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Formula Aim: To assist in the management of arthritis and degenerative diseases of the musculo-skeletal system by reducing inflammatory processes and pain, reduce the breakdown while supporting regeneration of connective tissue elements, improve micro-circulation, stimulate the production and provide the basic nutrients for joint regeneration.

The herbs that can assist are;

• anti-inflammatory activity (Devil’s Claw, Blackcurrant, Rosehip, Turmeric, Glucosamine)• analgesia (Devil’s Claw)• reducing or blocking joint tissue breakdown (Devil’s Claw, Blackcurrant, Turmeric)• regenerating connective tissue elements (Devil’s Claw, Blackcurrant, Gotu Kola)• establishing new blood vessels improving micro-circulation and nutrient supply

(Blackcurrant, Gotu Kola)• stimulate the production of joint building blocks (Turmeric, Gotu Kola)• nutrient supply for joint health (Blackcurrant, Rosehip, Turmeric, Glucosamine)

Devil’s Claw Root (Harpagophytum procumbens)

Devil’s Claw is the primary herb, used for its proven effect on osteoarthritis and degenerative diseases of the musculoskeletal system. More specifically its anti-inflammatory, analgesic, antioxidant and modulation of matrix-degrading enzymes activities.

Anti-inflammatory

It is generally accepted that a well manufactured extract of Devil's Claw will alleviate inflammatory conditions such as arthritis and rheumatism (Darshan et al., 2004).

• In 1997, an experiment demonstrated the anti-inflammatory effects of Devil's Claw. (An analytical study, 1997).

• Rats were injected with Freund's adjuvant in sub-plantar tissue of the right posterior paw and randomly assigned in acute (25, 50, or 100 mg/kg) or chronic (100 mg/kg) treatments with Devil's Claw solution test or vehicle. The results show that Devil's Claw extract increased the animals 'latency of paws' withdrawal, indicating a protective effect against the pain induced by the thermal stimulus, both in acute and chronic treatments. The data showed anti-inflammatory and peripheral analgesic properties of Devil's Claw (Andersen ML, 2004).

• Devil's Claw extract was shown to prevent the LPS-induced synthesis of tumour necrosis factor alpha (TNFá) in stimulated primary human monocytes in a dose-dependent manner. This suggested that Devil's Claw extract might have anti-inflammatory properties on the skeletal system. (Fiebich BL et al, 2001)

• Devil's Claw extract was shown to suppress PGE(2) synthesis and nitric oxide production by inhibiting lipopolysaccharide-stimulated enhancement of the cyclo oxygenase-2 and inducible nitric oxide synthase (iNOS) mRNAs expressions in L929 cells. These results suggest that Devil's Claw extract exerts anti-inflammatory and analgesic effects probably by

To support aged joints and provide relief from the symptoms of degenerative joint disease.

Devil’s Claw, Blackcurrant, Rosehip, Turmeric, Gotu Kola, Glucosamine

This document is for educational purposes only.Any similarity between actual products and theformula described herein is purely coincidental.

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FOR EDUCATIONAL PURPOSES ONLY

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suppressing cyclo oxygenase-2 and iNOS expressions.(Jang MH et al, 2003)

• Devil's Claw extracts were found to interfere with the transcriptional activation of iNOS. (Kaszkin M et al, 2004.)

• Inhibits NF-kappaâ activation, cyclo-oxygenase-2 and nitric oxide, limiting downstream inflammation and pain (Huang et al.,2006)

Analgesic

Several studies have demonstrated the analgesic effects of Devil's Claw (An analytical study, 1997). • In a study of mice and rats, Devil's Claw extract exerted anti-inflammatory and analgesic

effects in a dose-dependent fashion (Lanhers MC, 1992)

• Devil's Claw extract with at least 50 mg harpagoside in the daily dose may help pain management. The author believes that treatment with Devil's Claw extract may have a lower risk of adverse events than treatment with synthetic analgesics (Chrubasik S., 2004).

• 130 patients suffered from back pain were supplemented with Devil's Claw extract for eight weeks. 117 patients showed improvement of pain symptoms and mobility of the affected sections of their spine. No serious Devil's Claw side effects were observed (Laudahn D et al,

2001).• Strong evidence exists for the use of an aqueous Devil's Claw extract at a daily dose

equivalent of 50 mg harpagoside in the treatment of acute exacerbations of chronic non-specific low-back pain (Gagnier JJ 2004).

Effect on Osteoarthritis and degenerative diseases of the Musculoskeletal System.

Due to its anti-inflammatory and analgesic properties the benefits on osteoarthritis are almost expected.• In a 4 month-double-blind, randomized, multi-centre clinical study of 122 patients suffered

from osteoarthritis showed that 435 mg of Devil's Claw powder was as effective as 100 mg of diacerhein in the treatment of osteoarthritis. While, the frequency of side events (e.g. diarrhea) was significantly lower in the Devil's Claw group, the global tolerance assessment by patients at the end of treatment favoured the Devil's Claw powder (Chantre P, 2000)

• A multi-centre, randomized, double-blind, parallel-group study of 122 patients with hip and/or knee osteoarthritis demonstrated that high dose of Devil's Claw was as effective as diacerhein in the treatment of knee or hip osteoarthritis (Leblan D et al, 2000).

• In a 4 week-double-blinded study of 63 patients suffering from muscular tension or slight muscular pain of the back, shoulder and neck, Devil's Claw extract improved the patients’ score or performance on visual analogue scale, the pressure algometer test, the muscle stiffness test and the muscular ischaemia test. Tolerability for Devil's Claw extract was good; no serious adverse effects occurred (Wegener T., 2003).

• A 4 week-randomized, double-blind, placebo controlled study of patients with slight to moderate muscular tension at back, shoulder and neck showed the beneficial effects of Devil's Claw extract (2X480 mg/day) on sensory, motor and vascular mechanisms of muscle pain (Gobel H et al., 2001).

Devil's Claw has an ability to modulate the production of matrix-degrading enzymes.

• Arthritis and osteoarthritis are characterized by a loss of articular cartilage due to an imbalance between synthesis and degradation of the extracellular cartilage matrix. These diseases are accompanied by an increased induction of cytokines such as interleukin 1 beta (IL-1β) and tumour necrosis factor alpha (TNF-α). The increased release of cytokines leads to an enhanced production of matrix-degrading enzymes e.g. the matrix metalloproteinases (MMPs). Western blot analysis showed that the Devil's Claw extracts decreased significantly the production of MMPs in chondrocytes (Schulze-Tanzil G et al, 2004)

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Antioxidant

Devil's Claw extract is particularly rich in antioxidants (Betancor-Fernandez A et al, 2003) and has been demonstrated to scavenge super-oxide dose-dependently (Langmead L et al, 2002).

References

1. Andersen ML, Evaluation of acute and chronic treatments with Harpagophytum procumbens on Freund's adjuvant-

induced arthritis in rats. J Ethnopharmacol. 2004 Apr;91(2-3):325-30. 2. An analytical study, anti-inflammatory and analgesic effects of Harpagophytum procumbens and Harpagophytum

zeyheri. Planta Med. 1997 Apr;63(2): 171-6. 3. Betancor-Fernandez A et al, Screening pharmaceutical preparations containing extracts of turmeric rhizome,

artichoke leaf, devil's claw root and garlic or salmon oil for antioxidant capacity. J Pharm Pharmacol. 2003 Jul;55(7):981-6.

