Six ingredients for inflammation

The natural ingredients industry is delivering a range of natural anti-inflammatory bioactives to address the underlying cause of most degenerative disease states. Todd Runestad assesses the state of the science

Coronary heart disease, major depression, ageing and cancer are just some of the conditions characterised by an increased level of pro-inflammatory markers and mediators such as cytokines and eicosanoids. With pharmaceutical cox-2 inhibitors down for the count from their side effects, natural bioactives are just now coming into their own. Additional research will continue to tease out the mechanism of action for many natural ingredients, and may well find anti-inflammatory effects at their core.

From commodity ingredients such as vitamins C and E and dietary fibre to proprietary ones like LitoZin rose hip extract or Celadrin, the arsenal of natural products to address the many conditions with inflammation at their core will continue to expand. Consumers will be the better for it. Here is the state of the science behind six leading natural anti-inflammatory ingredients.

Omega-3 PUFAs
About twenty years ago researchers began looking at eicosanoid precursors as contributing mightily toward chronic inflammatory disorders. Prostaglandins, leukotrienes and other eicosanoids are synthesised from the PUFA arachidonic acid. It was suggested that alteration of cellular fatty acids may be a worthwhile approach to controlling inflammation.

Japanese researchers found that seniors who consumed large amounts of omega-3 fatty acids from fish had low levels of CRP

Two decades and hundreds of research studies later, it is now known that omega-3 PUFAs, in particular EPA and DHA, modulate the amount and types of eicosanoids such as prostaglandin E2 and leukotriene B4 that are made. In addition, mechanisms to control inflammation other than eicosanoid effects are now seen, including actions on intracellular signalling pathways and gene expression. 1 EPA and DHA are metabolised into anti-inflammatory prostaglandin E1. 2

This is in addition to the relatively simple arithmetic of omega-3s competing against pro-inflammatory omega-6 fatty acids, in particular EPA against arachidonic acid. Increasing the intake of omega-3 fatty acids while decreasing the omega-6 fatty acids in the diet has led to a decrease of nonsteroidal anti-inflammatory drugs used by people with rheumatoid arthritis and asthma.3,4

In short, omega-3 PUFAs have anti-inflammatory effects, and high dietary levels are associated with a lower incidence of inflammatory diseases. As R&D and product developers work closer with brand managers and marketers, this health message — of cutting back on foods and oils laden with omega-6s — ought to resonate throughout the food chain.

The carotenoid pigment astaxanthin has applications in a number of industries, ranging from its biggest use as aquaculture feed to the most lucrative in the nutraceutical and cosmetics fields. The micro-algae Haematococcus pluvialis is the richest source of natural astaxanthin. Carotenoids are known to take part in protecting marine animals against damage from free radicals.5

The cascade of inflammation begins with the release of pro-inflammatory cytokines such as tumour necrosis factor-alpha (TNF-alpha), interleukin-1B (IL-1B), and interleukin-6 (IL-6), as well as inflammatory mediators like nitric oxide and prostaglandin E2, which are synthesized by nitric oxide synthase and the cox enzymes.6

Beyond its pronounced effects as an antioxidant — one study showed astaxanthin to be 550 times stronger than vitamin E in singlet oxygen quenching — astaxanthin is showing benefits as an anti-inflammatory. 7 It appears to work through multiple pathways to combat inflammation throughout the entire body. It does act as a mild cox-1 and cox-2 inhibitor. It also suppresses the other inflammatory agents in the body such as prostaglandin E2, nitric oxide, IL-1B, TNF-alpha and C-reactive protein (CRP).

In one eight-week, double-blind, placebo-controlled human clinical trial, 15 subjects took 12mg/day BioAstin brand astaxanthin and eight took a placebo. CRP levels dropped a significant 20 per cent compared to placebo.8 CRP is one of the acute-phase proteins that increases during systemic inflammation.

A 2003 rat study found that astaxanthin inhibits iNOS enzyme activity, which decreases production of nitric oxide as well as prostaglandin E2 and TNF-alpha.9

Other research shows astaxanthin's utility with a range of inflammatory conditions including rheumatoid arthritis, carpal tunnel syndrome, tendonitis, joint and muscle soreness after exercise, and as an internal sunblock — another inflammatory condition because sunburn is an inflammation of the body's largest organ, the skin. Its effects are typically seen in two to four weeks.

