Turmeric (Curcuma longa) is a bright yellow, ancient spice and a traditional remedy that has been used as a medicine, condiment and flavoring based on records dating back to 600 BCE.  Turmeric's natural curcuminoid content inhibits 5-lipo-oxygenase (LOX) and cyclo-oxygenase (COX), resulting in a healthy inflammatory response (Chandra 1972; Arora 1971; Mukhopadhyay 1982). 

Protects From Oxidative Damage

Curcumin exhibits strong antioxidant activity (Toda 1985), enhances cellular resistance to oxidative damage (Mortellini 2000), and provides antioxidant protection against DNA damage (Garcea 2004). Curcumin also enhances the body's natural antioxidant glutathione levels; which in turn aids the liver in detoxification (Pizorrno 1999).  Turmeric has also been found to have hepatoprotective (i.e., liver-protective) properties against a variety of liver-toxic chemicals (Deshpande 1998; Park 2000; Kiso 1983; Donatus 1990; Soni 1993).

Joint Function & Healthy Inflammatory Response

In research on people with suboptimal joint function, curcumin was found to be useful for promoting a healthy inflammatory response, while promoting comfort and flexibility (Deodhar 1980).  In a double-blind study, curcumin was found to be superior to a placebo or other study compounds supporting a healthy post-surgical inflammatory response (Satoskar 1986).

Antimutgenic Effects

Animal research and human cell culture studies have demonstrated that curcumin has an anti-mutagenic effects (Kawamori 1999), and anti-angiogenic effects (reduced the growth of new blood vessels that would otherwise nourish the growth of mutagenic cells) (Thaloor 1998), as well as reducing the activity of several common mutagens (Mehta 1991; Soudamini 1989; Azuine 1992; Boone 1992).  This activity is consistent with COX-2 inhibition. 

Antimicrobial & Cardiovascular Support

Turmeric extract and curcumin has also reduced the growth of a variety of bacteria, parasites, and pathogenic fungi (Allen 1998; Apisariyakul 1995; Rasmussen 2000); and have provided a protective effect on the cardiovascular system including the promotion of healthy cholesterol and triglyceride levels within normal ranges, while decreasing susceptibility of low density lipoprotein (LDL) to lipid peroxidation (Ramirez-Tortosa 1999), and reducing platelet aggregation (Srivastava 1986). 

Gastrointestinal Support

Constituents of turmeric exert several protective effects on the gastrointestinal tract. A salt of curcumin was found to promote intestinal comfort, and p-tolymethylcarbinol, a turmeric component, was found capable of increasing gastrin, secretin, bicarbonate, and pancreatic enzyme secretion (Ammon 1991). In addition, a double-blind trial has found turmeric helpful for people with indigestion (Thamlikikul 1999), and effective in animal research in promoting healthy digestive function *Rafatulla 1991).

Extract Standardized for 95%

A turmeric extract standardized for 95% curcuminoids (including curcumin, demethoxycurcumin and bisdemethoxycurcumin) will provide you with the active components in this plant. This turmeric concentrate with 95% curcuminoids is an exceptional value.  Consider that whole turmeric naturally provides between 3 to 8 percent curcuminoids (Natural Standard 2009). Therefore, if you wanted to obtain a clinically relevant dose of 450 mg curcuminoids, you would have to consume 5.63 to 15 grams of whole turmeric.  With the 95% concentrate, however, a single capsule will provide the 475 mg curcuminoids.

References

• Allen PC, Danforth HD, Augustine PC. Dietary modulation of avian coccidiosis. Int J Parasitol 1998; 28:1131-1140.
• Ammon HPT, Wahl MA. Pharmacology of Cucuma longa. Planta Medica 1991;57:1-7.
• Apisariyakul A, Vanittanakom N, Buddhasukh D. Antifungal activity of turmeric oil extracted from Curcuma longa (Zingiberaceae). J Ethnopharmacol 1995; 49:163-169.
• Arora R, Basu N, Kapoor V, et al. Anti-inflammatory studies on Curcuma longa (turmeric). Ind J Med Res 1971;59:1289-1295.
• Azuine M, Bhide S. Chemopreventive effect of turmeric against stomach and skin tumors induced by chemical carcinogens in Swiss mice. Nutr Cancer 1992; 17:77-83.
• Boone CW, Steele VE, Kelloff GJ. Screening of chemopreventive (anticarcinogenic) compounds in rodents. Mut Res 1992; 267:251-255.
• Chandra D, Gupta S. Anti-inflammatory and anti-arthritic activity of volatile oil of Curcuma longa (Haldi). Ind J Med Res 1972; 60:138-142.
• Deodhar SD, Sethi R, Srimal RC. Preliminary studies on antirheumatic activity of curcumin (diferuloyl methane). Ind J Med Res 1980; 71:632-4.
• Deshpande UR, Gadre SG, Raste AS, et al. Protective effect of turmeric (Curcuma longa L.) extract on carbon tetrachloride-induced liver damage in rats. Indian J Exp Biol 1998;36:573-577.
• Donatus IA, Sardjoko, Vermeulen NP. Cytotoxic and cytoprotective activities of curcumin. Effects on paracetamol-induced cytotoxicity, lipid peroxidation and glutathione depletion in rat hepatocytes. Biochem Pharmacol 1990;39:1869-1875.
• Garcea G, Jones DJ, Singh R, et al. Detection of curcumin and its metabolites in hepatic tissue and portal blood of patients following oral administration. Br J Cancer. 2004;90(5):1011-1015.
• Kawamori T, Lubet R, Steele VE, et al. Chemopreventative effect of curcumin, a naturally occurring anti-inflammatory agent, during the promotion/progression stages of colon cancer. Cancer Res 1999;59:597-601.
• Kiso Y, Suzuki Y, Watanabe N, et al. Antihepatotoxic principles of Curcuma longa rhizomes. Planta Med 1983;49:185-187.
• Mehta RG, Moon RC. Characterization of effective chemopreventive agents in mammary gland in vitro using and initiation-promotion protocol. Anticancer Res 1991; 11:593-596.
• Mortellini R, Foresti R, Bassi R, Green CJ. Curcumin, an antioxidant and anti-inflammatory agent, induces heme oxygenase-1 and protects endothelial cells against oxidative stress. Free Radic Biol Med 2000;28:1303-1312.
• Mukhopadhyay A, Basu N, Ghatak N, et al. Anti-inflammatory and irritant activities of curcumin analogues in rats. Agents Actions 1982; 12:508-515.
• Natural Standard Research Collaboration. Turmeric (Curcuma longa Linn.) and Curcumin. Medline Plus, U.S. National Library of Medicine. Last updated August 26, 2009. Retrieved September 9, 2009 from http://www.nlm.nih.gov/medlineplus/druginfo/natural/patient-turmeric.html.
• Park E J, Jeon CH, Ko G, et al. Protective effect of curcumin in rat liver injury induced by carbon tetrachloride. J Pharm Pharmacol 2000;52:437-440.
• Pizorrno JE, Murray MT. Textbook of Natural Medicine, 2nd Ed. London: Churchill Livingstone; 1999;689-693.
• Rafatulla S, Tariq M, Alyahya MA, et al. Evaluation of turmeric (Curcuma longa) for gastric and duodenal antiulcer activity in rats. J Ethnopharmacol 1990; 29:25-34.
• Ramirez-Tortosa MC, Mesa MD, Aguilera MC, et al. Oral administration of a turmeric extract inhibits LDL oxidation and has hypocholesterolemic effects in rabbits with experimental atherosclerosis. Atherosclerosis 1999; 147:371-378.
• Rasmussen HB, Christensen SB, Kvist LP, Karazami A. A simple and efficient separation of the curcumins, the antiprotozoal constituents of Curcuma longa. Planta Med 2000; 66:396-398.
• Satoskar RR, Shah SJ, Shenoy SG. Evaluation of anti-inflammatory property of curcumin (diferuloyl methane) in patients with postoperative inflammation. Int J Clin Pharmacol Ther Toxicol 1986; 24:651-4.
• Soni KB, Rajan A, Kuttan R. Reversal of aflatoxin induced liver damage by turmeric and curcumin. Cancer Lett 1992;66:115-121.
• Soudamini NK, Kuttan R. Inhibition of chemical carcinogenesis by curcumin. J Ethnopharmacol 1989;27:227-233.
• Srivastava R, Puri V, Srimal RC, Dhawan BN. Effect of curcumin on platelet aggregation and vascular prostacyclin synthesis. Arzneim Forsch 1986; 36:715-717.
• Thaloor D, Singh AK, Sidhu GS, et al. Inhibition of angiogenic differentiation of human umbilical vein endothelial cells by curcumin. Cell Growth Differ 1998;9:305-312.
• Thamlikitkul V, Bunyapraphathara N, Dechatiwongse T, et al. Randomized double-blind study of Curcuma domestica Val for dyspepsia. J Med Assoc Thai 1989; 72:613-20.
• Toda S, Miyase T, Arich H, et al. Natural antioxidants. Antioxidative compounds isolated from rhizome of Curcuma longa L. Chem Pharmacol Bull 1985;33:1725-1728.

