobial prostato-vesiculitis (APV), a non-infectious inflammation of the prostate). The researchers wanted to determine if treatment with nonsteroidal anti-inflammatories (NSAIDS), including serrapeptase, could reduce inflammation and swelling of the prostate. The doctors conclude that in APV patients, the treatment with NSAIDS, including serrapeptase is an effective therapy, producing multiple positive effects.7

The efficacy of serrapeptase was evaluated in a multi-centre, double-blind, placebo-controlled study of 193 subjects suffering from acute or chronic ear, nose or throat disorders. It was concluded that serrapeptase has significant anti-inflammatory, anti-edemic and fibrinolytic activity and acts rapidly on localized inflammation.8

Other Applications Research

Research has demonstrated the mucolytic activity of serrapeptase (reduction is viscosity) in chronic airway disease and chronic sinusitis. The researchers concluded serrapeptase may exert a beneficial effect on mucus clearance by reducing viscosity of sputum in patients with chronic airway diseases.9-11

The potential applications for Peptizyme SP and Peptizyme SP EN are many and varied. Whether the application is fibrinolytic, anti-inflammatory, mucolytic and possibly analgesic, as well as others, Peptizyme SP, whether used by itself or in combination with other enzymes, is the cutting edge in systemic enzyme therapy.

References:

1 Moriya N,Nakata M, et al. Intestinal absorption of serrapeptase in rats. Biotechnol Appl Biochem. 1994 Aug;20 ( Pt 1):101-8.

2 Guyton, A. Function of the Human Body. WB Saunders pp. 83-84.

3 Malshe PC. A preliminary trial of serratiopeptidase in patients with carpal tunnel Syndrome. J Assoc Physicians India, 2000, 48(11):1130

4 Bracale G,Selvetella L. Clinical study of the efficacy of and tolerance to seaprose S in inflammatory venous disease. Controlled study versus serratio-peptidase. Minerva Cardioangiol. 1996 Oct;44(10):515-24.

5 Kee WH,Tan SL,Lee V,Salmon YM. The treatment of breast engorgement with Serrapeptase (Danzen): a randomised double-blind controlled trial. Singapore Med J. 1989 Feb;30(1):48-54.

6 Esch PM,Gerngross H,Fabian A. Reduction of postoperative swelling. Objective measurement of swelling of the upper ankle joint in treatment with serrapeptase — a prospective study Fortschr Med. 1989 Feb 10;107(4):67-8, 71-2.

7 Vicari E,La Vignera S,Battiato C,Arancio A. Treatment with non-steroidal anti-inflammatory drugs in patients with amicrobial chronic prostato-vesiculitis: transrectal ultrasound and seminal findings. Minerva Urol Nefrol 2005, 57(1):53-9

8 Mazzone A,Catalani M,Costanzo M, et al. Evaluation of Serratia peptidase in acute or chronic inflammation of otorhinolaryngology pathology: a multicentre, double-blind, randomized trial versus placebo. J Int Med Res. 1990 Sep-Oct;18(5):379-88.

9 Nakamura S,Hashimoto Y, et al. Effect of the proteolytic enzyme serrapeptase in patients with chronic airway disease. Respirology. 2003 Sep;8(3):316-20.

10 Majima Y,Inagaki M. The effect of an orally administered proteolytic enzyme on the elasticity and viscosity of nasal mucus. Arch Otorhinolaryngol. 1988;244(6):355-9.

11 Nakamura, S., et al. Effect of the proteolytic enzyme serrapeptase in patients with chronic airway disease. Respirology, 8(3): 316-20 2003.

Peptizyme® SP and Peptizyme® SP EN are Registered Trademarks of Specialty Enzymes and Biotechnologies. Copyright © 2012 All rights reserved.

Stratum Nutrition

20 Research Park Dr. Phone: (888) 403-5039 Email: info@stratumnutrition.com Website: www.stratumnutrition.com

BLIS K12 and BLIS M18 Oral Health Probiotics

The friendly bacteria found throughout the gastrointestinal (GI) tract are positive benefactors to general health. The right bacteria living in the intestinal tract can help digest food, keep body weight under control and help regulate the body’s use of nutrients. They also discourage the presence and growth of unfavorable microorganisms and help ensure that the body’s immune system functions properly.