Researchers in one study said astaxanthin's pronounced and widespread effects on inflammation were due to its potent antioxidant effects.6

The standardised extract of the bark of the French maritime pine (Pinus pinaster), Pycnogenol is one of those rare natural bioactives that works on a seemingly endless number of health conditions, from cardiovascular conditions to skin care, diabetes, asthma, allergies, menstrual disorders, varicose veins, cancer and inflammation.

Even more curious is the precise mechanism of action. Some studies show its utility as an antioxidant free radical scavenger. It binds to collagen and elastin. And it helps to vasodilate blood vessels.

What has been demonstrated is that Pycnogenol inhibits key triggers of inflammation. In a 2006 study on seven healthy human volunteers, 200mg/day exerted anti-inflammatory effects, apparently by inhibiting pro-inflammatory gene expression.10 This confirmed an earlier lab study that first postulated Pycnogenol works on a genetic level by suppressing TNF-alpha-induced activation of nuclear factor-kappa B (NF-kappaB) — a master switch known to regulate expression of more than 300 genes that promote an abnormal inflammatory response and can lead to disorders ranging from arthritis to cancer.11 Another small human study from 2006 found evidence that 200mg/day Pycnogenol inhibits pro-inflammatory eicosanoid-generating enzymes.12 A second arm of this study found that a single dose of 300mg significantly inhibited cox-1 and cox-2 enzymes after only 30 minutes.

Even the active principles are a matter of some debate, though chemical identification studies show that Pycnogenol is primarily composed of procyanidins and phenolic acids.13

The pungent yellow spice ground from the root of the Curcuma longa plant, curcumin is found in both turmeric and curry powders. Curcumin shuts down NF-kappaB.

When NF-kappaB is signaled, it releases pro-inflammatory cytokines such as TNF-alpha and IL-6.14 Numerous recent studies, working in a variety of experimental models, demonstrate that curcumin effectively targets NF-kappaB gene products.15

In addition, recent work suggests another anti-inflammatory mechanism of curcumin is that it inhibits prostaglandin E2 formation. It does this by targeting its precursor, IL-1B, as well as the cox-2 enzyme.16

This gene-receptor association was confirmed in another 2005 study, which found that curcumin can block the earliest events in the inflammation cascade by modifying the protein thiols, thereby altering the activity of the affected proteins.17

Dried extracts of the resin of the Boswellia serrata tree have been used since antiquity in India to treat inflammatory conditions. Boswellia contains anti-inflammatory triterpenoids called boswellic acids, or total organic acids.

The boswellic acids reduce inflammation by inhibiting production of pro-inflammatory 5-lipoxygenase (5-LO) chemicals and blocking leukotriene synthesis.18 Leukotrienes are important mediators in inflammatory and allergic processes that are produced from arachidonic acid, an essential fatty acid synthesised in the body via 5-LO.19,20 It has been suggested that the boswellic acids inhibit 5-LO by either directly interacting with 5-LO or by interacting with the 5-LO-activating protein.18 It appears the boswellic acids are unique in their inhibition of 5-LO as well as another pro-inflammatory enzyme, human leukocyte elastase.21

All patients receiving boswellia reported decreased knee pain and increased flexion

In one study of 30 patients with inflammatory bowel disease (chronic colitis), 20 were given boswellia extract 300mg three times a week for six weeks, and the other 10 were given boswellia, 1g three times a day. Of the 20 treated with 300mg boswellia, 14 went into remission, as did four of the 10 treated with 1g boswellia. The inflammatory process in colitis is associated with increased formation of leukotrienes. The key enzyme for leukotriene biosynthesis is 5-LO, which was found to be inhibited by boswellia. 22 A randomised, double-blind, placebo-controlled crossover study was conducted to assess the efficacy, safety and tolerability of Boswellia serrata extract in 30 patients with osteoarthritis of the knee for eight weeks. All patients receiving boswellia reported decreased knee pain, increased knee flexion and increased walking distance. The frequency of swelling in the knee joint was decreased. Boswellia serrata extract was well tolerated by the subjects except for minor gastrointestinal symptoms. 23