Excess body fat around the waist (abdominal and visceral fat; "having an apple shape") is not only undesirable from a cosmetic/fitness standpoint, but it can also be characteristic of metabolic syndrome-a cluster of conditions that occur together, increasing your risk of heart disease, stroke and diabetes[i]-which is estimated to be present in 76 million U.S. adults aged age 20 and older.[ii]  Consequently, there are many good reasons for reducing abdominal fat.  Of course a sensible program that includes dietary modification and exercise is absolutely required for the success of any weight loss program.  In addition, the process of reducing abdominal fat can be significantly augmented with the use glabridin as a component of licorice flavonoid oil.

Let's face it, virtually anyone with excess abdominal/visceral fat would like to lose it and shrink his/her waist to look better and to prevent metabolic syndrome. If fact, people spend literally over 100 billion dollars annually on weight loss products.[iii] Unfortunately, the vast majority of those people have minimal success in the first instance, and then tend to gain back what ever weight they've lost. One of the reasons for this is that they are using products that are not formulated to achieve the desired result.  Abdominal/visceral fat is not likely to respond well to common thermogenic/fat-burner products. In fact, only one natural product has been shown to significantly reduce abdominal/visceral fat. That product is glabridin.

Glabridin comes from the roots of licorice (Glycyrrhiza glabra L.), a plant with thousands of years of safe and effective use. Glabridin is a potent antioxidant and a flavonoid molecule (flavonoids are found in many plants throughout nature).[iv]

In one study[v], obese mice were fed on a high-fat diet containing glabridin-rich licorice flavonoid oil (LFO) for eight weeks, while another group of mice (the "control" group) did not receive LFO. Compared with mice in the control group, those given LFO significantly reduced their body weight and their abdominal/visceral fat. Scientists discovered that the fat cells of those mice treated with LFO had become smaller. This exciting development indicated that the fat cells wouldn't be storing as much fat again. Furthermore, an examination of the mice's DNA (cellular "blueprint") in the liver showed an increase in the activity of those genes responsible for burning fat (also called "beta-oxidation") and a reduction in the activity of genes responsible for building up new fat. Another LFO study on mice showed similar results.[vi]  Again, this was an exciting development suggesting that continued use of LFO would not only burn away existing fat, but help prevent new fat formation. Of course the real proof of the pudding is in human research, not animal research-and in the case of LFO, human clinical research has been conducted.

In an 8-week study, 84 overweight individuals received 900 mg daily of LFO or a placebo (a "fake" pill).  The results were that those taking the LFO were found to have significantly decreased body weight, body mass index (BMI), and abdominal fat-essentially the same type of results experienced in the mice study.  By contrast, the placebo group experienced no such benefits.  In this same study, as little as 300 mg of LFO was found to help reduce fat mass. This study offered proof that LFO is effective and reducing abdominal/visceral fat in humans.

Other human research also supports the effectiveness and safety of LFO. In another placebo-controlled, double-blind, 12-week study, 300 mg of LFO or placebo was taken daily by a total of 103 overweight subjects.  The results were that body weight increased in the placebo group, but not in the LFO group.[vii] Furthermore, in other research LFO has been shown to be safe when administered once daily up to 1200 mg daily.[viii] Based on these findings these human studies it was shown that LFO is a safe ingredient for long-term use, with potential weight-reducing effects.

References

[i] Mayo Clinic Staff. Metabolic syndrome. Mayo Foundation for Medical Education and Research. Nov. 7, 2007. Retrieved October 1, 2009 from http://www.mayoclinic.com/health/metabolic%20syndrome/DS00522.

[ii] Statistical Fact Sheet - Risk Factors 2009 Update: Metabolic Syndrome - Statistics. American Heart Association; 2009. Retrieved October 1, 2009 from http://www.americanheart.org/downloadable/heart/1236355725579METABOLIC.pdf.

[iii] Weight Loss Markets: Products, Services, Foods and Beverages. BCC Research. December 1, 2003. 305 Pages - Pub ID: WA952808.

[iv] Shibata S. A drug over the millennia: pharmacognosy, chemistry, and pharmacology of licorice. Yakugaku Zasshi 2000; 120:849-862.

[v] Aoki F, Honda S, Kishida H, Kitano M, Arai N, Tanaka H, Yokota S, Nakagawa K, Asakura T, Nakai Y, Mae T. Suppression by licorice flavonoids of abdominal fat accumulation and body weight gain in high-fat diet-induced obese C57BL/6J mice. Biosci Biotechnol Biochem 2007;71(1):206-14.

[vi] Nakagawa K, Kishida H, Arai N, Nishiyama T, Mae T. Licorice flavonoids suppress abdominal fat accumulation and increase in blood glucose level in obese diabetic KK-A(y) mice. Biol Pharm Bull 2004;27(11):1775-8.

[vii] Yuji T, Tatsumasa M, Mitsuaki K, et al. Licorice flavonoid oil effects body weight loss by reduction of body fat mass in overweight subjects. Journal of health science 2006;52(6):672-683.

[viii] Aoki F, Nakagawa K, Kitano M, Ikematsu H, Nakamura K, Yokota S, Tominaga Y, Arai N, Mae T. Clinical safety of licorice flavonoid oil (LFO) and pharmacokinetics of glabridin in healthy humans. J Am Coll Nutr 2007;26(3):209-18.

D-limonene a major constituent of several citrus oils (orange, lemon, mandarin, lime, and grapefruit), and is listed in the Code of Federal Regulations as generally recognized as safe (GRAS) for a flavoring agent that can be found in common food items such as fruit juices, soft drinks, baked goods, ice cream, and pudding [1-2]. In addition, d-limonene has some specific medicinal properties for human health, including natural heartburn protectant, slowing tumor progression and helping to dissolve gallstones.

Natural Heartburn Protectant

D-limonene has been shown to be effective in relieving occasional heartburn. In one study, 19 adults used d-limonene to relieve their symptoms. Participants took one capsule containing 1,000 mg d-limonene every day or every other day. On the second day of taking d-limonene, 32% of participants experienced a significant relief of symptoms; this relief rate improved gradually during the regimen. By day fourteen, 89% of participants achieved complete relief of symptoms [3].

In a double-blind, placebo-controlled study, 13 participants suffering from mild/moderate to severe heartburn received 1,000 mg d-limonene daily or every other day, or a placebo. On day four, 29% of participants in the d-limonene group experienced significant relief of symptoms, compared to no relief of symptoms in the placebo group. By day fourteen, 86% of participants achieved complete relief of symptoms, compared to 29 percent of participants in the placebo group [3].