Most are well aware of how important these bacteria are, and probiotics are a primary source of supplementation to support or replenish positive bacterial flora.

Beyond the Gut

While GI bacteria have been the mainstream focus of probiotics, bacteria are not just found in the gut. Our oral cavities (or mouths) also contain more than 600 species of bacteria that function in much the same way as the bacteria in our intestinal tracts.

Just like the bacteria in the GI tract, there are both good and bad bacterial strains in the mouth vying for control. The mouth is an entry point for pathogens as it comes into contact with billions of bacteria. If a healthy balance of oral bacteria is thrown off by stress, exposure to disease or antibiotics, it can quickly lead to problems such as bad breath, throat and ear infections. The microorganisms in the mouth are a first line of defense against pathogens and an important part of maintaining healthy oral bacteria.

Unfortunately, many simply don’t have a naturally occurring optimal balance of bacteria in the mouth. Therefore, interventions such as probiotic supplementation that promotes the health of the oral cavity can be one of the best proactive steps for maintaining optimal health.

BLIS K12 for Oral Health and ENT Immune Support

Bacterial infections of the ear, nose and throat and upper respiratory track, including otitis media, tonsillitis and pharyngitis, are a leading cause of patient visits to primary care physicians. These infections disproportionately affect infants, toddlers and young children, and have a significant economic burden, due to the disruption of family activities, absence from school and work, and the excessive use of antibiotics contributing to antibiotic resistance.1 Furthermore, if untreated or inadequately treated, these infections can result in serious long-term complications.

BLIS K12® is a specific oral probiotic strain of Streptococcus salivarius (S. salivarius) originally isolated from the mouth of a 12-year-old child who did not experience the normal occurrence of sore throats common in childhood. S. salivarius is one of the most numerous and beneficial species of bacteria found in a healthy human mouth. However, only a small number of individuals have K12-like strains inherently in the oral cavity.

The benefits of the K12 strain have been repeatedly demonstrated in human studies, which have shown such bacteria to combat pathogenic bacteria such as S. Pyogenes, a primary contributor to ENT (ear, nose and throat) infections. BLIS K12 colonizes in the mouth, crowding out the pathogenic bacteria strains by competitive inhibition and secretes bacteriocin-like inhibitory substances (BLIS) that provide an antimicrobial effect against colonization of unfavorable bacteria like S. Pyogenes.2

BLIS M18 for Dental Health

Dental cavities, bad breath or gum diseases are common problems people often experience in their oral cavity, as a result of imbalanced oral bacteria. Most people practice regular oral hygiene routines, such as brushing their teeth, flossing and using mouthwash to reduce the “bad” bacteria in their mouths and freshen breath. However, these practices, while important, only provide short-term results and in some cases can actually disrupt the natural balance of beneficial microorganisms in the oral cavity.

BLIS M18 is another unique strain of S. salivarius with health-promoting attributes for teeth and gums. Not all strains of S. salivarius act equally to inhibit oral and dental microbes. BLIS M18 is a naturally occurring strain that in vitro studies have shown is especially potent at inhibiting Streptococcus mutans (S. mutans).3 S. mutans is a harmful plaque-producing oral bacterium considered a leading causative of dental caries and tooth decay.

BLIS M18 resides along the gum line, where it produces bacteriocin-like inhibitory substances (BLIS) against S. mutans and also a number of enzymes like dextrinase and urease. These enzymes are important for protecting tooth surfaces by discouraging the buildup of plaque and neutralizing acid that can be harmful to teeth enamel and gums.

Probiotics for Oral Health

BLIS K12 and BLIS M18 are two heavily researched oral probiotics that offer benefits for oral health, affecting ENT health, halitosis and the health of teeth and gums. They are the logical complement to complete probiotic supplementation and maintenance of a healthy oral microbial balance.

References:

1 Medscape, Tonsillitis and Peritonsillar Abscess, http://emedicine.medscape.com/article/871977-overview#showall.

2 Dierksen KP and Tagg J. In D.R. Martin and T.J. (ed.). Streptococci and streptococcal diseases entering the new millennium. Securacopy, Auckland. P. 81-85 (2000).