When the body's immune system gets stimulated into action, NF-kappaB activates genes that turn on production of the cox-2 enzyme, one of the body's inflammatory agents. In 2000, when conjugated linoleic acid (CLA) was still not often discussed in the functional ingredients world, researchers at the American Chemical Society's national meeting presented a unique animal study. They found that the more CLA they fed to lab animals or in vitro, the more resistant they became at producing cox-2 and other inflammatory agents. What's more, the CLA not only decreased the production of cox-2 but it also decreased the activity of the cox-2 that was produced.24

In a 2004 cell study, other researchers found that CLA reduced the ability of NF-kappaB to attach to DNA, which in turn reduced gene activity related to inflammation. By reducing NF-kappaB activity, CLA decreased the pro-inflammatory activity of the cox-2 enzyme and prostaglandin E2. CLA also reduced activity of nitric oxide, which also can have pro-inflammatory effects. The 2004 study was the first report to show that CLA has anti-inflammatory properties by reducing the activity of NF-kappaB.25

The Chemical Society researchers in 2005 followed up with an animal study that confirmed their earlier work. They examined the effects of 10t,12c-CLA and 9c,11t-CLA on cox-2 expression and prostaglandin E2 (PGE2) production. The cox-2 expression level was inhibited 80 per cent by 10t, 12c-CLA compared to only 26 per cent by 9c,11t-CLA in vitro. PGE2 production was decreased from 5.39 to 1.12 by 10t,12c-CLA and from 5.7 to 4.5 by 9c,11t-CLA. In a separate arm, mice fed 10t,12c-CLA but not 9c,11t-CLA were found to have a 34 per cent decrease in cox-2 and a 43 per cent reduction of PGE2 release in the lung. They concluded that reduced cox-2 levels were attributable to the CLA inhibiting the NF-kappaB pathway.26

An important note is that the CLA researched and marketed for weight management is generally a 50:50 mixture of cis-9, trans-11 with trans-10, cis-12, whereas the isomer found to have better efficacy against inflammation is trans-10, cis-12. However, trans-10, cis-12 has shown to increase insulin resistance in susceptible people, whereas the combination does not appear to have that effect.27,28

