Inflammation Support + 90 Vcap

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• Ingredients
• How to Use

INFLAMMATION SUPPORT + by PHYSICIANS RESEARCH is a complex phytonutrient blend formulated to positively modulate the inflammatory response.  A potent bioflavonoid is included to relieve allergy symptoms by preventing histamine release.

The ingredients work synergistically to regulate the key inflammatory mediators in the body at the same time producing a potent antioxidant effect. 

Possible Indications for Inflammation Support + include:

• Osteoarthritis, Rheumatoid Arthritis, Joint Pain and Stiffness,
• Crohn's Disease, Colitis, Gastritis
• Autoimmune Diseases
• Asthma, Hay Fever, Hives, Eczema
• Migraine Headaches
• Acne & Skin Rashes

Any Inflammation in the body including:

• Bursitis
• Tendonitis
• Plantar Fasciitis
• Heart Disease
• Cancer
• Infections

Treat the Cause of your Symptoms:

Inflammation plays an Integral Role in Countless Chronic Diseases

New Research has shown that Chronic Inflammation anywhere in the body may lead to the development of Cancer.

Injury, infection, allergens, chronic disease and aging, all trigger the body’s defense mechanism through inflammation. Inflammatory mechanisms are regulated by balancing certain enzyme systems.  These mechanisms are integral in determining the health of the immune, cardiovascular, neurological, joint and connective tissue systems.

In addition to a large amount of pure Curcuminoids, INFLAMMATION SUPPORT + includes extracts of Green Tea, Rosemary, Holy Basil, Ginger, Barberry & Skullcap that provide many complementary compounds that normalize various inflammatory mechanisms.

Quercitin is included to offer a potent antioxidant & anti-inflammatory effect working through alternate pathways.  This powerful bioflavanoid also relieves allergy symptoms by stabilizing "mast" cells to prevent histamine release.

The synergistic effect of the elements in INFLAMMATION SUPPORT + acts to preserve the health of the all of the body's tissues, particularly connective tissues, including tendons, ligaments and cartilage. Patients with acute or chronic inflammation in degenerative diseases may benefit from INFLAMMATION SUPPORT +

Inflammatory mechanisms are regulated by the balance of cyclooxgenase 1 and 2 (COX-1 & COX-2) enzymes.  This process is integral in determining the health of the immune, cardiovascular, neurological, joint and connective tissue systems.

Injury, infection, allergens, chronic disease and aging, all trigger the body’s defense mechanism through inflammation.  The concomitant redness, swelling and pain in the tissues come from up-regulation of pro-inflammatory mediators.  The immune cells congregate in the inflamed area to clean up, and remove the initial offender.  In acute inflammation, this process is integral to healing and self-limiting.  In non-limiting instances, the inflammation can become destructive to the body’s own tissues, now preventing repair mechanisms.  Now, chronic inflammation can progress to debilitating states, as in osteoarthritis and rheumatoid arthritis. Evidence is arising that chronic inflammation is implicated in many degenerative disorders throughout the body, including cardiovascular disease, hypertension, neurodegeneration, diabetes, metabolic syndrome and carcinogenesis.

Arachidonic acid (AA) cascade is one pathway of chronic inflammation.  Inflammatory stimuli causes affected cells to release AA which forms Eicosanoids (prostaglandins, thromboxanes, prostacyclins, leukotrienes etc) via cyclooxygenase (COX) and lipoxygenase (LOX).  While COX-1 is constantly used in normal functions to regulate platelets and maintain the stomach lining through protective prostaglandins, COX-2 is induced in acute inflammation to produce pro-inflammatory prostaglandins such as ProstaGlandin E2 (PGE2).  Although LOX is constant like COX-1, its presence is increased by inflammatory stimuli, and trigger a series of reactions biosynthesizing leukotrienes, hydroxyeicosanoids, and lipoxins.  5-LOX is critical in producing the highly inflammatory cysteinal leukotrienes and leukotriene B4 (LTB4).