3 J. P. Burton, P. A. Wescombe, P. A. Cadieux, J. R. Tagg. Beneficial microbes for the oral cavity: time to harness the oral streptococci. Beneficial microbes, Vol 2 (2), 93-101.

VDF FutureCeuticals, Inc.

2692 N. State Rt. 1-17 Momence, IL 60954 Phone: (888) 452-6853 Fax: (815) 472-3529 Email: sales@futureceuticals.com Website: www.futureceuticals.com

Calcium Fructoborate Reduces Inflammation and Improves Lipid Profiles and Quality of Life in Human Subjects

Building upon earlier in vitro research suggesting calcium fructoborate’s strong potential to reduce inflammation1-3, a series of recently-published human clinical studies indicates that this patented, nature-identical plant-mineral complex available exclusively from VDF FutureCeuticals, Inc. may offer substantial benefits for healthy inflammatory response and inflammation-related conditions.

Calcium Fructoborate

Calcium fructoborate (CF) is a patented mineral complex found in legumes, fruits, vegetables, herbs and wine that has been the subject of more than a dozen published studies on its unique properties and potential health benefits, especially for conditions linked to inflammation such as bone, joint and cardiovascular conditions. Most recently, published human clinical research has demonstrated CF’s ability to modulate key markers associated with inflammation-related conditions such as osteoarthritis4,5 and angina pectoris6, and has included accompanying subjective reports of improvement in feelings of pain and comfort and in quality of life.4-6

In particular, the studies indicate that CF significantly improves elevated serum levels of CRP in humans. CRP is an immune recognition protein that is a sensitive marker of inflammation, commonly used as a diagnostic for presence of acute or chronic health problems. Elevated circulating levels of CRP have been associated with a wide range of inflammation-related conditions: diabetes7,8, cardiovascular disease and conditions9,10, osteoarthritis11 and osteoporosis and associated increased risk of fractures.12,13

A reduction in levels of CRP indicates a reduction of inflammation.

Clinical Study Results

• Study 1: A double-blind, placebo-controlled study on healthy subjects, 10 subjects per group. CF supplementation tested over a 14-day period at a serving of 108 mg twice per day. CRP was reduced by 37 percent versus baseline, pre-supplementation value. CF also induced a 19 percent increase in endogenous levels of calcitriol, the active form of vitamin D3 (1,25(OH)dihydroxy-vitamin D).6

• Study 2: A double-blind, placebo-controlled study on healthy subjects, 15 subjects per group. CF supplementation tested over a 14-day period at a serving of 28.5 mg twice daily. CRP was reduced by 60.25 percent versus baseline, pre-supplementation value. The CF group also experienced a reduction in elevated levels of erythrocyte sedimentation rate (-10.25 percent) and fibrinogen (-13.73 percent), other common measures of inflammation.5

• Study 3: A double-blind, active-controlled (existing treatment protocol) study on subjects with stable angina pectoris, 29 subjects per group. CF supplementation tested over a 60-day period at a serving of 112 mg once per day. CRP was reduced by 39.7 percent versus baseline, pre-supplementation value. The CF group also experienced a 5.9 percent reduction in total cholesterol, a 9.2 percent reduction in LDL cholesterol, a 5.1 percent increase in HDL cholesterol and a 48.8 percent reduction in angina episodes per week.6 With an appealing effective serving size, this patented plant-mineral complex stands out as a compelling, proven ingredient for products designed to support healthy inflammation management, cardiovascular health and bone health.

Calcium Fructoborate is available exclusively from FutureCeuticals. The company is cGMP and HACCP-certified, a voting member of the Council for Responsible Nutrition, a voting member of the International Probiotics Association and a member of the American Botanical Council.

References:

1 Scorei R, Ciubar R, Iancu C, Mitran V, Cimpean A, Iordachescu D. In vitro effects of calcium fructoborate on fMLP stimulated human neutrophil granulocytes. Biol Trace Elem Res 2007; 118:27-37.

2 Scorei RI, Ciofrangeanu C, Ion R et al. In vitro effects of calcium fructoborate upon production of inflammatory mediators by LPS-stimulated RAW 264.7 macrophages. Biol Trace Elem Res 2010; 135:334-344.