Results from these two studies suggest the beneficial effects of d-limonene appear to develop over time, with the best results attained after following a 10-capsule regimen. Research suggests d-limonene may neutralize the effect of gastric acid by coating the stomach wall and protecting the mucosal and esophageal lining from gastric acid exposure [3]. Some researchers believe d-limonene may support healthy peristalsis (movement of food and waste through the gastrointestinal tracts), which may also help [4].

Slows Tumor Progression

Research on cancer cells indicates that limonene may prevent lymphoma, breast, skin, liver, lung, colon, and gastric cancer. In fact, D-limonene taken orally in 21-day cycles concentrated in tumor tissue in patients with advanced cancer and may slowed disease progression [5]. Limonene might help reduce the risk of cancer by inducing phase I and phase II detoxification enzymes in the liver that metabolize carcinogens into harmless products. Limonene may also prevent tumor cell proliferation [6]. In addition, preliminary research suggests that limonene stimulates immune system activity [7].

Helps Dissolve Gallstones

During in-vitro laboratory experiements, d-limonene dissolved human gallstones within two hours [8]. In patients who had recently had gallstone surgery, infusion of 20 mL d-limonene every other day dissolved gallstones overlooked during surgery. In some patients gallstone dissolution occurred after only three infusions [8]. A study with 200 patients reported a direct infusion of 20-30 mL d-limonene (97% solution) completely or partially dissolved gallstones in 141 patients. The duration of the treatment ranged from three weeks to four months [9]. Although these studies all used direct infusion of d-limonene into the gallbladder, researchers have also suggested that systemic or "oral dissolution" may also be effective [10].

References

1.      Anonymous. Limonene monograph. Cri Rev Food Sci Nutr 1999;39:260-265.

2.      The United States Code of the Federal Regulations, Title 21, Part 182.60.

3.      Sun J. D-Limonene: Safety and Clinical Applications. Altern Med Rev 2007;12(3):259-264.

4.      Lis-Balchin M, Ochocka RJ, Deans SG, et al. Bioactivity of the enantiomers of limonene. Med Sci Res 1996;24:309-310.

5.      Vigushin DM, Poon GK, Boddy A, et al. Phase I and pharmacokinetic study of D-limonene in patients with advanced cancer. Cancer Research Campaign Phase I/II Clinical Trials Committee. Cancer Chemother Pharmacol 1998;42:111-7.

6.      Crowell PL. Prevention and therapy of cancer by dietary monoterpenes. J Nutr 1999;129:775S-778S.

7.      Raphael TJ, Kuttan G. Immunomodulatory activity of naturally occurring monoterpenes carvone, limonene, and perillic acid. Immunopharmacol Immunotoxicol 2003;25:285-94.

8.      Igimi H, Hisatsugu T, Nishimura M. The use of d-limonene preparation as a dissolving agent of gallstones. Am J Dig Dis 1976;21:926-939.

9.      Igimi H, Tamura R, Toraishi K, et al. Medical dissolution of gallstones. Clinical experience of d-limonene as a simple, safe, and effective solvent. Dig Dis Sci 1991;36:200-208.

10.  Plaisier PW, Vergunst H, Terpstra OT. Dissolution of gallstones. Dig Dis 1993;11(3):181-8.

Acetyl-L-carnitine (ALC) occurs naturally in the body. Carnitines (amino acids) produced in the body exist as a "carnitine pool" consisting of L-carnitine and several acetyl-carnitine esters. Intracellular enzymes and cell membrane transporters can rapidly interconvert the carnitines to the needed form and transport them between the tissues and extracellular space. ALC, the most important carnitine ester, is converted to L-carnitine.[1] [2] The distribution of inside the cell was found to be 60% as free l-carnitine, which was to be expected, and 40% as ALC, which underscores the importance of this unique substance in the body.[3]

Role with Acetylcholine & Memory

ALC is structurally related to acetylcholine. It also serves as a precursor to acetyl coenzyme A (a component of energy metabolism) and contributes acetyl groups to acetylcholine.¹ In doing so, it seems to promote acetylcholine release[4], which is considered to be the "memory neurotransmitter". This is consistent with other ALC related memory research.

ALC supplementation has been shown to improve some measures of cognitive function and memory in elderly people with age-related mental impairment.[5] [6] [7] Futhermore, ALC slowed the rate of disease progression, improved memory, and improved some measures of cognitive function and behavioral performance in some patients with Alzheimer's disease.[8] [9] [10] [11] In addition, ALC supplementation improved memory and visuospatial capacity in 30-60 year-old chronic alcoholics with cognitive impairment.[12]

Perhaps one reason why ALC is so effective for memory is a function of the blood-brain barrier. The blood-brain barrier is a selectively permeable protective membrane that controls whether substances in the blood can pass through into the brain tissue. ALC is able to cross the blood-brain barrier more effectively than L-carnitine, which makes it especially appropriate for promoting brain function.[13]

Promotes Fatty Acid Metabolism

Carnitines play an important role in lipid metabolism and energy production. They are essential for normal mitochondrial function, acting as a transporter of long-chain fatty acids into the mitochondria for where they are burned as an energy fuel (i.e. beta-oxidation).[14] [15] [16] [17]

Decrease Age-Related Testosterone Deficiency

ALC supplementation for 6 months, in combination with propionyl-L-carnitine, improved symptoms of androgen decline in older men sexual dysfunction, depression, and fatigue.[18]

Improve Diabetic Neuropathy

Patients with diabetic neuropathy had improved symptoms after taking 1500-3000 mg ALC daily in divided doses for a year. Acetyl-L-carnitine seems to increase nerve fibers, regenerate nerve fiber clusters, and improve vibratory sensations.[19] [20] [21] [22]

Increase Sperm Motility

Supplementing with ALC and L-carnitine for 6 months increased sperm motility in men with infertility.[23]

References

[1] Pettegrew JW, Levine J, McClure RJ. Acetyl-L-carnitine physical-chemical, metabolic, and therapeutic properties: relevance for its mode of action in Alzheimer's disease and geriatric depression. Mol Psychiatry 2000;5:616-32.

[2] Rebouche CJ. Kinetics, pharmacokinetics, and regulation of L-carnitine and acetyl-L-carnitine metabolism. Ann N Y Acad Sci 2004;1033:30-41.

[3] Frenkel, R., et al (eds). Carnitine Biosynthesis, Metabolism, and Functions (1980) New York: Academic Press; 1980:73-89.

[4] Mayeux R, Sano M. Treatment of Alzheimer's Disease. N Engl J Med 1999;341:1670-9.

[5] Cucinotta D, Passeri M, Ventura S, et al. Multicenter clinical placebo-controlled study with acetyl-L-carnitine (ALC) in the treatment of mildly demented elderly patients Drug Development Res 1988;14:213-6.

[6] Salvioli G, Neri M. L-acetylcarnitine treatment of mental decline in the elderly. Drugs Exp Clin Res 1994;20:169-76.

[7] Passeri M, Cucinotta D, Bonati PA, et al. Acetyl-L-carnitine in the treatment of mildly demented elderly patients. Int J Clin Pharmacol Res 1990;10:75-9.

[8] Pettegrew JW, Klunk WE, Panchalingam K, et al. Clinical and neurochemical effects of acetyl-L-carnitine in Alzheimer's disease. Neurobiol Aging 1995;16:1-4.

[9] Rai G, Wright G, Scott L, et al. Double-blind, placebo controlled study of acetyl-l-carnitine in patients with Alzheimer's dementia. Curr Med Res Opin 1990;11:638-47.