Activation of nuclear factor-kappa B (NF-κB) is another major inflammatory path.  NF-κB, a transcription factor, affects genes that encode proinflammatory cytokines, chemokines, and adhesion molecules.  Basically when cells are exposed to stimuli (cytokines, drugs, viruses, or bacterial endotoxins), NF-κB induces transcription of various inflammatory mediators (interleukin-1 (IL-1), IL-2, IL-6, IL-8, tumor necrosis factor-α (TNF-α), COX-2, and 5-LOX).

Conventional treatments, non-steroidal anti-inflammatory drugs (NSAIDs), corticosteroids, and selective inhibitors of the COX-2 enzymes have been linked with serious renal, gastrointestinal, and cardiovascular side effects. Anti-rheumatic drugs and biologics aim to reduce inflammatory cytokine activity with limited success.  Traditional use of botanicals is now supported with modern research to exemplify their ability to regulate key inflammatory mediators, such as COX-2, 5-LOX, and NF-κB.  Varied clinical studies demonstrate that the botanicals,Camellia sinensis, Rosmarinus officinalis, Ocimum tenuflorum, Zingiber officinale, Berberis vulgaris and Scutellaria baicalensis,may be recognized for their safety and efficacy as clinical options in managing inflammation.

TURMERIC Curcuma longa historically been used as both a spice and an Ayurvedic remedy for liver disease and inflammatory conditions. There are over thousands of citations in Medline relating to the biologic effect of Curcumin. Perhaps most of the activities associated with Curcumin are based on its ability to suppress inflammation. Curcumin has been shown to be effective in acute as well as chronic models of inflammation. The active component of Curcuma longa includes curcuminoids and sesquiterpenes providing not just potent anti-inflammatory effects, but also antioxidant, hepatoprotective, hypoglycemic, hypolipidemic and anti-proliferative benefits. The primarily beneficial curcuminoids have been shown to downregulate activation of the transcription factor NF-kB, thus leading to downregulation of the expression of TNF-a, adhesion molecules, MMPs, COX-2, 5 –LOX and other inflammatory intermediates, all of which are associated with arthritis.

The volatile oils and curcumin of Curcuma longa exhibit potent anti-inflammatory effects. Oral administration of Curcumin in instances of acute inflammation was found to be as effective as cortisone or phenylbutazone, and one-half as effective in cases of chronic inflammation. In rats with Freud’s adjuvant-induced arthritis, oral administration of Curcuma longa significantly reduced inflammatory swelling compared to controls. In monkeys, Curcumin was shown to inhibit neutrophil aggregation associated with inflammation.

The anti-inflammatory properties of Curcumin may be attributed to its ability to inhibit pro-inflammatory arachidonic acid, as well as neutrophil function during inflammatory states. Curcumin may also be applied topically to skin to counteract inflammation and irritation associated with inflammatory skin conditions and allergies. An in vitro study demonstrates Curcumin antioxidant role in down-regulating nitric oxide formation, a key element in inflammation and possibly in the process of carcinogenesis.

Anti-inflammatory and Antioxidant Properties
Several studies have shown that curcumin is a potent antioxidant. In fact, Curcumin has been found to be at least 10 times more active as an antioxidant than even vitamin E. Curcumin prevents the oxidation of hemoglobin and inhibits lipid peroxidation. The antioxidant activity of Curcumin could be mediated through antioxidant enzymes such as superoxide dismutase, catalase, and glutathione peroxidase. Curcumin has been shown to serve as a Michael acceptor reacting with glutathione and thioredoxin. Reaction of Curcumin with these agents reduces intracellular GSH in the cells. The suppression of lipid peroxidation by Curcumin could lead to suppression of inflammation.

Anticancer Properties
The anticancer potential of curcumin in various systems was recently reviewed. Curcumin has been shown to block transformation, tumor initiation, tumor promotion, invasion, angiogenesis, and metastasis. In vivo, curcumin suppresses carcinogenesis of the skin, forestomach, colon, and liver in mice. Curcumin also suppresses mammary carcinogenesis. Curcumin has been shown to inhibit the proliferation of a wide variety of tumor cells, including B-cell and T-cell leukemia, colon carcinoma, epidermoid carcinoma, and various breast carcinoma cells.