3 Scorei RI, Rotaru P. Calcium Fructoborate – Potential Anti-inflammatory Agent. Biol Trace Elem Res 2011; DOI: 10.1007/s12011-011-8972-6.

4 Reyes-Izquierdo T, Nemzer B, Gonzalez AE, Zhou Q, Argumedo R, Shu C, et al. Short-term Intake of Calcium Fructoborate Improves WOMAC and McGill Scores and Beneficially Modulates Biomarkers Associated with Knee Osteoarthritis: A Pilot Clinical Double-blinded Placebo-controlled Study. Am J Biomed Sci 2012; DOI: 10.5099/aj120200111.

5 Scorei R, Mitrut P, Petrisor I, Scorei ID. A double-blind, placebo-controlled pilot study to evaluate the effect of calcium fructoborate on systemic inflammation and dyslipidemia markers for middle-aged people with primary osteoarthritis. Biol Trace Elem Res 2011; DOI: 10.1007/s12011-011-9083-0.

6 Milataru C, Donoiu I, Craciun A, Scorei ID, Bulearca AM, Scorei RI. Oral resveratrol and calcium fructoborate supplementation in subjects with stable angina pectoris: Effects on lipid profiles, inflammation markers, and quality of life. Nutrition. [In press.]

7 Pradhan AD; Manson, JE; Rifai, N; Buring, JE; Ridker, PM. C-reactive protein, interleukin 6, and risk of developing type 2 diabetes mellitus. JAMA 286(3): 327–34. doi:10.1001/jama.286.3.327.

8 Dehghan A; Kardys, I; de Maat, MP; Uitterlinden, AG; Sijbrands, EJ; Bootsma, AH; Stijnen, T; Hofman, A et al. Genetic variation, C-reactive protein levels, and incidence of diabetes. Diabetes 56 (3): 872–8.doi:10.2337/db06-0922.

9 Cesari M, Penninx BW, Newman AB, Kritchevsky SB, Nicklas BJ, Sutton-Tyrell K, Rubin SM, Ding J, Simonsick EM, Harris TB, Pahor M. Inflammatory Markers and onset of cardiovascular events: results from the Health ABC study. Circulation 108:2317-2322.

10 Yeh ET, Willerson JT. Coming of age of C-reactive protein: using inflammation markers in cardiology. Circulation 107:370-371.

11 Spector TD, Hart DJ, Nandra D, Doyle DV, Mackillop N, Gallimore JR, Pepys MB. Low-level increases in serum C-reactive protein are present in early osteoarthritis of the knee and predict progressive disease. Arthritis Rheum 40:723-727.

12 Hardy R, Cooper MS. Bone loss in flammatory disorders. Journal of Endocrinology 201:301-309.

13 Koh JM, Khang YH, Jun CH, Bae S, Kim DJ, Chung YE, Kim GS. Higher Circulating hsCRP levels are associated with lower bone mineral density in healthy pre- and postmenopausal women: evidence for a link between systemic inflammation and osteoporosis.

Verdure Sciences

1250 E. Conner St. Noblesville, IN 46060 Phone: (317) 776-3600 Fax: (317) 776-0208 Email: info@vs-corp.com Website: www.vs-corp.com

New Evidence on Longvida: Efficacy and Safety of Brain Curcumin

A new paradigm for supporting healthy brain aging is now emerging, and encompasses three primary pathways: 1) reactive oxygen species and free radicals; 2) inflammatory modulation; and 3) regulation of lipid and protein aggregates.1 Based on this paradigm, curcumin possesses the characteristics of an ideal broad-spectrum neurosupportive agent. Curcumin’s antioxidant and inflammatory-modulating activities are well documented, but new pathways add significant power to its potential. Although further work needs to be done, placebo-controlled clinical trials suggest that curcumin may help support healthy levels of lipid and protein aggregates needed for healthy brain aging, including amyloid-beta.