[10] SanoM, Bell K, Cote L, et al. Double-blind parallel design pilot study of acetyl levocarnitine in patients with Alzheimer's disease. Arch Neurol 1992;49:1137-41.

[11] Bonavita E. Study of the efficacy and tolerability of L-acetylcarnitine therapy in the senile brain. Int J Clin Pharmacol Ther Toxicol 1986;24:511-6.

[12] Tempesta E, Troncon R, Janiri L, et al. Role of acetyl-L-carnitine in the treatment of cognitive deficit in chronic alcoholism. Int J Clin Pharmacol Res 1990;10:101-7.

[13] Tweed V. Basic Health Publications User's Guide to Carnitine and Acetyl-L-Carnitine. Laguna Beach, CA: Basic Health Publications; 2006.

[14] Hart AM, Wilson AD, Montovani C, et al. Acetyl-l-carnitine: a pathogenesis based treatment for HIV-associated antiretroviral toxic neuropathy. AIDS 2004;18:1549-60.

[15] Stanley CA. Carnitine deficiency disorders in children. Ann N Y Acad Sci 2004;1033:42-51.

[16] Evans AM, Fornasini G. Pharmacokinetics of L-carnitine. Clin Pharmacokinet 2003;42:941-67.

[17] Sima AAF, Calvani M, Mehra M, et al. Acetyl-L-carnitine improves pain, nerve regeneration, and vibratory perception in patients with chronic diabetic neuropathy: An analysis of two randomized, placebo-controlled trials. Diabetes Care 2005;28:89-94.

[18] Cavallini G, Caracciolo S, Vitali G, et al. Carnitine versus androgen administration in the treatment of sexual dysfunction, depressed mood, and fatigue associated with male aging. Urology 2004;63:641-6.

[19] Sima AAF, Calvani M, Mehra M, et al. Acetyl-L-carnitine improves pain, nerve regeneration, and vibratory perception in patients with chronic diabetic neuropathy: An analysis of two randomized, placebo-controlled trials. Diabetes Care 2005;28:89-94.

[20] Onofrj M, Fulgente T, Melchionda D, et al. L-acetylcarnitine as a new therapeutic approach for peripheral neuropathies with pain. Int J Clin Pharmacol Res 1995;15:9-15.

[21] De Grandis D, Minardi C. Acetyl-L-carnitine (levacecarnine) in the treatment of diabetic neuropathy. A long-term, randomised, double-blind, placebo-controlled study. Drugs R D 2002;3:223-31.

[22] Quatraro A, Roca P, Donzella C, et al. Acetyl-L-carnitine for symptomatic diabetic neuropathy. Diabetologia 1995;38:123.

[23] Lenzi A, Sgro P, Salacone P, et al. A placebo-controlled double-blind randomized trial of the use of combined l-carnitine and l-acetyl-carnitine treatment in men with asthenozoospermia. Fertil Steril 2004;81:1578-84.

When you think of dietary supplements for the joints and arthritis, chances are that you're thinking of glucosamine and chondroitin sulfate--which makes sense since there is good research to support the use of these nutraceuticals for this purpose.  What many people don't know, however, is that there are other nutraceuticals which also can be used effectively for arthritis.  Three of these are hyaluronic acid, calcium fructoborate and bromelain.

Hyaluronic acid

Hyaluronic acid (HA) is a naturally occuring substance found outside of cells, in the tissues and body fluids of all vertebrates. HA is a polysaccharide (long-chain sugar) chain found most primarily in cartilage, synovial fluid, skin, and the aqueous humor in the eye [1]--areas in the body where it serves as part of the supporting structure, cushioning and lubricating.

Research suggests that hyaluronic acid may prevent the breakdown of natural cushioning barriers in joint [2]. It seems that hyaluronic acid binds to cellular receptors on the surface membrane of cartilage and other cell types, supporting wound healing as well as reducing the enzymes that contribute to cartilage breakdown [3-4]. In randomized double-blind placebo-controlled study, 20 subjects with arthritis of the knee received either an oral form of hyaluronic acid or placebo for 8 weeks. The results were that daily supplementation with hyaluronic acid was useful to enhance several markers of quality of life in adults with knee arthritis, including improving pain and discomfort [5]. 

One form of hyaluronic acid that is significantly more effective than other forms is Hyal-Joint.  Hyal-Joint is 2 to 4 times more active in nourishing synovial fluid and supporting its health than regular hyaluronic acid. The increased activity comes from the unique (patent pending) composition of Hyal-Joint which naturally contains hyaluronic acid, as well as collagen and other proteoglycan which together create a special synergistic effect [6].

Fruitex-B® (aka, Calcium Fructoborate)

Fruitex-B®, which is also known as calcium fructoborate, is a form of the mineral boron. In research involving subjects with arthritis, 50% of the patients who received a daily supplement of 6 mg of boron noted improvements in joint pain associated with movement, while only 10% of subjects given a placebo experienced similar improvement [7]. Clinical studies demonstrate that Fruitex-B® especially effective in reducing pain in patients with arthritis [8]. The reason for the improvements in pain may be the result of boron helping to reduce joint inflammation [9-11].

Bromelain

Bromelain is a proteolytic (i.e., protein-digesting) enzyme found in pineapples.  Bromelain has proteolytic action on a variety of proteins, breaking them down into smaller peptides and amino acids [12].  Beyond its protein digesting capacity, research has shown that bromelain helps reduce inflammation. This was seen in a study where bromelain helped patients with arthritis, 73% of whom had good to excellent results [13].

References

1. Goa KL, Benfield P. Hyaluronic acid. A review of its pharmacology and use as a surgical aid in ophthalmology, and its therapeutic potential in joint disease and wound healing. Drugs 1994;47:536-66.
2. Dougados M. Sodium hyaluronate therapy in osteoarthritis: arguments for a potential beneficial structural effect. Semin Arthritis Rheum 2000;30(2 Suppl 1):19-25.
3. Chen WY, Abatangelo G. Functions of hyaluronan in wound repair. Wound Repair Regen 1999;7:79-89.
4. Petrella RJ, DiSilvestro MD, Hildebrand C. Effects of hyaluronate sodium on pain and physical functioning in osteoarthritis of the knee: a randomized, double-blind, placebo-controlled clinical trial. Arch Intern Med 2002;162:292-8.
5. Available at: http://www.hyal-joint.com/doc.php?op=uniqueness&tit=The%20uniqueness%20of%20Hyal-Joint. Accessed October 5, 2009.
6. Travers RL, Rennie GC, Newnham RE. Boron and arthritis: the result of a double-blind pilot study. J Nutr Med. 1990;1:127-32.
7. Available at: www.futureceuticals.com/proprietary/pdf/FruitexBBrochure.pdf. Accessed June 1, 2006
8. Hall IH, Rajendran KG, Chen SY, et al. Anti-inflammatory activity of amine-carboxyboranes in rodents. Arch Pharm (Weinheim). 1995 Jan;328(1):39-44.
9. Rajendran KG, Chen SY, Sood A, Spielvogel BF, Hall IH. The anti-osteoporotic activity of amine-carboxyboranes in rodents. Biomed Pharmacother. 1995;49(3):131-40.
10. Hall IH, Starnes CO, McPhail AT, et al. Anti-inflammatory activity of amine cyanoboranes, amine carboxyboranes, and related compounds. J Pharm Sci. 1980 Sep;69(9):1025-9.
11. Osol A, Robertson, P. The United States Dispensatory, 27th edition. Philadelphia: J.P. Lippincott Company; 1973: 201.
12. Cohen A, Goldman J. Bromelains therapy in rheumatoid arthritis. Pennsylvania Med J 1964; 67:27-30.

