Guest guest Posted April 20, 2004 Report Share Posted April 20, 2004 Herbs in Rheumatology by Jim Duke, PhD This issue of News from the Herbal Village is based, in part, on the draft of my book, Green Pharmacy, reviewing the so-called " green alternatives " (GA) or millennial medicines for some 125 modern ailments from the Herbal Village, stressing aromatherapeutic, herbal, food farmacy, nutritional and pharmaceutical alternatives. In preparing the book, I developed a GA database, not to encourage self diagnosis nor self medication, rather to elucidate and enumerate for intelligent readers some of the alternatives to which an increasingly large percentage of Americans are exposing themselves. Eisenberg (1993) indicated that Americans visit alternative practitioners more than conventional physicians. Many of these alternative therapists are encouraging the " green alternatives " covered in the GA database and Green Pharmacy. Until America performs unbiased head-on trials comparing the millennial green alternatives with the centennial synthetic alternatives (standard pharmaceuticals, some 25-60% ultimately derived from green alternatives, depending on the accounting system you use), America cannot be sure it is getting the best medicines. After 60 years as an outdoor botanist, the last 30 years as an ethnobotanist keenly interested in medical botany, I believe that in many cases the global green alternative is better than what we are getting. If I were diagnosed with arthritis, I’d much rather take some of the herbs listed below than steroids. I once endured a course of injected steroids prescribed for bursitis and I really prefer the GA. In retirement, as I told you in the first two issues, I am campaigning to get America to give the GA’s fair trial rather than keep them in the closet. DEFINITIONS: Rheumatoid arthritis, often called rheumatism or synovitis, is characterized by inflammation and pain, perhaps more frequently in the hands - especially the knuckles and second joints - in anyone, especially older people, often causing deformities as muscles weaken, tendons shrink, and ends of bones enlarge. (Time-Life Medical Advisor{TMA}1996). Infectious arthritis is caused by a bacterial or viral invasion of the joints, often following such diseases as gonorrhea, Lyme disease, staph infections and tuberculosis. Osteoarthritis, or degenerative joint disease, refers to pain and inflammation resulting from systematic loss of bone tissue in the joints. Some seem to have a genetic predisposition. (TMA, 1996) CIRCULATING IMMUNE COMPLEXES (CICs) Non-steroidal anti-inflammatory drugs (NSAIDs) *inhibit* cartilage repair (by inhibiting the production of the collagen matrix). Since osteoarthritis is caused or characterized in part by cartilage degeneration, the NSAIDs which 'suppress' the symptoms may *worsen* the target condition by inhibiting cartilage formation and hastening its 'destruction'. Individuals with rheumatoid arthritis may have " leaky guts " (increased intestinal permeability), especially if heavily dosing with NSAIDs. NSAIDs increase the leakiness of the gut, so that large dietary and bacterial molecules are absorbed into the body, leading to formation of complexes which can be deposited in the joints. Thus, the aspirin may ultimately aggravate more than alleviate. Cichoke (1996) notes that arthritis is associated with increased levels of immune complexes circulating in the blood. Normal antibodies in our immune system recognize and eliminate antigens (the enemy), like bacteria, cell wastes, toxins and viruses. Antibodies (shaped rather like the letter Y) flood the circulatory system, mopping up antigens (with the forked Y ends), forming aggregated clumps of antibody and antigen immune complexes (ICs). These IC’s are normally eliminated by the body. But abnormally, the body does not detect and/or or eliminate the circulating immune complexes (CICs). In this abnormal case, auto-immune diseases, (even rheumatoid arthritis) infections and/or malignant ailments can develop. Early breakdown and dissipation of the CICs (which can penetrate the joint cartilage from the synovial fluid) can moderate rheumatoid arthritis. ICs may act as antigens and stimulate the production of antibodies, resulting in the formation of gamma-globulins, which are contained in the ICs. The resulting antibodies, called rheumatoid factors, can be measured in the blood thus strengthening, if not positively, confirming the diagnosis of rheumatic joint disease. (Rheumatoid factors occur in several diseases such as some types of arthritis, endocarditis and hepatitis). Presence of rheumatoid factors, in conjunction with rheumatic symptoms, confirm the diagnosis of rheumatic disease. Several clinical tests confirm the beneficial effects of enzyme mixtures (including amylase, lipase, bromelain, chymotrypsin, pancreatin, papain, trypsin) in rheumatoid arthritis. One study helped 23 patients with arthritis of the large extremity joints, and seven with poly- arthritis of the fingers, using an enzyme mixture containing bromelain, chymotrypsin, pancreatin, papain, rutin, and trypsin. Acute and subacute cases clearly improved. Of patients with activated arthritis, treated six weeks with a specific enzyme mixture (containing trypsin, chymotrypsin, bromelain, papain, pancreatin, amylase, lipase, and the bioflavonoid, rutin), improved with no obvious side effects. (Cichoke, 1996) BUT, it may take months, and the required dose can be up to 30 tablets or more per day. That’s nearly a thousand capsules a month, more than 10,000 a year. Papaya and pineapple juice would be more pleasant, and perhaps cheaper, at least in Latin America. No one apparently knows whether the juice approach would be more or less effective at controlling CICs, if they are in fact the culprits that several scientists paint them to be. Cichoke summarizes: As a conditions of arthritis, CICs are present. Systematic enzyme therapy decreases the numbers of CICs and, in doing so, reduces the associated symptoms of the disease. . , without . . . serious and long-term side effects. Fight rheumatoid conditions without the serious side effects. I read Cichoke’s 1994 book during a couple of train trips and found it quite engaging. In the chapter where he talks about the CICs, he concludes rather emphatically, " Enzymes, through uncooked food and supplements, can help every system in your body function better. " I like the title for his arthritis chapter no. 12: More Precious than Gold. (Cichoke, 1994). The arthritis foundation keeps telling us that diet does not influence rheumatic conditions (except perhaps admitting that prunes may aggravate that podiatric form of arthritis known as gout.) Cichoke says, and I paraphrase very lightly: (1) In some people milk and milk products seem to aggravate the disease, (2) Diets low in saturated fat and high in EPA, help reduce or prevent the joint inflammation which makes arthritis so painful. EPA probably interferes with inflammatory prostaglandins, (3) Anti-oxidants can prevent oxidative joint damage, (4) Weight loss alleviates arthritis, and (5) European researchers have found enzymatic light at the end of the arthritic tunnel, if not the carpal tunnel. In this case, I side with Cichoke: diet, like exercise and weight loss, can alleviate many kinds of arthritis. Nature’s Herbs carries several plant-derived enzymes, like bromelain and papain, and herbs like ginger and turmeric, which also contain proteolytic enzymes, and may even be synergetic in breaking up CIC’s GREEN ALTERNATIVES Ashwagandha (Withania somnifera): Withaferin A " seems to be more potent than hydrocortisone in experimental (adjuvant-induced) arthritis in rats " which rather resembles human rheumatoid arthritis (RA). Most of the activities fall in dose ranges of 10-25 ppms. At inhibiting edema, the compound proved useful at 12-25 mg/kg body weight of albino rats intraperitoneally (ipr). A single dose lasted a long time, effectively suppressing inflammation after four hours. The effect of the compound called withanolide in suppressing granulation-tissue formation seemed similar to that of hydrocortisone. All that sounds good for both osteo- and rheumatoid arthritis. Some data suggests that it might suppress the immune system, which could be useful in RA. While some data suggests also that the plant may be poisonous, we still read that " The tender shoots are used as a vegetable " and " the seeds are used as a masticatory " (Wealth of India). Shoot extracts were anti-inflammatory in rats implanted with subcutaneous cotton pellets. 10 mg/kg doses i.p. significantly inhibited granuloma formation. Inhibition was comparable to 5 mg/kg hydrocortisone. Ashwagandha was also tested, along with Apium graveolens (celery), Myrtus communis (myrtle), Matricaria chamomilla, (chamomile), Achillea santolina (santolina), and aspirin on the suppression of carageenen-induced paw edema in rats. Aerial parts or flowers of plants were used in a water/ethanol extraction. 