4. Chantre P, Efficacy and tolerance of Harpagophytum procumbens versus diacerhein in treatment of osteoarthritis. Phytomedicine. 2000 Jun;7(3):177-83

5. Chrubasik S. Devil's claw extract as an example of the effectiveness of herbal analgesics Orthopade. 2004 Jul;33(7):804-8.

6. Darshan S, Doreswamy R. Patented anti-inflammatory plant drug development from traditional medicine. Phytother Res. 2004 May;18(5):343-57.

7. Fiebich BL et al, Inhibition of TNF-alpha synthesis in LPS-stimulated primary human monocytes by Harpagophytum (Devil's Claw) extract SteiHap 69. Phytomedicine. 2001 Jan;8(1):28-30.

8. Gagnier JJ Harpgophytum procumbens for osteoarthritis and low back pain: a systematic review. BMC Complement Altern Med. 2004 Sep 15;4(1):13.

9. Gobel H et al Effects of Harpagophytum procumbens on sensory, motor und vascular muscle reagibility in the treatment of unspecific back pain Schmerz. 2001 Feb;15(1):10-8.

10. Jang MH et al, Harpagophytum procumbens suppresses lipopolysaccharide-stimulated expressions of cyclo oxygenase-2 and inducible nitric oxide synthase in fibroblast cell line L929. J Pharmacol Sci. 2003 Nov;93 (3):367-71.

11. Kaszkin M et al, Downregulation of iNOS expression in rat mesangial cells by special extracts of Harpagophytum procumbens derives from harpagoside-dependent and independent effects. Phytomedicine. 2004 Nov;11(7-8):585-95.

12. Langmead L et al, Antioxidant effects of herbal therapies used by patients with inflammatory bowel disease: an in vitro study. Aliment Pharmacol Ther. 2002 Feb;16(2):197-205.

13. Lanhers MC Anti-inflammatory and analgesic effects of an aqueous extract of Harpagophytum procumbens. Planta Med. 1992 Apr;58(2):117-23.

14. Laudahn D et al, Efficacy and tolerance of Harpagophytum extract LI 174 in patients with chronic non-radicular back pain. Phytother Res. 2001 Nov;15(7):621-4.

15. Leblan D et al, Harpagophytum procumbens (Devil's Claw) in the treatment of knee and hip osteoarthritis. Four-month results of a prospective, multi-centre, double-blind trial versus diacerhein. Joint Bone Spine. 2000;67(5):462-7.

16. Schulze-Tanzil G et al, Effect of a Harpagophytum procumbens (DevilÂ’s Claw) extract on matrix metalloproteinases in human chondrocytes in vitro. Arzneimittelforschung. 2004;54(4):213-20.

17. Wegener T Treatment of patients with arthrosis of hip or knee with an aqueous extract of devil's claw (Harpagophytum procumbens DC.). Phytother Res. 2003 Dec;17(10):1165-72.

Blackcurrant Fruit (Ribes nigrum)

Blackcurrant has been chosen due to its high levels of anthocyanidins and Vitamin C. More specifically for its anti-inflammatory, antioxidant and tissue trophorestorative activity.

The berries are rich in polyphenolic compounds and especially in anthocyanins, demonstrating antioxidant activity. Antioxidant activities of plant products contribute multiple health benefits.

Blackcurrants are high in biotin, a key component of the claw and hoof wall. Although the dietary requirements for biotin in dogs and horses are not well defined, the responses to biotin supplementation to improve hoof quality are quite significant.(E. A. Buffa et al., 1992, H. Josseck et al.,

1995) After 5 months of supplementation hoof condition of all 55 of a group of thoroughbreds and draft horses showed marked improvement.(Comben et al., 1984)

Although traditionally Bilberry was considered the best source of anthocyanins which give the berries their deep purple colouring and have extremely high antioxidant activity. Bilberry is not

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grown in NZ on a commercial scale so must be sourced from Europe or USA. However recent trials by the New Zealand Institute for Plant and Food Research on NZ grown Blackcurrant have shown it to be equal to even the best bilberries for anthocyanin levels.

Figure 1. Typical Anthocyanin levels in common fruit (unit: mg/100g)

The fruit is also extraordinarily high vitamin C content at 160mg /100 g

Figure 2. Typical Vitamin C levels in common fruit (unit: mg/100g)

(

Summary of three trials carried out by the New Zealand Black Currant Cooperative.

Anthocyanins increase bloodflow.

In a human trial subjects consumed anthocyanin (100mg) equivalent to two tablespoons of blackcurrant berries.• Anthocyanin content of plasma reached a maximum after 1 hour, and decreased to 50% by

4 hours.• After 1 hour the forearm blood flow increased significantly (about 40%) compared to

placebo.In another study 50mg of anthocyanin was shown to improve blood circulation in cold hands.• Hands were soaked in cold water at 10°C for 1 minute. For subjects who had consumed

blackcurrants hand temperature returned to normal after 7 minutes, compared to 13 minutes for the placebo group.

http://www.nzblackcurrants.com).

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Fruit mg Anthocyan/100g fresh product

Major Anthocyanidin

Raspberry rubus idaeus 40 Cyanidin

Blackberry rubus caesiuss 160 Cyanidin

Bilberry Vaccinium myrtillus 165 Delphinidin, Malvidin, Petunidin

Black Currant Ribes nigrum 270 Cyanidin, Delphinidin

Fruit mg/100g

Blackcurrant 160

Kiwifruit 93

Orange 36

Cranberry 13

Blueberry 10

Bilberry 1

Fruit mg/100g

Blackcurrant 160

Kiwifruit 93

Orange 36

Cranberry 13

Blueberry 10

Bilberry 1

(http://www.nzblackcurrants.com).

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Blackcurrants reduce muscle stiffness by increasing peripheral blood flow and reducing muscle fatigue.• Subjects consumed anthocyanin (50mg) equivalent to one tablespoon of blackcurrant

berries and carried out keyboard work for 30 minutes.• Total haemoglobin was significantly higher (about 40%) in the blackcurrant intake group.

Oxygenated haemoglobin was significantly higher in the blackcurrant intake group.• There was significant stiffening of the trapezius (shoulder) muscle during typing in the

placebo but not the blackcurrant intake group. However, final stiffness was not significantly different between the two.

(http://www.nzblackcurrants.com)

The Importance of Anthocyanidins In the course of inflammation, enzymes damage connective tissue in capillaries, causing

blood to leak into surrounding tissues. Oxidants are released and further damage blood-vessel walls.

Anthocyanins protect in several ways. First, they neutralize enzymes that destroy connective tissue. Second, their antioxidant capacity prevents oxidants from damaging connective

tissue. Finally, they repair damaged proteins in the blood-vessel walls.

Studies to support use

Animal experiments have shown that supplementation with anthocyanins effectively prevents inflammation and subsequent blood-vessel damage (Bertuglia S. et al., 1995).

Anthocyanins anti-inflammatory ability has been shown to help dampen allergic reactions. In one study, Bulgarian researchers gave animals histamine and serotonin, both of which cause allergic reactions and increase capillary permeability. The animals were supplemented with a variety of flavonoids. Anthocyanins were found to have the strongest anti-inflammatory effect of any flavonoid tested (Borissova P, et al. 1994).