Methylsenocysteine (MSC) is a relatively simple organic selenium compound formed naturally in various plants, including garlic, wild leeks, onions and broccoli grown on high selenium soil.[1] It is the preferred form of selenium for a few different reasons. First, for the past 15 years or so, selenium research on the incidence of cancer cell development has focused heavily on MSC, and MSC rich foods have shown good activity in reducing the incidence of cancer cell development without excess tissue accumulation or toxicity.[2]

Second, MSC is easily converted to methylselenol[3], and methylselenol has been shown to reduce cancer cell development through a process called apoptosis, or programmed cell death. Cells eliminated by apoptosis don't leave a messy residue to trigger inflammation and spread cell death. Methylselenol is also known to reduce angiogenesis, the growth of new blood vessels necessary to promote the development of cancer cells.[4]

Third, MSC is a relatively nontoxic form of selenium. Consider that selenite/selenate forms of selenium (e.g. sodium selenite) are more frequently metabolized to the toxic metabolite hydrogen selenide (H2Se).[5] Then consider that because cells cannot distinguish selenomethionine from the essential amino acid methionine, some selenomethionine become incorporated into general body proteins, increasing tissue selenium levels which may risk toxicity[6]. By contrast, once methylselenol is formed from MSC, it is soon transformed into dimethylselenide, which is rapidly excreted in the breath, or converted to trimethylselenonium, which is thoroughly excreted in the urine.[7]

References

[1] Whanger, P. Selenocompounds in plants and animals and their biological significance. J Am Coll Nutr 2002, 21:223-32.

[2] Ip, C. and Lisk, D. Characterization of selenium profiles and anticarcinogenic responses in rats fed natural sources of selenium-rich products. Carcinogenesis 1994, 15:573-76.

[3] Medina, D. et al. Se-methylselenocysteine: A new compound for chemoprevention of breast cancer. Nutr Cancer 2001, 40:12-17.

[4] Lu, J. and Jiang, C. Antiangiogenic activity of selenium in cancer chemoprevention: metabolite-specific effects. Nutr Cancer 2001, 40:64-73.

[5] Passwater, R. Selenium Against Cancer and AIDS. New Canaan CT: Keats, 1996:47-48.

[6] Ip, C. Lessons from basic research in selenium and cancer prevention. J Nutr 1998, 128:1845-54.

[7] Satyanarayana S, Sekhar JR, Kumar KE, Shannika LB, Rajanna B, Rajanna S. Influence of selenium (antioxidant) on gliclazide induced hypoglycaemia/anti hyperglycaemia in normal/alloxan-induced diabetic rats. Mol Cell Biochem. 2006;283:123-7.

In analyzing hundreds of articles published over three decades, researchers have concluded that current recommendations for vitamin K are not being met, which may place people at increased risk accelerated bone fragility, arterial and kidney calcification, cardiovascular disease, and possibly cancer.[1]

Although vitamin K is primarily known for its role in facilitating blood coagulation, various vitamin K-related proteins play other important roles as well in promoting bone health and cardiovascular health, while avoiding inappropriate calcification and inhibiting the growth of certain types of cancer cells.

The results of this new analysis support the "triage theory", first proposed by Dr. Ames (one of the researchers in the current study) in 2006[2] to explain why age-related diseases like heart disease, cancer, and dementia may be unintended consequences of mechanisms developed during evolution to protect against episodic vitamin/mineral shortages. The theory basically holds that the body will use scarce micronutrients for absolutely essential functions such as energy production (needed for short-term survival), making them unavailable for other needs which ultimately would trigger the "triage response", accelerating cancer, aging, and neural decay (long-term survival).

The solution to the problem would be to provide a higher intake of the micronutrient in question-in this case vitamin K. This makes a good case for vitamin K supplementation.

References

[1] McCann JC, Ames BN. Vitamin K, an example of triage theory: is micronutrient inadequacy linked to diseases of aging? Amer J Clin Nutr Published online ahead of print, doi: 10.3945/ajcn.2009.27930.

[2] Ames BN. Low micronutrient intake may accelerate the degenerative diseases of aging through allocation of scarce micronutrients by triage. PNAS 2006;103:17589-17594.

In order to answer this question fairly, we must first agree upon the definition of what constitutes a natural vitamin.

Definitions of natural

Some would choose to define a natural vitamin based upon its source. In this instance, the definition of a natural vitamin would be, "Vitamins provided from food or plant sources."  In this case, the vitamin C found in a fresh glass of orange juice would be considered to be natural vitamin C.  Others consider the chemical form of a vitamin to be the factor that dictates whether or not it is natural.  For example, since the chemical form of vitamin C found in orange juice is L-ascorbic acid, then L-ascorbic acid would be considered natural even though it was derived via the conversion of corn syrup to glucose, and then via further enzymatic steps in the laboratory that would ultimately yield purified, crystallized vitamin C.

The issue of potency

If you decided that you wanted only natural source vitamins, and if you go by the former, fundamentalist definition of natural, you would have to prepare yourself to accept the fact that there is no way you will be able to achieve high intakes of virtually any vitamin in supplemental form. Consider that a cup of fresh orange juice will provide you with about 124 mg of vitamin C.[1] If you were able to cause all the liquid in the orange juice to evaporate without destroying the heat and light-sensitive vitamin C, and then put the remaining powder into a capsule, you would still only get a little over 100 mg of "natural" vitamin C. If you wanted at least 1000 mg, you would have to take about 10 capsules, which isn't particularly practical. On the other hand, if you went by the latter definition of natural, you could easily get 1,000 mg of vitamin C in a single tablet.

Whole food source vitamins

Right about know, you may be thinking, "Wait a minute! What about whole food source vitamins? They're all natural and I can get them in higher potencies." Again, this is an issue of definition. If you're going by the fundamentalist definition, then so-called "whole food" vitamins are synthetic, not natural. If you doubt this, just go to the website of almost any brand selling "whole food" vitamins, and carefully read how these vitamins are created.

Initially, the marketing copy on these websites generally present the vitamins as coming from a whole food, not chemical isolates.  As a matter of fact, one website touts that their products do not contain "the synthetic vitamins, minerals and chemical herbal isolates you'll find in most supplements." However, when you examine the process closer, you learn that the distained isolated and synthetic vitamins are simply mixed together with whole foods in a type of broth, or more eloquently stated, "cultured in organic media." The finished vitamins are then said to be delivered "in their safest and most active form within the infinite complexity of whole food." Let's be fair.  Just because synthetic vitamins are mixed with whole foods, do you really think that they're now natural and from a whole food source?

Answering the original question

So, back to the original question: "Are natural vitamins better for you than synthetic vitamins?" With the exception of vitamin E, the short answer is "no." The reason for this answer is that there is no published data demonstrating greater absorption or efficacy for natural over synthetic vitamins. For example, in a review examining vitamin C bioavailability, studies found that ascorbic acid bioavailability is equivalent in ascorbic acid tablets, orange juice, whole orange sections, and cooked broccoli, while the bioavailability of ascorbic acid in raw broccoli was 20% lower.[2]

Adherents to the fundamentalist definition will say that it's okay to get far less of a natural vitamin since it will work better in the body than natural.  However, there is no published data to support this position.  Rather, the data often suggests that it is the higher doses of "synthetic" vitamins that yield positive health benefits. For example, the research shows a benefit in reducing the duration and severity of a cold if megadoses (in the grams) of vitamin C are used[3] [4], while smaller doses tend to yield little results.

Natural vitamin E is better than synthetic

Vitamin E, it turns out, is different than other vitamins.  Natural vitamin E (d-alpha tocopherol/yl) is better absorbed then synthetic vitamin E (dl-alpha tocopherol/yl).   SEQ CHAPTER \h \r 1A 1981 study published in The American Journal of Clinical Nutrition[5] demonstrated that the natural vitamin E was 3.48 times more active in the human body than the synthetic vitamin E; even though the same number of IUs were used in the test subjects.