1. Simopoulos AP. Omega-3 fatty acids in inflammation and autoimmune diseases. J Am Coll Nutr 2002;21(6):495-505.
2. Das UN. Essential fatty acid metabolism in patients with essential hypertension, diabetes mellitus and coronary heart disease. Prostaglanding Leukot Essent Fatty Acids 1995;52:387-91.
3. Sundrarjun T, et al. Effects of n-3 fatty acids on serum interleukin-6, tumour necrosis factor-alpha and soluble tumour necrosis factor receptor p55 in active rheumatoid arthritis. J Int Med Res 2004 Sep-Oct;32(5):443-54.
4. Nagakura T, et al. Dietary supplementation with fish oil rich in omega-3 polyunsaturated fatty acids in children with bronchial asthma. Eur Respir J 2000 Nov;16(5):861-5.
5. Wang X, et al. Astaxanthin-rich algal meal and vitamin C inhibit Helicobacter pylori infections in BALB/cA mice. Antimicrob Agents Chemother 2000;44:2452-7.
6. Seon-Jin L, et al. Astaxanthin inhibits nitric oxide production and inflammatory gene expression by suppressing IkB kinase-dependent NF-kB activation. Mol Cells 2003;16(1);97-105.
7. Shimizu, N. et al. Carotenoids as single oxygen quenchers in marine organisms. Fisheries Sci 1996; 62;134-7.
8. Spiller GA, et al. Effect of daily use of natural astaxanthin on C-reactive protein. Unpublished.
9. Ohgami K, et al. Effects of astaxanthin on lipopolysaccharide-induced inflammation in vitro and in vivo. Ophthamol Visual Sci 2003 Jun;44(4):2694-2701.
10. Grimm T, et al. Inhibition of NF-kappaB activation and MMP-9 secretion by plasma of human volunteers after ingestion of maritime pine bark extract (Pycnogenol). J Inflamm 2006 Jan 27;3:1
11. Peng Q, et al. Pycnogenol inhibits tumor necrosis factor-alpha-induced nuclear factor kappa B activation and adhesion molecule expression in human vascular endothelial cells. Cell Mol Life Sci 2000 May;57(5):834-41.
12. Schafer A, et al. Inhibition of COX-1 and COX-2 activity by plasma of human volunteers after ingestion of French maritime pine bark extract (Pycnogenol). Biomed Pharmacother 2006 Jan;60(1):5-9.
13. Rohdewald P. A review of the French maritime pine bark extract (Pycnogenol), a herbal medication with a diverse clinical pharmacology. Int J Clin Pharmacol Ther 2002 Apr;40(4):158-68.
14. Kim KH, et al. The inhibitory effect of curcumin on the growth of human colon cancer cells in vitro. Korean J Gastroenterol 2005 Apr;45(4):277-84.
15. Shishodia S, et al. Curcumin (diferuloylmethane) inhibits constitutive NF-kappaB activation, induces G1/S arrst, suppresses proliferation, and induces apoptosis in mantle cell lymphoma. Biochem Pharmacol 2005 Sep 1;70(5):700-13.
16. Moon Y, et al. Curcumin suppresses interleukin 1 (beta)-mediated microsomal prostaglandin E synthase 1 by altering early growth response gene EGR-1 and other signaling pathways. J Pharmacol Exp Ther 2005 Nov;315(2):788-95.
17. Jurrmann N, et al. Curcumin blocks interleukin-1 signaling by inhibiting the recruitment of the IL-1 receptor-asociated kinase IRAK in murine thymoma EL-4 cells. J Nutr 2005 Aug;135(8):1859-64.
18. Safayhi H, et al. Boswellic acids: novel, specific, nonredox inhibitors of 5-lipoxygenase. J Pharmacol Exp Ther 1992;261(3):1143-6.
19. Henderson WR. The role of leukotrienes in inflammation. Ann Intern Med 1994;121:684-97.
20. Hutchinson F, et al. 5-lipoxygenase. Ann Rev Biochem 1993;63:383-417.
21. Sailer E-R, et al. Characterization of acetyl-11-keto-b-boswellic acid and arachidonate-binding regulatory site of 5-lipoxygenase using photoaffinity labeling. Eur J Biochem 1998;256:364-8.
22. Effects of gum resin of Boswellia serrata in patients with chronic colitis. Planta Med 2001 Jul;67(5):391-5.
23. Efficacy and tolerability of Boswellia serrata extract in treatment of osteoarthritis of knee — a randomized double blind placebo controlled trial. Phytomedicine 2003 Jan;10(1):3-7.
24. Cook ME, et al. Regulation of inducible prostanoids and leukotrienes by conjugated linoleic acid (CLA). American Chemical Society 220th National Meeting. Aug 21. Washington DC.
25. Cheng WL, Lii CK, Chen HW, et al. Contribution of conjugated linoleic acid to the suppression of inflammatory responses through the regulation of the NF-kB pathway. J Agric Food Chem 2004;52:71-8.
26. Li G, et al. 10t,12c-conjugated linoleic acid inhibits lipopolysaccharide-induced cyclooxygenase expression in vitro and in vivo. J Lipid Res 2005 Oct;46(10):2134-42.
27. Riserus U, et al. Treatment with dietary trans10cis12 conjugated linoleic acid causes isomer-specific insulin resistance in obese men with the metabolic syndrome. Diabetes Care 2002;25:1516—21.
28. Riserus U, et al. Supplementation with conjugated linoleic acid causes isomer-dependent oxidative stress and elevated C-reactive protein: a potential link to fatty acid-induced insulin resistance. Circulation 2002;106:1925—9.

Inflammation nation: olive oil and antioxidants
Two other families of nutrients have bearing on the inflammatory process. The omega-9 fatty acids, such as oleic acid (found in olive oil, macadamia nut oil, and avocadoes) have a mild anti-inflammatory effect, and they seem to be synergistic with the omega-3s.1

Antioxidants can also reduce inflammation. Free radicals, secreted by white blood cells, fuel the inflammatory response, such as by activating gene-transcription factors (e.g., nuclear factor kappa beta) that turn on pro-inflammatory genes. Because antioxidants quench free radicals, they can help dampen inflammatory reactions. Several studies have found that supplemental vitamin E can reduce CRP levels in people.2,3

— Jack Challem

1. Hwang D. Essential fatty acids and immune response. FASEB Journal, 1989;3:2052-2061.
2. Upritchard JE, et al. Effect of supplementation with tomato juice, vitamin E, and vitamin C on LDL oxidation and products of inflammatory activity in type 2 diabetes. Diabetes Care 2000, 23:733-738.
3. Devaraj S, Jialal I. Alpha tocopherol supplementation decreases serum C-reactive protein and monocyte interleukin-6 levels in normal volunteers and type 2 diabetic patients. Free Radical Biology & Medicine 2000; 29:790-792.