Dietary polyphenols have been found to inhibit cellular enzymes, such as PLA2, COX and LOX, in order to reduce arachidonic acid, prostaglandins and leukotrienes production, thus exerting an important anti-inflammatory action (Yoon JH, et al., 2005, Baumann J, et al., 1980, Welton

AF, et al.,1986, Laughton MJ, et al.,1991, A viram et al., 1998). Some study results suggest that polyphenols inhibit NO release by suppressing NOS

enzymes expression and/or NOS activity (Kim HP, et al., 2004, Sutherland BA, et al., 2006). Cyanidin-3-glucoside (Cy3G) induced eNOS expression and escalated NO production (Xu JW,

et al., 2004). Increased eNOS expression may help to ameliorate endothelial dysfunction giving a long-term beneficial effect of supplementation.

Anthocyanins in the fruit have demonstrated in laboratory experiments a potential to inhibit inflammation mechanisms (Heinonen, M. 2007, Seeram, NP. (2008)

Vitamin C

Vitamin C (L-ascorbic acid) is found in rose hips, blackcurrants, and citrus fruits but can also be synthesised from glucose. It is an antioxidant, since it protects the body against oxidative stress (Padayatty, et al., 2003). It is also a cofactor in several collagen synthesis reactions that cause the most severe symptoms of scurvy when they are dysfunctional (Vitamin C 2007). Collagen is found throughout the body. It is an important component of connective tissues, tendons, ligaments, cartilage, bone and blood vessels.

The Importance of Vitamin C

Collagen synthesis reactions are especially important in wound-healing and in preventing bleeding

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from capillaries. Vitamin C is essential to the development and maintenance of scar tissue, blood vessels, and cartilage( MedlinePlus Encyclopaedia Ascorbic acid).

Articular cartilage accumulates ascorbic acid (Stabler TV, et al., 2003). Ascorbic acid serves as a cofactor for enzymes crucial in collagen synthesis. In vitro, ascorbate and ascorbic acid increased protein and proteoglycan synthesis by articular chondrocytes (Clark AG, et al 2002, Schwartz ER, et al.,1977, Daniel et al.,1984) and increased the levels of type I and II collagen (Clark AG, et al 2002, Sandell LJ et al., 1988).

There is some debate as to the necessity for Vitamin C supplementation as dogs produce their own vitamin C unlike humans and guinea pigs who must have it in their diet. It is therefore thought Vitamin C supplementation is unnecessary, but is believed will do no harm as the excess is excreted. Under conditions of stress, disease, surgery or injury the requirement for vitamin C may exceed the capacity for synthesis.

If supplementation is required then some believe they will get enough for their needs from a balanced diet. Although many dogs are perceived to be fed a balanced diet they are not receiving the raw diet they would be eating in the wild, most meat is cooked or heated which destroys the Vitamin C. There therefore may be a real need for supplementation.

Recommended moderate doses of Vitamin C are approximately 250 mg to 500mg twice daily for the average dog.

Studies to support use

Ascorbate has been demonstrated to be an effective antioxidant. This review presents evidence which supports the importance of vitamin C as a component of the overall antioxidant protective mechanisms found in cells and tissues. The data are consistent and form a strong consensus for investigating the importance of the antioxidant function of vitamin C in the maintenance of human health. (Bendich A, et al., 1986)

Vitamin C deficiency is detrimental to immune function, resulting in reduced resistance to some pathogens. Routine supplementation is not indicated in the general population, though there is some evidence that it reduces symptom severity but not incidence of the common cold. Effects are most pronounced in cases of physical strain or insufficient dietary intake.(Hemilä, et al., 2007, Ströhle A, et al., February 2009).

A study found a threefold reduction in risk of OA progression from vit C intake and an inverse association between vit C intake and cartilage loss (McAlindon TE, Jacques P, Zhang Y,

Hannan MT, Aliabadi P, Weissman B, Rush D, Levy D, Felson et al.,1996).

A study where a group of guinea pigs were feed on supplemented levels of vitamin C or minimal diet group after surgically inducing osteoarthritis in a joint. Early stages of pathology in both diet groups were characterized by formation of repair cartilage. As the disease progressed, pitting, ulcerations, and eburnation occurred in the minimal diet group. Cartilage weight in normal joints was greater for guinea pigs kept on high levels of vitamin C. It is likely that this stimulated synthesis of cartilage in the supplemented animals protected against the erosion of the articular cartilage which characterized the more severe disease process in the guinea pigs on minimal levels of vitamin C. (Schwartz ER. et al.,1981)

References

1. Aviram M, Fuhrman B. Polyphenolic flavonoids inhibit macrophage-mediated oxidation of LDL and attenuate

atherogenesis. Atherosclerosis 1998;137 Suppl:S45-50. 2. Baumann J, von Bruchhausen F, Wurm G. Flavonoids and related compounds as inhibition of arachidonic acid

peroxidation. Prostaglandins 1980;20:627-39.

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3. Bendich A, Machlin LJ , Scandurra O (1986). The antioxidant role of vitamin C. Advances in Free Radical Biology & Medicine, Volume 2, Issue 2, 1986, Pages 419-444

4. Bertuglia S, et al. Effect of Vaccinium myrtillus anthocyanosides on ischemia reperfusion injury in hamster cheek pouch microcirculation. Pharmacol Res 1995;31(3/4):183-7.

5. Borissova P, et al. Anti-inflammatory effects of flavonoids in the natural juice from Aronia melanocarpa, rutin, and rutin-magnesium. Complex on an experimental model of inflammation induced by histamine and serotonin. Acta Physiol Pharmacol Bulg 1994;20(1):25-30.

6. Buffa EA, Van Den Berg SS , Verstraete FJM , Swart NGN. Effect of dietary biotin supplement on equine hoof horn growth rate and hardness. Equine Veterinary Journal, Volume 24, Issue 6, pages 472–474, November 1992.

7. Clark AG, Rohrbaugh AL, Otterness I, Kraus VB: The effects of ascorbic acid on cartilage metabolism in guinea pig articular cartilage explants. Matrix Biol 2002, 21:175-184.

8. Comben N, R. J. Clark, and D. J. B. Sutherland. 1984. Clinical observations on the response of equine hoof defects to dietary supplementation with biotin. Vet. Rec. 115:642–645.

9. Daniel JC, Pauli BU, Kuettner KE: Synthesis of cartilage matrix by mammalian chondrocytes in vitro. III. Effects of ascorbate. J Cell Biol 1984, 99:1960-1969.

10. Kim HP, Son KH, Chang HW, Kang SS. Anti-inflammatory plant flavonoids and cellular action mechanisms. J Pharmacol Sci 2004;96:229-45.

11. Heinonen, M (2007). "Antioxidant activity and antimicrobial effect of berry phenolics--a Finnish perspective". Molecular nutrition & food research 51 (6): 684–91. doi:10.1002/mnfr.200700006. PMID 17492800.

12. Hemilä, Harri; Chalker, Elizabeth; Douglas, Bob; Hemilä, Harri (2007). "Vitamin C for preventing and treating the common cold". Cochrane database of systematic reviews (3): CD000980. doi:10.1002/14651858.CD000980.pub3. PMID 17636648.

13. 14. http://www.nzblackcurrants.com/blackcurrants-vs-bilberries-blueberries/15. http://www.nzblackcurrants.com/assets/pdfs/BCNZBlackcurrantExtractsClinicaTrials16July09.pdf16. Josseck H , Zenker W, Geyer H. Hoof horn abnormalities in Lipizzaner horses and the effect of dietary biotin on

macroscopic aspects of hoof horn quality. Equine Veterinary Journal, Volume 27, Issue 3, pages 175–182, May 1995 10.1111

17. Laughton MJ, Evans PJ, Moroney MA, Hoult JR, Halliwell B. Inhibition of mammalian 5-lipoxygenase and cyclo oxygenase by flavonoids and phenolic dietary additives. Relationship to antioxidant activity and to iron ion-reducing ability. Biochem Pharmacol 1991;42:1673-81.