Conclusion

If you want high/mega potency doses of a nutrient, your only real option is to utilize synthetic vitamins. In any case, it really doesn't matter whether the vitamin is synthetic or natural.  Either way, you're going to get good absorption. 

References

[1] USDA National Nutrient Database for Standard Reference, Release 21; 2008

[2] Gregory JF 3rd. Ascorbic acid bioavailability in foods and supplements. Nutr Rev 1993;51(10):301-3.

[3] Hemila H. Vitamin C supplementation and common cold symptoms: factors affecting the magnitude of the benefit. Med Hypotheses 1999; 52(2):171-8.

[4] Gorton HC, Jarvis K. The effectiveness of vitamin C in preventing and relieving the symptoms of virus-induced respiratory infections. J Manipulative Physiol Ther 1999; 22(8):530-3.

[5] Machlin LJ, Brin M. Bioequivalence of RRR-alpha- tocopheryl acetate and all-rac-alpha-tocopheryl acetate.  Am J Clin Nutr 1981; 34(8):1633-6.

 

Turmeric (Curcuma longa) is a bright yellow, ancient spice and a traditional remedy that has been used as a medicine, condiment and flavoring based on records dating back to 600 BCE.  The rhizome (underground stem) is the part of the plant used, and its key constituents include curcumin and essential oils (p-tolymethylcarbinol). Its health value is essentially due to its curcumin content.  The curcumin inhibits 5-lipo-oxygenase (LOX) and cyclo-oxygenase (COX), resulting in a healthy inflammatory response.[1] [2] [3] 

Joint Function & Healthy Inflammatory Response

In research on people with suboptimal joint function, curcumin was found to be useful for promoting a healthy inflammatory response, while promoting comfort and flexibility.[4]  In a double-blind study, curcumin was found to be superior to a placebo or other study compounds supporting a healthy post-surgical inflammatory response.[5]

Antioxidant & Hepatoprotective Activity

Curcumin also exhibits strong antioxidant activity[6], enhances cellular resistance to oxidative damage[7], and provides antioxidant protection against DNA damage.[8] Curcumin also enhances the body's natural antioxidant glutathione levels; which in turn aids the liver in detoxification.[9]  Turmeric has also been found to have hepatoprotective (i.e., liver-protective) properties against a variety of liver-toxic chemicals.[10] [11] [12] [13] [14]

Antimutgenic Effects

Animal research and human cell culture studies have demonstrated that curcumin has an anti-mutagenic effects[15], and anti-angiogenic effects (reduced the growth of new blood vessels that would otherwise nourish the growth of mutagenic cells)[16], as well as reducing the activity of several common mutagens.[17] [18] [19] [20]  This activity is consistent with COX-2 inhibition.  

Antimicrobial & Cardiovascular Support

Turmeric extract and curcumin has also reduced the growth of a variety of bacteria, parasites, and pathogenic fungi [21] [22] [23]; and have provided a protective effect on the cardiovascular system including the promotion of healthy cholesterol and triglyceride levels within normal ranges, while decreasing susceptibility of low density lipoprotein (LDL) to lipid peroxidation[24], and reducing platelet aggregation.[25] 

Gastrointestinal Support

Constituents of turmeric exert several protective effects on the gastrointestinal tract. A salt of curcumin was found to promote intestinal comfort, and p-tolymethylcarbinol, a turmeric component, was found capable of increasing gastrin, secretin, bicarbonate, and pancreatic enzyme secretion.[26] In addition, a double-blind trial has found turmeric helpful for people with indigestion,[27] and effective in animal research in promoting healthy digestive function.[28]

References

[1] Chandra D, Gupta S. Anti-inflammatory and anti-arthritic activity of volatile oil of Curcuma longa (Haldi). Ind J Med Res 1972; 60:138-142.

[2] Arora R, Basu N, Kapoor V, et al. Anti-inflammatory studies on Curcuma longa (turmeric). Ind J Med Res 1971;59:1289-1295.

[3] Mukhopadhyay A, Basu N, Ghatak N, et al. Anti-inflammatory and irritant activities of curcumin analogues in rats. Agents Actions 1982; 12:508-515.

[4] Deodhar SD, Sethi R, Srimal RC. Preliminary studies on antirheumatic activity of curcumin (diferuloyl methane). Ind J Med Res 1980; 71:632-4.

[5] Satoskar RR, Shah SJ, Shenoy SG. Evaluation of anti-inflammatory property of curcumin (diferuloyl methane) in patients with postoperative inflammation. Int J Clin Pharmacol Ther Toxicol 1986; 24:651-4.

[6] Toda S, Miyase T, Arich H, et al. Natural antioxidants. Antioxidative compounds isolated from rhizome of Curcuma longa L. Chem Pharmacol Bull 1985;33:1725-1728.

[7] Mortellini R, Foresti R, Bassi R, Green CJ. Curcumin, an antioxidant and anti-inflammatory agent, induces heme oxygenase-1 and protects endothelial cells against oxidative stress. Free Radic Biol Med 2000;28:1303-1312.

[8] Garcea G, Jones DJ, Singh R, et al. Detection of curcumin and its metabolites in hepatic tissue and portal blood of patients following oral administration. Br J Cancer. 2004;90(5):1011-1015.

[9] Pizorrno JE, Murray MT. Textbook of Natural Medicine, 2nd Ed. London: Churchill Livingstone; 1999;689-693.

[10] Deshpande UR, Gadre SG, Raste AS, et al. Protective effect of turmeric (Curcuma longa L.) extract on carbon tetrachloride-induced liver damage in rats. Indian J Exp Biol 1998;36:573-577.

[11] Park E J, Jeon CH, Ko G, et al. Protective effect of curcumin in rat liver injury induced by carbon tetrachloride. J Pharm Pharmacol 2000;52:437-440.

[12] Kiso Y, Suzuki Y, Watanabe N, et al. Antihepatotoxic principles of Curcuma longa rhizomes. Planta Med 1983;49:185-187.

[13] Donatus IA, Sardjoko, Vermeulen NP. Cytotoxic and cytoprotective activities of curcumin. Effects on paracetamol-induced cytotoxicity, lipid peroxidation and glutathione depletion in rat hepatocytes. Biochem Pharmacol 1990;39:1869-1875.

[14] Soni KB, Rajan A, Kuttan R. Reversal of aflatoxin induced liver damage by turmeric and curcumin. Cancer Lett 1992;66:115-121.

[15] Kawamori T, Lubet R, Steele VE, et al. Chemopreventative effect of curcumin, a naturally occurring anti-inflammatory agent, during the promotion/progression stages of colon cancer. Cancer Res 1999;59:597-601.

[16] Thaloor D, Singh AK, Sidhu GS, et al. Inhibition of angiogenic differentiation of human umbilical vein endothelial cells by curcumin. Cell Growth Differ 1998;9:305-312.

[17] Mehta RG, Moon RC. Characterization of effective chemopreventive agents in mammary gland in vitro using and initiation-promotion protocol. Anticancer Res 1991; 11:593-596.

[18] Soudamini NK, Kuttan R. Inhibition of chemical carcinogenesis by curcumin. J Ethnopharmacol 1989;27:227-233.

[19] Azuine M, Bhide S. Chemopreventive effect of turmeric against stomach and skin tumors induced by chemical carcinogens in Swiss mice. Nutr Cancer 1992; 17:77-83.

[20] Boone CW, Steele VE, Kelloff GJ. Screening of chemopreventive (anticarcinogenic) compounds in rodents. Mut Res 1992; 267:251-255.

[21] Allen PC, Danforth HD, Augustine PC. Dietary modulation of avian coccidiosis. Int J Parasitol 1998; 28:1131-1140.