Jack Challem: How dietary and biochemical imbalances fuel one of the major causes of disease
Inflammation, which we typically associate with redness and pain, is at its best a normal and protective process. After we're injured, be it a bruise or a cut, inflammation stimulates the healing process and helps fight infections. But a more subtle form of inflammation, sometimes called silent or low-gradeinflammation, sets the stage for coronary artery disease, Alzheimer's and about one-third of cancers.

In the 1990s, researchers developed an inexpensive medical test — high-sensitive C-reactive protein (hsCRP) — to measure this subtle form of inflammation. The availability of the hsCRP test prompted a wave of new research. As a result, in less than 10 years biomedical researchers have increasingly become convinced that chronic low-grade inflammation is the root cause of coronary artery disease.

The co-inventor of the hsCRP test, Paul M Ridker, MD, of the Harvard Medical School, found that high blood levels of C-reactive protein (CRP) were associated with three times the risk of a heart attack in men and four-and-one-half times the risk in women.1,2 Subsequent research found that high levels of CRP were far more accurate than low-density lipoprotein (LDL) cholesterol in predicting cardiovascular disease risk.3

Inflammation maintains a sustained level of immune activity, much like when a mechanic sets a car's engine idle too high. Inflammation increases the risk of cholesterol deposits rupturing, leading to blood-vessel blockages and a heart attack.4 It also stiffens blood vessels, leading to impaired blood flow.5 Normally, undulations in flexible blood-vessel walls help the heart circulate blood.

CRP and inflammation
Several processes relating to inflammation appear to set the stage for heart disease. In one scenario, elevated blood levels of homocysteine, a potentially toxic amino acid, injure cells in the artery wall. In response, the body deposits low-density lipoprotein (LDL) cholesterol, much like a salve, into the matrix of artery cells.6

Although LDL per se does not attract white blood cells, oxidized LDL does. Monocytes and other types of white blood cells attack oxidized LDL as they would a bacterial infection. These immune cells engulf globules of oxidized LDL and then become stuck in the artery's cellular matrix.7 The immune cells leak out free radicals and cytokines, which further stimulate the inflammatory response. Meanwhile, the cholesterol deposit continues to grow.

A similar process, but one with far more systemic consequences, occurs with the accumulation of abdominal adipocytes — fat cells around the belly — perhaps better known as a 'beer belly.' Adipocytes secrete a variety of pro-inflammatory cytokines, including interleukin-6 (IL-6), arguably the most inflammatory cytokine, and its byproduct, CRP. Cytokines are cell-communication molecules, and IL-6 and CRP signal the immune system to maintain or increase its inflammatory response. White blood cells infiltrate the spaces between the fat cells and release still more pro-inflammatory IL-6 and CRP.8

Abdominal obesity is regarded as the principal risk factor for type-2 diabetes and heart disease. Studies have found that all three conditions have an undercurrent of low-grade inflammation, leading to what could best be described as an 'inflammation syndrome.9,10 Essentially, the immune system is revved up, and without a bacterial infection to fight, the immune cells maintain chronic low-grade inflammation and attack their host.

Omega-3, -6 and -9 pathways
Identifying the causes of disease is often like peeling off the skin of an onion. Inflammation may be the underlying cause of heart disease and arthritis, but what is the cause of an inflammatory reaction that seems to know no end?

Prescription treatments for inflammation, such as cox-2 inhibitor drugs and aspirin, skirt the periphery of the problem. These drugs target downstream enzymes in the omega-6 and omega-3 fatty acid pathways. But peel back one more layer, and a major part of the problem is an imbalance between these two biochemical pathways.

The omega-6 pathway is primarily pro-inflammatory, and the parent dietary molecule is linoleic acid, found in corn, soy and safflower oils. Through a number of steps, it is converted to arachidonic acid and then to very potent inflammatory compounds, such as prostaglandin E2.11,12

Meanwhile, the omega-3 pathway is so weakly inflammatory that it is often considered anti-inflammatory. The parent molecule is alpha-linolenic acid, found in flax, vegetables and seafood, and it is converted to docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA).