18. McAlindon TE, Jacques P, Zhang Y, Hannan MT, Aliabadi P, Weissman B, Rush D, Levy D, Felson DT: Do antioxidant micronutrients protect against the development and progression of knee osteoarthritis Arthritis Rheum 1996, 39:648-656.

19. Padayatty, Sebastian J.; Katz, Arie; Wang, Yaohui; Eck, Peter; Kwon, Oran; Lee, Je-Hyuk; Chen, Shenglin; Corpe, Christopher et al. (2003). "Vitamin C as an antioxidant: evaluation of its role in disease prevention.". Journal of the American College of Nutrition 22 (1): 18–35. PMID 12569111.

20. Sandell LJ, Daniel JC: Effects of ascorbic acid on collagen mRNA levels in short term chondrocyte cultures. Connect Tissue Res 1988, 17:11-22.

21. Schwartz, E. R., Oh, W. H. and Leveille, C. R. (1981), Experimentally Induced Osteoarthritis in Guinea Pigs. Arthritis & Rheumatism, 24: 1345–1355. DOI: 10.1002/art.1780241103

22. Seeram, NP (2008). "Berry fruits: compositional elements, biochemical activities, and the impact of their intake on human health, performance, and disease". Journal of agricultural and food chemistry 56 (3): 627–9. doi:10.1021/jf071988k. PMID 18211023.

23. Stabler TV, Kraus VB: Ascorbic acid accumulates in cartilage in vivo. Clin Chim Acta 2003, 334:157-162. 24. Ströhle A, Hahn A (February 2009). "[Vitamin C and immune function]" (in German). Medizinische Monatsschrift

Für Pharmazeuten 32 (2): 49–54; quiz 55–6. PMID 19263912. 25. Sutherland BA, Rahman RM, Appleton I. Mechanisms of action of green tea catechins, with a focus on ischemia-

induced neurodegeneration. J Nutr Biochem 2006;17:291-306.26. Schwartz ER, Adamy L: Effect of ascorbic acid on arylsulfatase activities and sulfated proteoglycan metabolism in

chondrocyte cultures. J Clin Invest 1977, 60:96-106. 27. "Vitamin C – Risk Assessment" (PDF). UK Food Standards Agency.

http://www.food.gov.uk/multimedia/pdfs/evm_c.pdf. Retrieved 2007-02-19.28. Welton AF, Tobias LD, Fiedler-Nagy C, Anderson W, Hope W, Meyers K, Coffey JW. Effect of flavonoids on arachidonic

acid metabolism. Prog Clin Biol Res 1986;213:231-42.29. Xu JW, Ikeda K, Yamori Y. Upregulation of endothelial nitric oxide synthase by cyanidin-3-glucoside, a typical

anthocyanin pigment. Hypertension 2004;44:217-22. 30. Yoon JH, Baek SJ. Molecular targets of dietary polyphenols with anti-inflammatory properties. Yonsei Med J

2005;46:585- 96.

Rosehips Fruit (Rosa canina)

The historic and present uses of Rosehips focus on some of its key constituents: Vitamin C one of the richest plant sources available, biotin, carotenoids, anti-oxidants such as flavonoids; anthocyanins and proanthocyanidins, glycoside:galactolipid, fatty acids, pectins; tannins; sugar and

http://www.nzblackcurrants.com

plant acids. (ESCOP Monographs, 2009, D. P. James, 1950). It has long been valued by herbalists as a source of natural Vitamin C and as an aid to arthritic conditions.

http://www.jacn.org/cgi/content/full/22/1/18.

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Vitamin C acts as a cofactor for enzymes crucial in collagen synthesis which is especially important in

joint health and wound-healing. is essential to the development and maintenance of scar tissue, blood vessels and cartilage

(MedlinePlus). In vitro, ascorbate and ascorbic acid increased protein and proteoglycan synthesis by

articular chondrocytes (Clark AG, et al., 2002, Schwartz ER, et al., 1977, Daniel JC, et al., 1984) and increased the levels of type I and II collagen. (Clark AG, et al., 2002, Sandell LJ, et al., 1988)

Carotenoids Precursors to vitamin A and antioxidant. Carotenoids in Rosehip beta-cryptoxanthin and zeaxanthin have shown to provide a 41%

reduction in the risk of developing rheumatoid arthritis. In a study published in the August 2005 issue of the American Journal of Clinical Nutrition, researchers in the UK, following 25,000 people, found that among those who developed inflammatory polyarthritis, average intakes of beta-cryptoxanthin and zeaxanthin-were 40% and 20% lower, respectively, than in those who did not develop the inflammatory disease. In contrast, those whose diets provided the highest intakes of beta-cryptoxanthin were only half as likely to develop arthritis over 7 to 15 years as those with the lowest intakes.(Pattison DJ, et al., 2005)

Biotin A key component of the claw and hoof wall. Rosehips are relatively high in biotin. Although the dietary requirements for biotin in dogs

or horses are not well defined, the responses to biotin supplementation to improve hoof quality are quite significant. (E. A. Buffa et al., 1992, H. Josseck et al., 1995)

After 5 months of supplementation hoof condition of all 55 of a group of thoroughbreds and draft horses showed marked improvement. (Comben et al., 1984)

Antioxidants Help the body reduce the inflammatory action of free-radicals. When comparing patients dietary antioxidant consumption, patients who consumed low

levels have been shown to display a increased rate of joint deterioration.(K Kartikey, et al., 2009)

Anthocyanins The fruit have demonstrated in laboratory experiments a potential to inhibit inflammation

mechanisms (Heinonen, M, 2007, Seeram, NP, 2008)

Pectin Various fruit pectins have promoted pain-free joint movement, they are believed to act by

returning connective tissue to its previously smooth, elastic, lubricated condition. There are no studies on Rosehip pectins to support this.

Glycoside - galactolipid Recently Rosehip became prominent following the discovery of a different constituent; a

galactolipid that contributes to the anti-inflammatory action and the publication of papers that demonstrate its efficacy. (Jäger et al., 2008)

Just as in humans the European research has shown Rosehip to be a worthwhile treatment todecrease pain, inflammation, and improve mobility in horses with osteoarthritis.

The double blind trial conducted by the Frederiksberg Hospital, University of Copenhagen used a proprietary brand of rosehip extract. The 74 trotting horses were administered 210g of the powder with their food once a day for three months. The results showed that the

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Ÿ supplemented horses trotted faster over 1,000 metres and were more lithe after strenuous exercise compared to the placebo group. In addition, supplemented horses had significant alterations in three separate measures of anti-inflammatory activity than the placebo group. (Winther et al., 2008)

Ÿ A literature search has revealed other studies that have also showed that straight rosehip powder or a normal ethanolic extract is also effective. (Orhan DD, etal., 2007, Nadia O, 2006).