[22] Apisariyakul A, Vanittanakom N, Buddhasukh D. Antifungal activity of turmeric oil extracted from Curcuma longa (Zingiberaceae). J Ethnopharmacol 1995; 49:163-169.

[23] Rasmussen HB, Christensen SB, Kvist LP, Karazami A. A simple and efficient separation of the curcumins, the antiprotozoal constituents of Curcuma longa. Planta Med 2000; 66:396-398.

[24] Ramirez-Tortosa MC, Mesa MD, Aguilera MC, et al. Oral administration of a turmeric extract inhibits LDL oxidation and has hypocholesterolemic effects in rabbits with experimental atherosclerosis. Atherosclerosis 1999; 147:371-378.

[25] Srivastava R, Puri V, Srimal RC, Dhawan BN. Effect of curcumin on platelet aggregation and vascular prostacyclin synthesis. Arzneim Forsch 1986; 36:715-717.

[26] Ammon HPT, Wahl MA. Pharmacology of Cucuma longa. Planta Medica 1991;57:1-7.

[27] Thamlikitkul V, Bunyapraphathara N, Dechatiwongse T, et al. Randomized double-blind study of Curcuma domestica Val for dyspepsia. J Med Assoc Thai 1989; 72:613-20.

[28] Rafatulla S, Tariq M, Alyahya MA, et al. Evaluation of turmeric (Curcuma longa) for gastric and duodenal antiulcer activity in rats. J Ethnopharmacol 1990; 29:25-34.

In 1999, the Food and Drug Administration (FDA) officially recognized the cholesterol-lowering effects of soy protein, but allowing a new health claim which stated that 25 grams of soy protein per day may reduce the risk of heart disease. Now, in a new study published in the Journal of Nutrition, researchers have found that in increased intakes of soy protein may reduce cholesterol levels in people with type-2 diabetes. This study emphasized prevention by studying adults with type-2 diabetes who are free of diabetic complications and not taking glycemic or lipid-lowering mediations.

In a double -blind, randomized, crossover, placebo-controlled intervention study (Pipe et al 2009), 29 type-2 diabetics were assigned to consume a daily dose of 40 grams of soy protein isolate (SPI), which also contained 80 mg of aglycone isoflavones, or milk protein isolate for 57 days. At the end of the intervention they underwent a 28 day washout period, and then were assigned to receive the other protein. The results of the study showed that when using the soy protein, subjects experienced a significant reduction in LDL cholesterol levels of 0.17 mmol/l, and a reduction in the ratio of LDL to HDL cholesterol of 0.03 points.

Another result from soy protein consumption was a drop in the ratio of apolipoprotein B:apolipoprotein A-I, compared to the milk protein intervention. Apolipoprotein B is the main apolipoprotein of LDL cholesterol and is responsible for the transport of cholesterol to tissues. In high concentrations it has been linked to plaque formation in the blood vessels.

The researchers concluded, "These data demonstrate that consumption of soy protein can modulate some serum lipids in a direction beneficial for CVD risk in adults with type 2 diabetes,"

By Gene Bruno, MS, MHS

Probiotics, or friendly bacteria, are generally known for the role they play in gut health or-thanks to yogurt commercials-immune health. Based upon new research, the role of probiotics in immune health has expanded to include reducing cold and flu symptoms in children.

In a double-blind, placebo-controlled study (Leyer et al, 2009), 326 children (3-5 years of age) received either Lactobacillus acidophilus NCFM, or L. acidophilus NCFM in combination with Bifidobacterium lactis Bi-07, or a placebo twice daily for 6 months. The results were as follows:

Statistics indicate that the common cold is prevalent amongst children. Most children have about 6 to 10 colds annually and, in families with children in school, the number of colds each child gets each year increases dramatically to 12. Furthermore, every year an average of 5% to 20% of the population gets the flu, with young children being especially at risk. Also, between 8400 and 11,700 children 2 or more years of age are hospitalized from flu complications.

In consideration of these statistics, and given the relative safety of probiotics, the use of L. acidophilus NCFM alone or in combination with B. lactis Bi-07 appears to be a good method for treating cold and flu symptoms naturally.

Reference

Acai (pronounced ah-sigh-ee) is the berry from an Amazonian palm tree.  It contains an interesting mix of nutrients and phytochemicals including protein, lipids, calcium, vitamin A, phosphorus, iron, vitamin B1, vitamin C, several anthocyanins, proanthocyanidins, and other flavonoids. The anthocyanins are pigments that give the ripe fruit its purple color. Anthocyanins are also potent antioxidants. Acai fruit pulp has a very high antioxidant capacity. It has more antioxidant content than cranberry, raspberry, blackberry, strawberry, or blueberry.[1] [2] [3] [4]

Other benefits

In addition to its antioxidant properties, what else can acai do?  Apparently it has anti-inflammatory properties due to its ability act as a cyclooxygenase-1 (COX-1) and COX-2 inhibitor.[5] [6] In addition, reports are that acai is a traditional remedy for diabetes. Although there is no published evidence to support this benefit, it is known that oxidative stress may contribute to diabetes[7], and it is also known that anthocyanins may improve insulin secretion.[8]

Weight loss?

So what does all this have to do with weight loss? When perusing the internet there are many websites that claim acai is good for losing weight.  For example, one writer from eHow.com states, "I don't believe that Acai Berries hold a "magic key" that will help you lose weight, but it will help make your body healthy. When your body is healthy and well-balanced, it will be easier to reach your perfect weight."[9]

So basically, this author offers no real support that acai will actually help promote weight loss- just that it will help make you healthier which, in return, may help you loss weight. Following this same logic, the same could be said for a multivitamin. Anyone out there losing weight by taking Centrum^®?

Another website touting acai's weight loss benefits states, "The berry's natural concoction of essential fatty acids, fiber, phytosterols and amino acids work together to help your body burn fat more efficiently, process food more quickly and shed the unwanted pounds that you'd like to lose."[10] Really?  How exactly does that happen? I can't say because the author offers absolutely no support for the claim.

Another website alludes to a weigh loss mechanism through detoxification: "Acai berries also provide essential amino acids, a good source of carbohydrates and fibers, healthy fatty acids, and phytosterols which can speed up the metabolism considerably. This makes detoxification of impurities from the system move much faster."[11]  Sounds good, but where's the proof? Any studies, any history of traditional use? Nope.

There are more websites making similar claims, but none of them offer any substantiation for the alleged weight loss benefits of acai.

Conclusion

In short, acai offers some great antioxidant properties, so use it for that purpose if you desire. If you're taking it to help you lose weight, however, you may be sorely disappointed.

References

[1] Del Pozo-Insfran D, Brenes CH, Talcott ST. Phytochemical composition and pigment stability of Acai (Euterpe oleracea Mart.). J Agric Food Chem 2004;52:1539-45.

[2] Cordova-Fraga T, de Araujo DB, Sanchez TA, et al. Euterpe Oleracea (Acai) as an alternative oral contrast agent in MRI of the gastrointestinal system: preliminary results. Magn Reson Imaging 2004;22:389-93.

[3] Schauss AG, Wu X, Prior RL, et al. Phytochemical and nutrient composition of the freeze-dried Amazonian palm berry, Euterpe oleraceae mart. (acai). J Agric Food Chem 2006;54:8598-603.

[4] dos Santos GM, Maia GA, de Sousa PH, da Costa JM, de Figueiredo RW, do Prado GM. [Correlation between antioxidant activity and bioactive compounds of açaí (Euterpe oleracea Mart) comercial pulps] Arch Latinoam Nutr. 2008;58(2):187-92.

[5] Schauss AG, Wu X, Prior RL, et al. Antioxidant capacity and other bioactivities of the freeze-dried Amazonian palm berry, Euterpe oleraceae mart. (acai). J Agric Food Chem 2006;54:8604-10.