There are clear advantages to including ample omega-3 fatty acids in the diet. A recent study by Japanese researchers found that seniors who consumed large amounts of omega-3 fatty acids from fish had low levels of CRP. People with the greatest consumption of omega-3s had about half the CRP levels as those who ate small amounts of these healthy fats.13 Some studies have found direct CRP-lowering benefits from omega-3 supplements.14

The omega-9 fatty acids, such as oleic acid (found in olive oil, macadamia-nut oil and avocadoes), have a mild anti-inflammatory effect, and they seem to be synergistic with the omega-3s.15

Jack Challem is the author of The Inflammation Syndrome (Wiley, 2003) and Feed Your Genes Right (Wiley, 2005). His next book, The Food-Mood Solution, will be published in February 2007.

1. Ridker PM, et al. Inflammation, aspirin, and the risk of cardiovascular disease in apparently healthy men. N Engl J Med 1997;336:973-9.
2. Ridker PM, et al. C-reactive protein and other markers of inflammation in the prediction of cardiovascular disease in women. N Engl J Med 2000;342:836-43.
3. Ridker PM, et al. Comparison of C-reactive protein and low-density lipoprotein cholesterol levels in the prediction of first cardiovascular events. N Engl J Med 2002;347:1557-65.
4. Burke AP, et al. Elevated C-reactive protein values and atherosclerosis in sudden coronary death: association with different pathologies. Circulation 2002;105:2019-23.
5. Vlachopoulos C, et al. Acute systemic inflammation increases arterial stiffness and decreases wave reflections in healthy individuals. Circulation 2005;112:2193-2200.
6. McCully KS. Chemical pathology of homocysteine. I. Atherogenesis. Ann Clin Lab Sci 1993;23:477-93.
7. Jialal I, Devaraj S. The role of oxidized low density lipoprotein in atherogenesis. J Nutr 1996;126(4 Suppl):1053S-7S.
8. Bastard JP, et al. Recent advances in the relationship between obesity, inflammation, and insulin resistance. Eur Cytokine Netw 2006;17:4-12.
9. Kahn SE, et al. Obesity is a major determinant of the association of C-reactive protein levels and the metabolic syndrome in type 2 diabetes. Diabetes 2006;55:2357-64.
10. de Rekeneire N, et al. Diabetes, hyperglycemia, and inflammation in older individuals: the health, aging and body composition study. Diabetes Care 2006;29:1902-8.
11. Heller A, Koch T, et al. Lipid mediators in inflammatory disorders. Drugs 1998;55:487-96.
12. Grimble RF. Nutritional modulation of cytokine biology. Nutrition 1998;14:634-640.
13. Niu K, et al. Dietary long-chain n-3 fatty acids of marine origin and serum c-reactive protein concentrations are associated in a population with a diet rich in marine products. Am J Clin Nutr 2006;84:223-9.
14. Lau CS, et al. Effects of fish oil supplementation on non-steroidal anti-inflammatory drug requirement in patients with mild rheumatoid arthritis — a double-blind placebo controlled study. Br J Rheumatol 1993;32:982-9.
15. Hwang D. Essential fatty acids and immune response. FASEB Journal, 1989;3:2052-2061


Select suppliers
Targeting inflammation with a variety of ingredients solutions

Tonalin brand conjugated linoleic acid is the industry's top-selling CLA brand.

Croda Health Care
Incromega omega-3 concentrates provide EPA up to 70 per cent purity to target a range of inflammatory conditions.

BioAstin natural astaxanthin is an antioxidant and anti-inflammatory carotenoid grown in Hawaii.

InterHealth Nutraceuticals
UC-II is a patented undenatured type II collagen complex that promotes healthy joints while improving joint mobility and flexibility.

Biocell Technology
BioCell Collagen II is a natural hydrolysed type II collagen ingredient with chondroitin and hyaluronic acid.

Lipid Nutrition
Clarinol branded CLA comes in three forms for supplements, foods and beverages.

Lyc-O-Mato brand broad-spectrum tomato extract inhibits inflammation marker TNF-alpha by one third.

Natural Health Science/Horphag Research
Exclusive suppliers of the French maritime pine bark.

Pacific Rainbow
Celadrin is a compound developed through a proprietary process of esterifying oils and aimed at the joint-health market.

PL Thomas
5-Loxin is a standardised Boswellia serrata extract.

Curcumin C3 Complex is standardised to 95 per cent curcuminoids.

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