References

1. Buffa EA, Van Den Berg SS , Verstraete FJM , Swart NGN. Effect of dietary biotin supplement on equine hoof horn

growth rate and hardness. Equine Veterinary Journal, Volume 24, Issue 6, pages 472–474, November 1992.2. Clark AG, Rohrbaugh AL, Otterness I, Kraus VB: The effects of ascorbic acid on cartilage metabolism in guinea pig

articular cartilage explants. Matrix Biol 2002, 21:175-184. 3. Comben N, R. J. Clark, and D. J. B. Sutherland. 1984. Clinical observations on the response of equine hoof defects

to dietary supplementation with biotin. Vet. Rec. 115:642–645. 4. Daniel JC, Pauli BU, Kuettner KE: Synthesis of cartilage matrix by mammalian chondrocytes in vitro. III. Effects of

ascorbate. J Cell Biol 1984, 99:1960-1969. 5. Didem Deliorman Orhan, Ali Hartevioglu, Esra Küpeli and Erdem Yesilada. In vivo anti-inflammatory and anti-

nociceptive activity of the crude extract and fractions from Rosa canina L. fruits. Journal of Ethnopharmacology, Volume 112, Issue 2, 13 June 2007, Pages 394-400

6. ESCOP Monographs: the Scientific Foundation for Herbal Medicinal Products, 2009.7. Heinonen, M (2007). "Antioxidant activity and antimicrobial effect of berry phenolics--a Finnish perspective".

Molecular nutrition & food research 51 (6): 684–91. doi:10.1002/mnfr.200700006. PMID 17492800. 8. Jäger AK, Petersen KN, Thomasen G, Brøgger Christensen S. Isolation of linoleic and á-linolenic acids as COX-1 and

-2 inhibitors in rose hip. Phytotherapy Research. Volume 22, Issue 7, pages 982–984, July 2008 9. James DP. Nicotinic Acid, Pantothenic Acid and Biotin in Fruits, Vegetables and Nuts: University of Bristol Research

Station, Long Ashton 1950.10. Josseck H , Zenker W, Geyer H. Hoof horn abnormalities in Lipizzaner horses and the effect of dietary biotin on

macroscopic aspects of hoof horn quality. Equine Veterinary Journal, Volume 27, Issue 3, pages 175–182, May 1995 10.1111

11. Kartikey K, Singh G, Kidyore B, Somsunder YA. Association of dietary w-6/w-3 fatty acid ratio and inflammation with risk of hip fracture. Open Nutra J, 2009 - tsimtsoum.net

12. MedlinePlus Encyclopaedia Ascorbic acid 13. Osman, Nadia,, Effects of Probiotics and Plant Components on Murine Experimental Colitis and Acute Liver Failure,

2006. Lund University Faculty of Engineering, LTH at Lund University.14. Pattison DJ, Symmons DP, Lunt M, Welch A, Bingham SA, Day NE, Silman AJ. Dietary beta-cryptoxanthin and

inflammatory polyarthritis: results from a population-based prospective study. Am J Clin Nutr. 2005 Aug;82(2):451-5. 2005. PMID:16087992.

15. Sandell LJ, Daniel JC: Effects of ascorbic acid on collagen mRNA levels in short term chondrocyte cultures. Connect Tissue Res 1988, 17:11-22.

16. Schwartz ER, Adamy L: Effect of ascorbic acid on arylsulfatase activities and sulfated proteoglycan metabolism in chondrocyte cultures. J Clin Invest 1977, 60:96-106.

17. Seeram, NP (2008). "Berry fruits: compositional elements, biochemical activities, and the impact of their intake on human health, performance, and disease". Journal of agricultural and food chemistry 56 (3): 627–9. doi:10.1021/jf071988k. PMID 18211023.

18. Winther K, Falk-Ronne J, Kharazmi A et al. OARSI, Rome, 18-21 September 5 2008

Turmeric Root (Curcuma longa)

Turmeric is a widely used spice and colouring/flavouring agent. The FDA classifyturmeric as ‘generally recognized as safe’. Turmeric has a long history of use for its anti-inflammatory and anti-arthritic effects. Research supports this with recent findings showing that it would also be excellent for prevention. The root and stem have been used for centuries in India to help minimize swelling associated with sprains, strains, and arthritis

Turmeric has anti-inflammatory effects (But et al., 1997), with efficacy rivaling that of both cortisone and phenylbutazone (Mukhopadhyay, et al., 1982).

The issue of absorption

Isolated curcumin is not well absorbed in the intestinal tract (Bisht et al., 2009). This has proven an

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obstacle in the scientific application of curcumin for managing the effects of rheumatoid arthritis (Henrotin et al., 2009; Bisht et al., 2009).

An enhanced preparation of curcumin standardized to a 95% concentration of curcuminoids that reincorporate many of the components of raw turmeric root that are normally removed during the extraction process. This enhanced extract was found to be 6 to 7 times more bioavailable than conventional curcumin extracts. Importantly, this enhanced curcumin was absorbed more rapidly and retained longer in the blood, compared with standard curcumin preparations (Antony et al., 2008;

Benny et al., 2006).

Turmeric contains;Curcumin: 3–5% (Budavari, 1996; Iwu, 1993 ; Wichtl, 1996) gives turmeric its characteristic yellow-orange colour. Ÿ Curcumin and its derivatives are active anti-inflammatory constituents (Arora et al., 1971, Gupta et al.,

1972, Chandra et al., 1972, Tripathi et al., 1973, Ghatak et al., 1972, Srimal et al., 1973, Mukhopadhyay et al., 1982,

and Rao et al., 1982). Ÿ The primary mode of action is by shutting down a pro-inflammatory proteins (Shishodia et al., 2005).Ÿ Curcumin has been shown to inhibit key inflammation-producing enzymes (lipooxygenase, cyclo-

oxygenase, and phospholipase A2), thus disrupting the inflammatory cascade at three different stages essentially switching off inflammation.

Ÿ Curcumin is a specific for rheumatoid arthritis, providing multi-modal relief from inflammation and other symptoms of rheumatoid arthritis, suppressing inflammatory cytokines throughout the body and reducing joint swelling, pain, and stiffness. Inhibit NF-kB, down regulating multiple inflammatory pathways (Shishodia et al., 2007; Jurenka, 2009).

Ÿ Curcumin was found to be effective after oral administration in the acute carrageenin-induced oedema test in mice and rats (Ammon et al.,1991).

Ÿ Research has shown curcumin to be a powerful antioxidant, ten times more active than vitamin E (Khopde, et al.,1999; Srinivas et al.,1991).

Ÿ Part of the anti-inflammatory activity of curcumin may be due to its ability to scavenge oxygen radicals, which have been implicated in the inflammation process ( Masuda et al., 1993, Kunchandy et

al., 1990).Ÿ Curcumin also increase normally functioning immune cell numbers in people with recurrent

infections (Zuccotti et al., 2009).Ÿ In animal models of inflammatory arthritis, curcumin can produce a remarkable antigen-specific

suppression of inflammation, meaning that only the dangerous inflammatory response is quenched, leaving healthier immune functions unaffected (Capini et al., 2009).

Ÿ Curcumin suppresses destructive enzymes (matrix metalloproteinases) that dissolve cartilage (Henrotin et al., 2009; Onodera et al., 2000).

Ÿ It also blocks numerous inflammatory signalling molecules that aggravate painful joint inflammation (Li et al., 2001; Kawasaki et al., 2003).

Ÿ Curcumin is a powerful inhibitor of migration inhibitory factor, now thought to play a significant role in many of the symptoms of rheumatoid arthritis (Molnar & Garai, 2005).