Cardioprotective Effects
Curcumin has been effective against atherosclerosis and myocardial infarction. The proliferation of peripheral blood mononuclear cells (PBMCs) and vascular smooth muscle cells (VSMCs), which are hallmarks of atherosclerosis, is inhibited by curcumin. Curcumin prevents the oxidation of low-density lipoproteins (LDLs), inhibits platelet aggregation, and reduces the incidence of myocardial infarction.

Skin Diseases
Curcumin has been shown to be effective against different skin diseases including skin carcinogenesis, psoriasis, scleroderma, and dermatitis. Numerous reports suggest that Curcumin accelerates wound healing. In addition, Curcumin also prevents the formation of scars and plays a role in muscle regeneration following trauma.

Diabetes
In type II diabetes, administration of Curcumin reduced the blood sugar, hemoglobin, and glycosylated hemoglobin levels significantly in an alloxan-induced diabetic rat model. Diabetic rats maintained on a Curcumin diet for 8 weeks excreted less albumin, urea, creatinine, and inorganic phosphorus. Dietary Curcumin also partially reversed the abnormalities in plasma albumin, urea, creatine, and inorganic phosphorus in diabetic animals.

Rheumatoid Arthritis
Curcumin has also been shown to possess anti-rheumatic and anti-arthritic effects, most likely through the down-regulation of COX2, tumor necrosis factor (TNF), and other inflammatory cytokines.

Multiple Sclerosis
Multiple sclerosis is characterized by the destruction of oligodendrocytes and myelin sheath in the CNS. Curcumin inhibits experimental allergic encephalomyelitis by blocking interleukin (IL)-12 signaling in T cells, suggesting it would be effective in the treatment of multiple sclerosis.

Alzheimer’s Disease
Curcumin can suppress oxidative damage, inflammation, cognitive deficits, and amyloid accumulation in Alzheimer’s disease.

Inflammatory Bowel Disease
Ukil et al. recently investigated the protective effects of Curcumin on inflammatory bowel disease induced in a mouse model. Pretreatment of mice with Curcumin for 10 days significantly ameliorated the appearance of diarrhea and the disruption of the colonic architecture.

Cystic Fibrosis
Cystic fibrosis, the most common lethal hereditary disease in the Caucasian population, is caused by mutations in the cystic fibrosis transmembrane conductance regulator gene. In a recent report, Egan et al. demonstrated that Curcumin corrected the cystic fibrosis defects in DeltaF508 CF mice.

Curcumin was found to be a potent and selective inhibitor of human immunodeficiency virus (HIV-1) long-terminal repeat-directed gene expression, which governs the transcription of type 1 HIV-1 provirus. It has also been shown to prevent cataractogenesis in an in vitro rat model. Treatment with Curcumin also prevented experimental alcoholic liver disease. Curcumin has a protective effect on cyclophosphamide-induced early lung injury. Nephrotoxicity, a problem observed in patients who are administered chemotherapeutic agents, can be prevented with Curcumin.

QUERCITIN Styphnolobium japonicum, a bioflavonoid, is a plant pigment and a powerful antioxidant in the oxidation of LDL. Quercetin appears to have many beneficial effects on human health, including cardiovascular protection, anti-cancer activity, anti-ulcer effects, anti-allergy activity, cataract prevention, antiviral activity, and anti-inflammatory effects.

Quercetin is a flavonoid aglycone of rutin and is found in a wide variety of vegetables and herbs. Quercetin inhibits inflammatory processes attributed to activated neutrophils due to membrane stabilization, potent antioxidant effects and inhibition of the enzyme hyaluronidase (which prevents the breakdown of collagen matrix). Membrane stabilization results in prevention of mast cell and basophil degranulation and decreased inflammation by inhibition of neutrophil lysosomal enzyme secretion and leukotriene production.

Quercetin’s mast-cell-stabilizing effects make it an obvious choice for use in preventing histamine release in allergy cases, similar to the synthetic flavonoid analogue cromolyn sodium. Absorption of the pure aglycone quercetin is poor; however, much of quercetin’s anti-allergy effects may be due to anti-inflammatory and anti-histaminic effects in the gut.