[6] Jensen GS, Wu X, Patterson KM, Barnes J, Carter SG, Scherwitz L, Beaman R, Endres JR, Schauss AG. In vitro and in vivo antioxidant and anti-inflammatory capacities of an antioxidant-rich fruit and berry juice blend. Results of a pilot and randomized, double-blinded, placebo-controlled, crossover study. J Agric Food Chem 2008 24;56(18):8326-33.

[7] Maxwell SR, et al. Poor glycaemic control is associated with reduced serum free radical scavenging (antioxidant) activity in non-insulin-dependent diabetes mellitus. Ann Clin Biochem 1997;34( Pt 6):638-44.

[8] Jayaprakasam B, Vareed SK, Olson LK, Nair MG. Insulin secretion by anthocyanins and anthocyanidins. J Agric Food Chem 2005;53:28-31.

[9] Huether K. How to Use Acai Berry for Weight Loss. eHow. Retrieved February 11, 2009 from http://www.ehow.com/how_4456371_use-acai-berry-weight-loss.html.

[10] Acai Berry the New Weight Loss Superfood. ProjectSwole2.0. July 17th, 2008. http://www.projectswole.com/diet/acai-berry-the-new-weight-loss-superfood/

[11] Ahmed M. Acai Berry Detox and Weight Loss - What You Really Need to Know. Ezine @rticles. Retrieved February 11, 2009 from http://ezinearticles.com/?Acai-Berry-Detox-and-Weight-Loss---What-You-Really-Need-to-Know&id=1790074.

Serrapeptase is a protein-digesting enzyme from the silk worm[1]. The type of protein it digests is not protein from your food, but rather certain types of protein-related substances in your body that are related to pain and inflammation. Research shows that once you swallow a tablet that contains serrapeptase, the serrapeptase is absorbed in your intestines[2] [3] and provides anti-inflammatory and pain-decreasing effects in inflamed or damaged tissue. [4] [5] [6]

These types of positive effects were reported in a study conducted by Dr. Laurent Bannock of the Santa Fe Center for Nutritional Medicine.[7] Dr. Bannock's patients complained primarily of osteoarthritis symptoms, an inflammatory condition, as well as rheumatoid arthritis, and even more inflammatory condition, and included other healthy challenges such as high cholesterol levels. In the study, Dr. Bannock gave his patients Naprinol^®, a dietary supplement containing serrapeptase and other protein-digesting enzymes, and available through Arthur Andrew Medical (http://www.arthurandrew.com/ or (800)-448-5015).

The results were that his patients experienced a significant reduction in pain and inflammation, with biochemical markers of inflammation being reduced by as much as 80% in some cases. In addition, patients experienced reductions in cholesterol and triglyceride levels-in some cases by 131 and 124 points, respectively.

In addition, serrapeptase was found to improve sinus congestion in individuals suffering from sinusitis.[8] When patients with chronic sinusitis supplemented with serrapeptase daily, nasal mucus secretions were thinned out,[9] there was significantly reduced pain, nasal secretions, nasal obstruction, and improved sense of smell.[10]

[1] Sandhya KV, Devi SG, Mathew ST. Quantitation of serrapeptase in formulations by UV method in the microplate format. Curr Drug Deliv 2008;5(4):303-5.

[2] Tachibana M, Mizukoshi O, Harada Y, et al. A multi-centre, double-blind study of serrapeptase versus placebo in post-antrotomy buccal swelling. Pharmatherapeutica 1984;3:526-30.

[3] Moriya N, Nakata M, Nakamura M, Takaoka M, Iwasa S, Kato K, Kakinuma A. Intestinal absorption of serrapeptase (TSP) in rats. Biotechnol Appl Biochem 1994;20(Pt 1):101-8.

[4] Tachibana M, Mizukoshi O, Harada Y, et al. A multi-centre, double-blind study of serrapeptase versus placebo in post-antrotomy buccal swelling. Pharmatherapeutica 1984;3:526-30.

[5] 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;18:379-88.

[6] 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;18:379-88.

[7] The End of Heart Disease and Arthritis. The Doctors' Prescription for Healthy Living 2008;10(1):8 pages.

[8] Majima Y, Hirata K, Takeuchi K, Hattori M, Sakakura Y. Effects of orally administered drugs on dynamic viscoelasticity of human nasal mucus. Am Rev Respir Dis 1990;141(1):79-83.

[9] Majima Y, Inagaki M, Hirata K, Takeuchi K, Morishita A, Sakakura Y. The effect of an orally administered proteolytic enzyme on the elasticity and viscosity of nasal mucus. Arch Otorhinolaryngol. 1988;244(6):355-9.

[10] 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;18:379-88.

 Tags: arthritis, cardiovascular, heart health, sinusitus, silk worms, supplements, nutrition

Previously, the incidence of vitamin B6 deficiency was thought to be relatively rare, affecting less than 200,000 people in the US population .[3]  New research from Tufts University, however, suggests that vitamin B6 deficiency is actually common, affecting large segments of the US population.[4]

In a study published in the American Journal of Clinical Nutrition³, researchers analyzed blood taken from 7,822 men, women and children (aged one year and up) for pyridoxal 5´-phosphate (PLP), the active form of vitamin B6.  PLP levels of less than 20 nmol/L were considered to represent a state of vitamin B6 deficiency. 

The results were that 11% of those who used dietary supplements, and nearly 25% of non-users, had PLP blood levels of less than 20 nmol/L, with a higher incidence among:

• women of reproductive age, especially current and former users of oral contraceptives
• male smokers
• non-Hispanic African-American men
• men and women over 65 years of age.

These deficiencies occurred despite the fact that many participants reported consuming more than the Recommended Daily Allowance for vitamin B6 in their diet.

Considering that there was a lower incidence of vitamin B6 deficiency among dietary supplement users (some of whom may not have been using supplements with vitamin B6), it appears prudent for Americans to supplement with this nutrient.  The use of a good multiple vitamin or B-complex product should provide adequate vitamin B6, as well as the other B vitamins.

[1] Bruno Jr EJ, Ziegenfuss TN. Water-soluble Vitamins: Research Update.  Current Sports Medicine Reports 2005; 4:207-213.

[2] Theodoratou SM, et al. Dietary Vitamin B6 Intake and the Risk of Colorectal Cancer. Cancer Epidemiology Biomarkers & Prevention 2008; 17:171-182.

[3] Pyridoxine deficiency. National Institutes of Health, Office of Rare Diseases.  Retrieved May 22, 2008 from http://rarediseases.info.nih.gov/GARD/Disease.aspx?PageID=4&diseaseID=4616.

[4] Morris MS, Picciano, MF, Jacques PF, Selhub, J. Trends of Vitamin B6 Status in US Population Sample. American Journal of Clinical Nutrition 2008;  87:1446 -54.

[1] Soleas GJ, Diamandis EP, Goldberg DM. Resveratrol: A molecule whose time has come? And gone? Clin Biochem 1997;30:91-113.

[2] Baur JA, Sinclair DA. Therapeutic potential of resveratrol: the in vivo evidence. Nature reviews. Drug discovery 2006; 5(6):493-506.

[3] Labinskyy N, Csiszar A, Veress G, Stef G, Pacher P, Oroszi G, Wu J, Ungvari Z. Vascular dysfunction in aging: potential effects of resveratrol, an anti-inflammatory phytoestrogen. Current medicinal chemistry 2006; 13(9):989-96.

[4] Okunieff P, Sun W, Wang W, Kim H, Yang S. Anti-cancer effect of resveratrol is associated with induction of apoptosis via a mitochondrial pathway alignment. Advances in Experimental Medicine and Biology 2008;614:179-86.

 Keywords: wine, resveratrol, cancer, cancer prevention, Mediterranean diet