Ÿ Curcumin also blocks the multiple effects of the inflammatory cytokine IL-1beta, which contributes to much of the devastating, painful destruction of joint cartilage symptomatic of rheumatoid arthritis. Lab studies show that curcumin slows the degeneration of cartilage caused by IL-1beta while restoring normal cartilage protein production (Shakibaei et al., 2005).

Ÿ RA cartilage deterioration is also mediated by an enzyme called collagenase, whose action is also powerfully neutralized by curcumin (Jackson et al., 2006).

Ÿ A newly discovered cytokine called IL-18 may also play a role in rheumatoid arthritis by triggering vascular endothelial growth factor (VEGF), an agent that triggers blood vessel growth (angiogenesis) and thickens joint membranes. Curcumin downregulates IL-18’s stimulatory effect on VEGF, thus reducing angiogenesis and promoting healthy joint membranes (Cho et al.,

2006)

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Volatile oils

Ÿ Have exhibited anti-inflammatory activity in rats against adjuvant-induced arthritis, carrageenin-induced paw oedema, and hyaluronidase-induced inflammation (Yegnanarayan et al., 1976). The anti-inflammatory activity appears to be mediated through the inhibition of the enzymes trypsin and hyaluronidase (Permpiphat et al., 1990).

Polysaccharides

Ÿ Immunologically active arabinogalactan (Bruneton, 1995; Wichtl, 1996), Ÿ Phagocytosis activating ukonan A and C (Gonda et al., 1992; Gonda et al., 1993).

minerals, carotene, vitamin C

A number of animal studies support curcumin’s ability to relieve the pain and swelling of both osteo and rheumatoid arthritis. One study found that when curcumin was given to arthritic rats, it lowered levels of an inflammatory protein by a stunning 73 percent (Joe, et al., 1997).

The effectiveness of curcumin and phenylbutazone on postoperative inflammation was investigated in a double-blind study, both drugs produced a better anti-inflammatory response than a placebo (Satoskar et al., 1986).

Another study, also in rats, showed that turmeric extract profoundly curbed joint inflammation and joint destruction (Funk, et al., 2006).

A study in dogs with osteoarthritis found that turmeric extract reduced lameness and joint pain (Innes, et al., 2003 ).

In a double-blind, crossover study consisting of eighteen patients with rheumatoid arthritis, after just two weeks of receiving either curcumin (1200 mg/day) or phenylbutazone (30 mg/day) showed significant improvements in morning stiffness, joint swelling, and walking ability (Deodhar et

al., 1980; McCaleb, et al., 2000).

In 2006, rheumatologists undertook a study examining curcumin’s efficacy in treating RA (Funk et al.,

2006 Nov). They induced rheumatoid-like arthritis in lab rats and then treated them with turmeric extracts rich in curcumin. The scientists reported that the extract “profoundly inhibited joint inflammation and periarticular joint destruction…[and] prevented local activation of NF-kB and the subsequent expression of NF-kB-regulated genes mediating joint inflammation and destruction.” In fact, they conducted other research showing that they could prevent lab-induced rheumatoid arthritis in animals through the use of a special curcumin formulation (Funk et al., 2006 Mar).

Human cell studies have additionally shown that curcumin suppresses the inflammatory chemicals that contribute to the development of osteoarthritis,(Shakibaei, et al., 2007) and decreases some of the abnormal changes in joint tissue that characterize rheumatoid arthritis(Park, et al., 2007).

In an as-yet-unpublished, randomized, controlled trial, researchers compared this enhanced curcumin preparation to the commonly-used NSAID diclofenac. Forty-five subjects with mild to moderate disease activity as rated on a standard score were enrolled and randomly assigned to 3 groups. One group received 500 mg of enhanced curcumin twice daily, another both 500 mg enhanced curcumin and 50 mg diclofenac, and a third group 50 mg diclofenac only. Their conditions were evaluated over the next 8 weeks, including blood testing and disease scoring.The greatest reduction in the disease activity score was attained by the patients treated exclusively with enhanced curcumin. The diclofenac group experienced the least improvement! Similarly, the supplement-only group showed the greatest improvement in the inflammatory blood markers C-reactive protein and antistreptolysin O (ASO) (Chandran et al., 2009).

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REFERENCES

1. Ammon HP, Wahl MA. Pharmacology of Curcuma longa. Planta medica,1991, 57:1–7.2. Antony B, Merina B, Iyer S, Judy N, Lennertz K, Joyal S. A pilot cross-over study to evaluate human oral

bioavailability of BCM-95® CG (Biocurcumax™), a novel bioenhanced preparation of curcumin. Indian J Pharm Sci. 2008 J-uAlug; 70(4):445-50.

3. Arora RB et al. Anti-inflammatory studies on Curcuma longa (turmeric). Indian journal of medical research, 1971, 59:1289–1295.

4. Benny M, Antony B. Bioavailability of Biocurcumax (BCM-095™). Spice India. 2006 Sept 9;19(9):1-51.5. Bisht S, Maitra A. Systemic delivery of curcumin: 21st century solutions for an ancient conundrum. Curr Drug

Discov Technol. 2009 Sep;6(3):192-9.6. Bruneton, J. 1995. Pharmacognosy, Phytochemistry, Medicinal Plants. Paris: Lavoisier Publishing.

th7. Budavari, S. (ed.). 1996. The Merck Index: An Encyclopedia of Chemicals, Drugs, and Biologicals, 12 ed. Whitehouse Station, N.J.: Merck & Co., Inc. 450, 1674.

8. But, P.P.H. et al. (eds.). 1997. International Collation of Traditional and Folk Medicine. Singapore: World Scientific. 207–208.

9. Capini C, Jaturanpinyo M, Chang HI, et al. Antigen-specific suppression of inflammatory arthritis using liposomes. J Immunol. 2009 Mar 15;182(6):3556-65.

10. Chandra D, Gupta SS. Anti-inflammatory and antiarthritic activity of volatile oil of Curcuma longa. Indian journal of medical research, 1972, 60:138–142.

11. Chandran B, Chakkiath VK, Thomas SPO. A Multicentre, Randomized, Controlled Human Clinical Study to Assess the Efficacy and Safety of Biocurcumax TM (BCM-95) Compared to Diclofenac sodium in the Management of Active Rheumatoid Arthritis. Kerala, India: Arjuna Natural Extracts Limited; 2009.

12. Cho ML, Jung YO, Moon YM, et al. Interleukin-18 induces the production of vascular endothelial growth factor (VEGF) in rheumatoid arthritis synovial fibroblasts via AP-1-dependent pathways. Immunol Lett. 2006 Mar 15;103(2):159-66.

13. Deodhar SD, Sethi R, Srimal RC. Preliminary study on anti-rheumatic activity of curcumin (diferuloyl methane). Indian journal of medical research, 1980, 71:632–634.

14. Funk JL, Frye JB, Oyarzo JN, et al. Efficacy and mechanism of action of turmeric supplements in the treatment of experimental arthritis. Arthritis Rheum. 2006 Nov;54(11):3452-64.

15. Funk JL, et al. Effi cacy and mechanism of action of turmeric supplements in the treatment of experimental arthritis. Arthritis Rheum. 2006 Nov;54(11):3452-64.

16. Ghatak N, Basu N. Sodium curcuminate as an effective antiinflammatory agent. Indian journal of experimental biology, 1972, 10:235–236.

17. Gonda, R., M. Tomoda, K. Takada, N. Ohara, N. Shimizu. 1992. The core structure of ukonan A, a phagocytosis-activating polysaccharide from the rhizome of Curcuma longa, and immunological activities of degradation products. Chem Pharm Bull (Tokyo) 40(4):990–993.