Quercetin is indicated in any inflammatory condition, as it inhibits the formation of the inflammatory mediators prostaglandins and leukotrienes, as well as histamine release. This may be especially helpful in asthma, as leukotriene B4 is a potent bronchial constrictor. Quercetin’s inhibition of xanthine oxidase decreases the formation of uric acid, and thus it may be of value in the treatment of gout.

Quercetin is one of several flavonoids that have effects on mast cells and basophils; thus, some research suggests, it might be useful in some allergies, such as hay fever. Quercetin can help prevent the release of histamine and other mediators of allergic reactions, possibly by stabilizing cell membranes so that they are less reactive to allergens. Quercetin also exhibits anti-inflammatory properties, inhibiting formation of inflammatory prostaglandins and leukotrienes.

Quercetin showed benefit in category III chronic prostatitis syndromes (nonbacterial chronic prostatitis and prostatodynia), which was confirmed in a prospective, randomized, double-blind, placebo-controlled trial. Several of Quercetin’s activities, including anti-inflammatory, anti-oxidant and immune-modulating actions, are believed to play roles in achieving these effects. There was evidence that Quercetin prevented oxidative-mediated cellular injury, which the researchers suggested would apply whether the injury was due to infective, inflammatory or auto-immune mechanisms.

GREEN TEA Camellia sinensis is produced from steaming fresh leaves at high temperatures, thereby inactivating the oxidizing enzymes and leaving the polyphenol content intact. The polyphenols found in tea are more commonly known as flavanols or catechins and comprise 30-40 percent of the extractable solids of dried green tea leaves. The main catechins in green tea are epicatechin, epicatechin-3-gallate, epigallocatechin, and epigallocatechin-3-gallate (EGCG), with the latter being the highest in concentration.

Green tea polyphenols have demonstrated significant antioxidant, anti-carcinogenic, anti-inflammatory, thermogenic, probiotic, and antimicrobial properties in numerous human, animal, and in vitro studies. Green tea and its polyphenol constituents have been extensively researched in their beneficial roles in combating cancer, cardiovascular disease, diabetes, obesity, osteoporosis, cognitive dysfunction, and inflammatory disorders. The main benefit of Green Tea on health is from its anti-inflammatory effect.

Many chronic disease states and inflammatory conditions are a result of oxidative stress and subsequent generation of free radicals. Some of these include heart disease (resulting from LDL oxidation), renal disease and failure, several types of cancer, skin exposure damage caused by ultraviolet (A and B) rays, as well as diseases associated with aging.

Green tea polyphenols are potent free radical scavengers due to the hydroxyl groups in their chemical structure. The hydroxyl groups can form complexes with free radicals and neutralize them, preventing the progression of the disease process.

The green tea polyphenols possess antioxidant, antimicrobial, anti-inflammatory and anti-carcinogenic properties. Green tea and its constituents have exhibited a variety of anti-inflammatory effects, raising hopes that they might be helpful in treating some forms of arthritis, dermatosis, gout and other inflammatory conditions. Inflammatory cytokines, tumor necrosis factor and interferon-gamma and RA-specific immunoglobulin-G were all reduced in the animals given the green tea polyphenols.

ROSEMARY Rosmarinus officinalis Many dietary plants and the phytochemicals they contain possess cancer preventive properties. Green tea and rosemary, as extracts, and catechins, carnosol and curcumin, as purified compounds, have been shown to inhibit 120tetradecanoylphorbol-13-acetate (TPA)-induced inflammation on mouse skin, colon and stomach cancers.

Carnosol is a naturally occurring phytopolyphenol found in rosemary. Carnosol functions as antioxidant and anticarcinogen. Rosmarinus officinalis exhibited dose-dependent viability suppression and significant tumor necrosis factor-alpha (TNF-α) production, with a non-cytotoxic character. Conclusively, rosemary can be considered an herbal anti-inflammatory and anti-tumor agent.

The pathophysiology of Osteoarthritis (OA) involves inflammatory cytokines, such as interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α). These cytokines are known to induce production of PGE2 via the COX-2 pathway as part of the inflammatory process. Rheumatoid arthritis is also characterized by IL-1β- and TNF-α mediated inflammation, similar to OA, and has been shown to involve generation of PGE2 by COX-2. Furthermore, inhibitors of COX-2 activity like Rosemary have been shown to decrease production of PGE2 and effectively provide pain relief for patients with chronic arthritic conditions.