However, a critical factor is often overlooked in the current use of curcumin as a neurosupportive ingredient: its limited bioavailability. With a molecular weight (MW) of 368, curcumin is considered as highly active compared to its main metabolite, curcumin glucuronide (MW 546). Curcumin glucuronide has not been shown to cross the blood-brain barrier, and is quickly excreted from the body, minimizing its potential to support healthy brain aging. Likewise, “enhanced” forms of curcumin have been unable to demonstrate absorption of actual curcumin, detecting only the glucuronide form in blood.2-6

Longvida® Optimized Curcumin, based on patent-pending solid-lipid curcumin particle, or SLCP™ Technology, was developed by Verdure Sciences in collaboration with the University of California—Los Angeles (UCLA) to address these challenges. Longvida reaches neurosupportive blood levels of free (unmetabolized) curcumin, at a level 65 times greater than non-optimized curcumin.7

Likewise, in research presented at the International Conference for Natural Product Research in August 2012, a single dose of just 40 mg curcumin from Longvida led to blood concentrations of free curcumin that achieve the minimum target level of 0.1 micromolar.8

However, improved bioavailability is only a means to an end, and randomized, placebo-controlled trials (RCT) are necessary to evaluate efficacy. According to a new RCT performed at The Ohio State University, a single daily dose of Longvida (containing 80 mg curcumin) administered for 30 days led to significant improvement in levels of several biomarkers key for healthy brain aging, including an 11 percent reduction in plasma amyloid-beta.9

Regulation of healthy levels of blood lipids, particularly plasma triglycerides and cholesterol, are also critical for supporting healthy brain aging.10 For example, the function of apolipoprotein E4 (ApoE4), a key marker for healthy brain aging, is to transport and eliminate triglycerides. After 30 days of SLCP-based Longvida, a significant 14 percent reduction in plasma triglycerides was observed (p<0.05), coinciding with a trend for decrease of plasma cholesterol. Curcumin is a key regulator of several steps in the oxidative stress and inflammatory cascade that are highly correlated with amyloid-beta and cognitive function. Two of these major markers include catalase and C-reactive protein.11-13 In subjects taking Longvida, a 72 percent increase in catalase (p<0.01) and an 11 percent reduction in CRP was observed (p<0.05 from baseline).

Other keys for endothelial and cerebrovascular health include soluble intracellular cell adhesion molecule-1 (sICAM-1) and nitric oxide (NO).14,15 After 30 days of Longvida, a significant 14 percent reduction in sICAM-1 (p<0.05) and a 37 percent increase in endothelial NO (p<0.05) was observed.

Longvida: Generally Recognized As Safe

In August 2012, Longvida was determined to be generally recognized as safe (GRAS) by an independent, internationally recognized panel of scientists.16 The safety determination is based on more than a dozen clinical, preclinical and safety studies on Longvida. Longvida adheres to the most stringent global standards for quality and purity, and contains no piperine, crude lecithin, volatile oils, gluten, sugar, salt, artificial preservatives or additives.

References:

1 Frautschy and Cole. Mol Neurobiol. 2010 Jun;41(2-3):392-409.

2 Baum et al. Letter in J Clin Psychopharm. 2008:28(1), 110-114.

3 Baum et al. Pharmacol Res. 2007 Dec;56(6):509-14.

4 Cuomo et al. J Nat Prod. 2011 Mar 17.

5 Lao et al. BMC Complement Altern Med. 2006;6:10.

6 Marczylo et al. Cancer Chemother Pharmacol. 2007 Jul;60(2):171-7.

7 Gota et al. J Agric Food Chem. 2010 Feb 24;58(4):2095-9.

8 Shah et al. Planta Med 2012; 78. DOI: 10.1055/s-0032-1320664.

9 DiSilvestro et al. FASEB. April 23 2012.

10 Razay et al. Arch Neurol. 2007;64(1):93-96.

11 Kuo et al. Lancet Neurol. 2005 Jun;4(6):371-80.

12 Milton et al. Biochem J. (1999) 344, 293-296

13 Torres et al. J Alzheimers Dis. 2011;26(1):59-68.

14 Frohman et al. J Neurol Sci. 1991 Nov;106(1):105-11.

15 Nielsen et al. Neurobiol Dis. 2007 Apr;26(1):27-35.

16 Thomas et al. GRAS Expert Panel Statement, 2012.