18. Gonda, R., M. Tomoda, N. Ohara, K. Takada. 1993. Arabinogalactan core structure and immunological activities of ukonan C, an acidic polysaccharide from the rhizome of Curcuma longa. Biol Pharm Bull 16(3):235–238.

19. Gupta SS, Chandra D, Mishra N. Anti-inflammatory and antihyaluronidase activity of volatile oil of Curcuma longa (Haldi). Indian journal of physiology and pharmacology, 1972, 16:254.

20. Henrotin Y, Clutterbuck AL, Allaway D, et al. Biological actions of curcumin on articular chondrocytes. Osteoarthritis Cartilage. 2009 Oct 8.

21. Innes JF, et al. Randomised, double-blind, placebo-controlled parallel group study of P54FP for the treatment of dogs with osteoarthritis. Vet Rec. 2003 Apr 12;152(15):457- 60.

22. Iwu, M.M. 1993. Handbook of African Medicinal Plants. Boca Raton: CRC Press. 164–166.23. Jackson JK, Higo T, Hunter WL, Burt HM. The antioxidants curcumin and quercetin inhibit inflammatory processes

associated with arthritis. Inflamm Res. 2006 Apr;55(4):168-75.24. Joe B, et al. Presence of an acidic glycoprotein in the serum of arthritic rats: modulation by capsaicin and curcumin.

Mol Cell Biochem. 1997 Apr;169(1-2):125-34.25. Jurenka JS. Anti-inflammatory properties of curcumin, a major constituent of Curcuma longa: a review of preclinical

and clinical research. Altern Med Rev. 2009 Jun;14(2):141-53.26. Kawasaki H, Komai K, Nakamura M, et al. Human wee1 kinase is directly transactivated by and increased in

association with c-Fos/AP-1: rheumatoid synovial cells overexpressing these genes go into aberrant mitosis. Oncogene. 2003 Oct 9;22 (44):6839-44.

27. Khopde SM, et al. Free radical scavenging ability and antioxidant efficiency of curcumin and its substituted analogue. Biophys Chem. 1999;80:85-91.

28. Kunchandy E, Rao MN. Oxygen radical scavenging activity of curcumin.International journal of pharmacognosy, 1990, 58:237–240.

29. Li WQ, Dehnade F, Zafarullah M. Oncostatin M-induced matrix metalloproteinase and tissue inhibitor of metalloproteinase-3 genes expression in chondrocytes requires Janus kinase/STAT signaling pathway. J Immunol. 2001 Mar 1;166(5):3491-8.

30. Masuda T et al. Anti-oxidative and anti-inflammatory curcumin-related phenolics from rhizomes of Curcuma domestica. Phytochemistry, 1993, 32:1557–1560.

31. McCaleb R, Leigh E, and K Morien. The Encyclopedia of Popular Herbs: Your Complete Guide to the Leading Medicinal Plants. Roseville, CA: Prima Health, 2000, p. 378.

32. Molnar V, Garai J. Plant-derived anti-inflammatory compounds affect MIF tautomerase activity. Int Immunopharmacol. 2005 May;5(5):849-56.

33. Mukhopadhyay A, et al. Anti-infl ammatory and irritant activities of curcumin analogues in rats. Agents Actions. 1982;12:508-15.1982;12:508-15.

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34. Onodera S, Kaneda K, Mizue Y, Koyama Y, Fujinaga M, Nishihira J. Macrophage migration inhibitory factor up-regulates expression of matrix metalloproteinases in synovial fibroblasts of rheumatoid arthritis. J Biol Chem. 2000 Jan 7;275(1):444-50.

35. Park C, et al. Curcumin induces apoptosis and inhibits prostaglandin E(2) production in synovial fibroblasts of patients with rheumatoid arthritis. Int J Mol Med. 2007 Sep;20(3):365-72.

36. Permpiphat U et al. Pharmacological study of Curcuma longa. In: Proceedings of the Symposium of the Department of Medical Science, Mahidol University, Bangkok, Thailand, Dec 3–4, 1990.

37. Satoskar RR, Shah Shenoy SG. Evaluation of antiinflammatory property of curcumin (diferuloyl methane) in patient with postoperative inflammation. International journal of clinical pharmacology, therapy and toxicology, 1986, 24:651–654.

38. Shakibaei M, Schulze-Tanzil G, John T, Mobasheri A. Curcumin protects human chondrocytes from IL-l1beta-induced inhibition of collagen type II and beta1-integrin expression and activation of caspase-3: an immunomorphological study. Ann Anat. 2005 Nov;187(5-6):487-97.

39. Shakibaei M, et al. Suppression of NF-kappaB activation by curcumin leads to inhibition of expression of cyclo-oxygenase-2 and matrix metallo-proteinase-9 in human articular chondrocytes: Implications for the treatment of osteoarthritis. Biochem Pharmacol. 2007 May 1;73(9):1434-45.

40. Shishodia S, Sethi G, Aggarwal B. Curcumin: Getting back to the roots. Ann NY Acad Sci. 2005 Nov;1056:206-17.41. Shishodia S, Singh T, Chaturvedi MM. Modulation of transcription factors by curcumin. Adv Exp Med Biol.

2007;595:127-4842. Srimal RC, Dhawan BN. Pharmacology of diferuloyl methane (curcumin), a non- steroidal anti-inflammatory agent.

Journal of pharmacy and pharmacology, 1973, 25:447–452.43. Srinivas, L. and V.K. Shalini. 1991. DNA damage by smoke: protection by turmeric and other inhibitors of ROS. Free

Radic Biol Med 11(3):277–283. 44. Rao TS, Basu N, Siddiqui HH. Anti-inflammatory activity of curcumin analogs. Indian journal of medical research,

1982, 75:574–578.45. Tripathi RM, Gupta SS, Chandra D. Anti-trypsin and antihyaluronidase activity of volatile oil of Curcuma longa

(Haldi). Indian journal of pharmacology, 1973, 5:260– 261. 46. Wichtl, M. 1996. Monographien—Kommentar. In: Braun, R. et al. 1997. Standardzulassungen f r

Fertigarzneimittel—Text and Kommentar. Stuttgart: Deutscher Apotheker Verlag.47. Yegnanarayan R, Saraf AP, Balwani JH. Comparison of antiinflammatory activity of various extracts of Curcuma

longa (Linn). Indian journal of medical research, 1976, 64:601–608.48. Zuccotti GV, Trabattoni D, Morelli M, Borgonovo S, Schneider L, Clerici M. Immune modulation by lactoferrin and

curcumin in children with recurrent respiratory infections. J Biol Regul Homeost Agents. 2009 Apr-Jun;23(2):119-23.

Gotu Kola (Centella asiatica)

Gotu Kola has been chosen for its proven ability to ensure efficient regeneration and repair. In the management and control of osteoarthritis and other degenerative diseases of the musculoskeletal system the production of new connective tissue is an important aspect, and to date Gotu Kola stands out in this area.

Interestingly, Gotu Kola not only can be used topically it can be taken internally to encourage healing. There are many herbs that are effective topically, but there are relatively few herbs that can promote healing following ingestion. The significance of this is that it suggests that the healing potential of Gotu Kola is not just confined to the skin, and can be used to promote healing in any tissue ie; skin, bones etc.