There are preliminary data that suggest this Rosemary combination inhibits production of PGE2 in vitro. Consistent with this observation, sera from human subjects that consumed the Rosemary combo has been shown to inhibit PGE2 production in LPS-stimulated RAW264.7 cells. The results presented in this study support previous findings and further suggest that this Rosemary combo is beneficial in the management of pain from PGE2-mediated inflammation.

HOLY BASIL Ocimum tenuiflorum leaves contain many active constituents such as eugenol, luteolin, oleanolic acid, and ursolic acid. Ursolic acid, a triterpenoid, is often used as a marker agent in Holy Basil. Holy Basil has shown various effects, including hypotensive, cardiac depressant, smooth muscle cell relaxant and anti-stress activities. In vitro and in vivo studies show ursolic acid functions as a hepatoprotective, antimicrobial, anti-mutagenic, anti-ulcer, and anti-inflammatory compound.

Ursolic acid modulates inflammation through COX-2 & 5-LOX inhibition to suppress eicosanoid production. Studies even show Ursolic acid inhibiting histamine secretion from stimulated immune cells. Rheumatoid arthritis induced animals show Ursolic acid dramatically reduce plasma PGE2 levels, paw swelling, and joint abnormalities. The anti-inflammatory activity is also seen in whole extracts of Holy Basil, equivalent to 300 mg/kg of sodium salicylate, emphasizing that Holy Basil was found to have measurable and significant analgesic effects in rats.

Lipid peroxidation can play a crucial role in inflammation, cancer and cardiac diseases. A study found that Holy Basil extracts and their fractions are strong inhibitors of in vitro lipid peroxidation.

It was also found that Holy Basil possesses significant anti-inflammatory and anti-ulcer activity. Earlier studies showed the herb to possess significant anti-inflammatory, antipyretic, analgesic and anti-arthritic properties.

Leaves of the holy basil plant have been found to contain a number of active constituents such as eugenol, luteolin, oleanolic acid, and ursolic acid. Ursolic acid, a triterpenoid, is often used as a marker agent in holy basil and has a number of beneficial health effects. In vitro and in vivo studies show ursolic acid functions as a hepatoprotective, antimicrobial, anti-mutagenic, anti-ulcer, and anti-inflammatory compound. The anti-inflammatory activity of ursolic acid is mediated primarily by suppression of eicosanoid production via inhibition of COX-2 and 5-LOX. Studies suggest ursolic acid also inhibits histamine secretion from stimulated leukocytes.

GINGER Zingiber officinale has been used for thousands of years in Ayurvedic medicine and other systems of traditional medicine as an anti-inflammatory agent. Five constituents of ginger, including gingerols and shogaols, have been identified as inhibitors of inflammatory prostaglandin synthesis through modulation of eicosanoid and cytokine pathways, the same mechanism by which aspirin and other NSAIDs exert their anti-inflammatory and analgesic effects. Gingerols alter genetic expression of COX-2 mRNA reducing enzyme production and directly inhibiting COX-2 activity. Other constituents, 6-shogaol and gingerdione have been shown to antagonize 5-LOX activity. Ginger extracts also block production of the inflammatory cytokines, TNF-α and IL-1β, macrophage inflammatory protein 1α (MIP-1α), monocyte chemoattractant protein-1 (MCP-1), and interferon-inducible protein 10 (IP-10).

Oral Ginger extract is as effective as sulfasalazine in reducing colonic mucosal injury in rat models of Inflammatory Bowel Disease (IBD).

COMMON BARBERRY Berberis vulgaris has been naturalized in the United States but originates from Europe. B. vulgaris roots, stems and leaves have been used extensively in the Middle East, Europe and America for the treatment of infections, as a bitter tonic, and a variety of other medicinal purposes.

While Berberis vulgaris has not had sufficient testing in clinical trials, laboratory studies have shown that B. vulgaris is active in antimicrobial and anti-inflammatory responses. Berberis vulgaris is rich in berberine and berbamine. From the roots and bark, berberine is the main alkaloid isolated.