Positive results were obtained for oral use of Gotu Kola taken for three to eight weeks in 50 patients with leg ulcers (Huriez, 1972). In 1996 Suguna et al., showed oral and topical administration of Gotu Kola extract produced faster skin growth and higher rates of wound contraction compared to controls.

Oral administration of Gotu Kola has been used successfully to treat keloids and hypertrophic scars. In a study of 227 patients Bosse et al., 1979, found treatment with Gotu Kola for a period of two to 18 months had therapeutic value in both preventing and reducing keloids (excessive scar formation on the skin).

The area where Gotu Kola excels is in wound healing. By promoting efficient regeneration and repair through its ability to stimulate the activity of fibroblasts (including osteoblasts) and epithelial cells, several clinical trials support its ability to boost healing where other treatments failed. (Chakrabarty & Deshmukh 1976, Nebout 1974).

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For efficient healing it is vital to have a good blood supply to the area. Gotu Kola helps strengthen veins and capillaries. (Cesarone et al. 2001). Clinical trials have established that Gotu Kola improves microcirculation along with production of connective tissue, and overall wound healing, (Belcaro et

1989; Grimaldi et al., 1990; Tincani et al., 1963; Arpaia et al., 1990). Some studies have shown that it speeds up the healing process, especially in terms of the production and strengthening of connective tissue. (Vogel et al.,1990; Suguna et al., 1996)

These effects have been noted after various surgical procedures (Castellani et al., 1966; Sevin, 1962); and other traumatic injuries. (Stassen 1964); and clinical trials have found that Gotu Kola helps correct and prevent the formation of scars. (Bosse et al., 1979).

Widgerow et al., 2000, found collagen synthesis was a mechanism of action. Through stimulation of scar maturation by the production of type I collagen and a resulting decrease in the inflammatory reaction.

Poizot & Dumez,1978 had already found Gotu Kola acted specifically to shorten the immediate phase of healing, probably due to the increased glycosaminoglycan production. Maquart, et al., 1999 found Gotu Kola stimulated glycosaminoglycan production (glycosaminoglycans are the first component of the extracellular matrix to be synthesized during the wound healing process). Glycosaminoglycans (GAGs) include hyaluronic acid a component in the synovial fluid a lubricant in body joints; chondroitin 4- and 6-sulfates which can be found in connective tissues, cartilage, and tendons; keratan sulfate found in joints and act as a cushion to absorb mechanical shock; dermatan sulfate which is believed to play a role in wound repair.

References:

1. Widgerow AD, Chait LA, Stals R, et al. Aesthetic Plast Surg 2000;24(3):227-234.2. Maquart FX, Chastang F, Simeon A, et al. Eur J Dermatol 1999;9(4):289-296.3. Poizot A, Dumez D. C R Acad Sci Hebd Seances Acad Sci D 1978;286(10):789-792.4. Suguna L, Sivakumar P, Chandrakasan G. Indian J Exp Biol 1996;34(12):1208-1211.5. Bosse JP, Papillon J, Frenette G et al. Ann Plast Surg 1979;3(1):13-21.6. Huriez CL. Lille Med 1972;3(17:Suppl):574-9.7. Cesarone MR, Incandela L, De Sanctis MT, et al. "Flight microangiopathy in medium- to long-distance flights:

prevention of oedema and microcirculation alterations with total triterpenic fraction of Centella asiatica." Angiology 2001; 52(Suppl 2): S33-37

8. Chakrabarty T, Deshmukh S. "Centella asiatica in the Treatment of Leprosy." Sci Culture 1976; 42(11): 5739. Nebout M. Results of a controlled experiment of the titrated extract of Centella asiatica in a leper population with

perforative foot lesions." Bull Soc Pathol Exot 1974; 67(5): 471-47810. Belcaro G, Laurora G, Cesarone MR, et al. "Efficacy of Centellase in the treatment of venous hypertension evaluated

by a combined micro-circulatory model." Curr Ther Res 1989; 46: 1,015-1,02611. Grimaldi R, De Ponti F, D'Angelo L, et al. "Pharmacokinetics of the total triterpenic fraction of Centella asiatica after

single and multiple administrations to healthy volunteers. A new assay for asiatic acid." J Ethnopharmacol 1990; 28(2): 235-241

12. Tincani GP, Riva PC, Baldini E. "[Cutaneous Enzymatic Activity In the Processes of Regeneration. I. Effect of asiaticoside on Leucine Aminopeptidase (LAP) and the Sulfhydryl Groups in Normal Subjects]." G Ital Dermatol 1963; 104: 429-440

13. Arpaia MR, Ferrone R, Amitrano M ,et al. "Effects of Centella asiatica extract on mucopolysaccharide metabolism in subjects with varicose veins." Int J Clin Pharmacol Res 1990; 10(4): 229-233

14. Vogel HG, De Souza N, D'Sa A. Acta Therapeut 1990; 16: 285-29815. Suguna L, Sivakumar P, Chandrakasan G. "Effects of Centella asiatica extract on dermal wound healing in rats."

Indian J Exp Biol 1996; 34(12): 1,208-1,21116. Castellani L, Gillet JY, Lavernhe G, Dellenbach P. "[Asiaticoside and cicatrization of episiotomies]." Bull Fed Soc

Gynecol Obstet Lang Fr 1966; 18(2): 184-18617. Sevin P. "[Some observations on the use of asiaticoside (Madecassol) in general surgery.]" Progr Med (Paris)

1962;Â 90: 23-2418. Stassen P. "[The Use of Asiaticoside in Traumatology]." Rev Med Liege 1964; 19: 305-30819. Bosse JP, Papillon J, Frenette G, et al. "Clinical study of a new antikeloid agent." Ann Plast Surg 1979; 3(1): 13-21

Glucosamine HydrochlorideGlucosamine is a natural compound found in high concentrations in joint cartilage.

Cartilage covers the articulating surfaces of bones acting as a protective cushion allowing the joints

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to function as they should. However, as we age, repetitive use and injury, the cartilage layer can become thinner and in some cases, osteoarthritis occurs.

It has been thought that glucosamine is a key factor to the healing, protection and regrowth of cartilage.

Glucosamine benefits in Osteoarthritis Management

• This study found Glucosamine inhibited inducible NO synthesis via inhibition of iNOS protein expression, which provides a biochemical basis for the use of glucosamine in treating chronic inflammatory diseases such as arthritis (CJ Meininger, KA Kelly, H Li, TE Haynes, 2000).

• A dosage of 1.5 gram of glucosamine daily for 2-4 weeks is just as effective as low doses of NSAIDs in alleviating pain; research finds. (Ned Tijdschr Geneeskd. 2002)

• Another study shows a great decrease in symptom severity after 4-6 weeks oral or intramuscular administration of glucosamine.(Drug Aging. 2003)

• Injection of glucosamine, chondroitin sulfate, dextrose and DMSO may help chronic intractable low back pain. (Spine J. 2003)

References

1. Biochmical injection treatment for discogenic lowback pain: a pilot study. Spine J. 2003 May-Jun; 3(3):220-6. 2. CJ Meininger, KA Kelly, H Li, TE Haynes, 2000. Glucosamine inhibits inducible nitric oxide synthesis. Biophysical

Research.3. Glucosamine and chondroitin sulfate as a possible treatment for osteoarthritis, Ned Tijdschr Geneeskd. 2002 Sep

28;146(39):1819-23. 4. Glucosamine: a review of its use in the managment of osteoarthritis. Drug Aging. 2003;20(14):1041-60

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