Berberine was shown to inhibit activator protein 1, a central transcription factor in inflammation and carcinogenesis during in vitro studies using human cell lines. Recent studies indicate berberine has wide-ranging anti-inflammatory activity. In vitro, berberine inhibits two major intracellular inducers of inflammation: mitogen-activated protein kinase (MAPK) and NF-κB. As a result, berberine also reduces production of inflammatory mediators TNF-α, IL-1β, IL-6, CRP, COX-2, and PGE2.

Another example of berberine’s anti-inflammatory activity is its significant inhibitory effects on lymphocyte transformation, which may be a result of the inhibition of DNA synthesis in activated lymphocytes. During platelet activation due to tissue injury, it was observed that berberine had a direct affect on many parts of the inflammatory process, including dose-dependent inhibition or arachidonic acid release from cell membrane phospholipids, inhibition of thrombus formation, and the inhibition of thromboxane A2 from platelets.

BAIKAL SKULLCAP Scutellaria baicalensis is used to regulate inflammation. Baicalin (BA, 7-glucuronic acid, 5, 6, -dihydroxy flavon) is a flavonoid compound purified from the medicinal plantS. baicalensis. BA  interferes with chemokines or chemokine receptors, which are critical mediators of inflammation and infection. In addition, BA possesses potent anti-inflammatory and antioxidant properties.

BA was tested to see whether it could interfere with chemokines or chemokine receptors, which are critical mediators of inflammation and infection. The results suggest that one possible anti-inflammatory mechanisms of BA is to bind a variety of chemokines and limit their biological function. The anti-inflammatory effects Chinese skullcap flavones are attributed mainly to their capacity to downregulate transcriptional expression of inducible nitric oxide synthase (iNOS), COX-2, and 5-LOX enzymes and thus reduce production of nitric oxide, prostaglandins, and leukotrienes. Baicalin also modulates activation of pro-inflammatory NF-κB cascade demonstrating significant in vivo anti-inflammatory activity.

INDICATIONS:

• Inflammation
• Infections
• Osteoarthritis
• Joint Pain and Stiffness
• Cadiovascular disease
• Cellular growth & differentiation
• Autoimmune diseases
• Asthma
• Acne
• Inflammatory Bowel disease
• Infection

Adult: 2 capsule 2X daily empty stomach (1/2 hour before meals)

Recommended Dose: Adult: 1 capsule three times daily with food.

Recommended Use: lnflammation Support+ contains Curcumin which is used in herbal medicine to help relieve joint inflammation, and provides antioxidants for the maintenance of good health.

Duration of Use: For use beyond 2 weeks, consult a health care practitioner.

Cautions: Consult a health care practitioner prior to use if you have diabetes, gallstones or a bile duct obstruction, stomach ulcers or excess stomach acid, severe circulatory disorders, iron deficiency or bleeding tendencies. Consult a health care practitioner prior to use if you are taking any prescription drugs, nutritional or herbal supplements, heart or blood pressure medication, including anti-platelet medication or blood thinners. Consult a health care practitioner if abdominal discomfort, heartburn or throat irritation persists. Consult a health care practitioner if symptoms persist or worsen. Use of alcohol while taking this may increase sedative effect. May cause hypoglycaemia in diabetics; monitor blood sugar. 

If you have a liver disorder, consult a healthcare practitioner prior to use. Stop use if you develop symptoms of liver trouble such as yellowing of the skin/eyes (jaundice), stomach pain, dark urine, sweating, nausea, unusual tiredness and/or loss of appetite and consult a healthcare practitioner.

Rare, unpredictable cases of liver injury associated with green tea extract containing products have been reported (in Canada and internationally).

Contraindications: Do not take it you are pregnant, nursing, or have a stomach or spleen dysfunction. Do not use if you or your partner are attempting to conceive.

Hypoallergenic: This product contains NO gluten, dairy, beef, egg, com, soy, peanut, pineapple, yeast or sugar.

Do not use if bottle seal is broken or missing.

Store in a cool, dry place (59°F-85°F) away from direct light.

KEEP OUT OF REACH OF CHILDREN.