1% Carageenen solution was injected into the plantar region of the hind foot, followed by the various plant extracts at 10 mg/kg i. p. A treatment dose (at one tenth of a lethal dose (LD50) was used for each plant extract, and 1/5 (100 mg/kg) and 2/5 LD50 (200 mg/kg) used for aspirin. Three hour paw volume was measured; inhibition of edema was greatest in W. somnifera > Apium graveolens > Achillea santolina > Matricara chamomilla > Myrtus communis. All plant extracts inhibited edema better than 100 mg/kg aspirin, but only W. somnifera was as effective as 200 mg/kg aspirin. However, the dose of W. somnifera (like all the herbs studied!) is a smaller percentage of LD50, and has no reported gastrointestinal irritation side effects, so this may be a promising alternative to aspirin. (Al- Hindawi et al. 1992 - abstracted by C. Leigh Broadhurst) Bilberry (Vaccinium myrtillus): More promoting oligomeric procyanidins (OPCs) like Pycnogenol® or red wine than bil- or blueberries, Schwitters (1993) notes that OPCs, by means of their activity against free radicals, can help prevent alterations of the synovial liquid by depolymerization of hyaluronic-acid during articular diseases as well as collagen degradation during so called collagen disease (such as MS). Hyaluronidase is involved in inflammation, releasing histamine during degranulation of mast cells, wherein histamine is contained in blister- like vesicles. Hyaluronidase breaks down the " blisters " , releasing the histamine. Bioflavanols (OPCs) block an activator of hyaluronidase, hence exerting an anti-histamine, anti-allergic, and anti-inflammatory activity. Leukotrienes are 3-4 magnitudes more active than histamine, and are implicated in allergies, arthritis, asthma, diabetic retinopathy (via vascular leakage), immune suppressions, inflammations, and insect stings. (Schwitters, 1993) Boswellia aka Indian Frankincense (Boswellia serrata): I’d not be afraid to try the resin from Boswellia serrata, used for centuries in Asia in the treatment of arthritic conditions. Boswellic- acid extracts from the gum show anti-arthritic activity in experimental animals, retarding inflammation, maintaining glycosaminoglycan synthesis, and improving circulation to the joints. (Reddy et al, 1989) Alpha, beta-boswellic-acid completely inhibits the complement pathway at only 0.1 æM. Ammon et al (1993) found that boswellic acids specifically inhibit 5-LO in vitro (IC50=1.5-7.5 æM) without inhibiting 12-LO or CO. This important mechanism allows boswellic acids to act as anti-inflammatory agents without the attendant side effects of broad spectrum NSAIDs which block the cyclooxygenase reaction, or glucocorticosteroids which interfere with the phospholipase-A2 reaction. Boswellin, (a standardized extract of 60-65% boswellic acids,) improves the blood supply to the joints and prevents the breakdown of tissues affected by arthritis (Sabinsa Corp, 1995). In a double-blind, placebo-controlled study of 42 osteoarthritics (Kulkarni et al. 1991) taking a combination of Boswellia, Curcuma, Withania and zinc for three months, pain and disability was significantly reduced, with no significant side effects; 39 patients preferred the combo to placebo. In a clinical trial (Gupta et al. 1987) 95% of 175 RA patients, reported moderate to excellent improvement after 3-4 weeks of treatment, with reduced morning stiffness, pain, and swollen joints. Grip strength and physical performance also improved. In a foreword, James Brady, MD, Boca Raton, Florida, says: " The major use of Boswellia serrata in contemporary medicine is as an anti-arthritic and anti-inflammatory plant-derived extract. Its anti-inflammatory actions, supported by solid science, are indicated in clinical medicine for the treatment of rheumatoid arthritis, osteoarthritis, juvenile rheumatoid arthritis, soft-tissue rheumatism, gout, low back pain, myositis, and fibrositis and are attributed primarily to the presence of boswellic acids. Boswellic acid inhibits leukotriene synthesis via inhibition of 5- lipoxygenase. Compared to nordihydroguaiaretic acid (NDGA), both inhibit 5-lipoxygenase, but only NDGA also inhibits cyclooxygenase and 12-lipoxygenase. At reducing edema, boswellia, however, is not a whole lot better than phenylbutazone, IC39-75 = 50-200 mg/kg orl rat, cf IC40- 47 at 50-100 mg/kg phenylabutazione. And, at the molar level, it’s not clear that beta-boswellic- acid is better than aesculetin. Further 10 mg boswellic acid ointment was not as effective as 5 mg phenylbutazone ointment. As Sabinsa puts it, boswellic acids are effective at higher concentrations than phenylbutazone. " Translate: it takes less phenylbutazone to do the trick, orally or topically. " The therapeutic, anti-inflammatory effect of boswellic acids was comparable in strength to that produced by a topical application of curcuminoids. " (Majeed et al, 1996.) In his new newsletter, even Dr. Andy Weil (1996) recommends boswellia and its extract Boswellin to relieve inflammation of the joints. Burdock (Arctium lappa): I get many inquiries on the Essiac formula (burdock, rhubarb, sheep sorrel, slippery elm). While I think burdock could have given Jackie Onassis a few extra years Willix (Health & Longevity {H & L}, May 1995) is more positive, recommending " Essiac tea, with boiled unfluoridated water, to boost your immune system and prevent disease, 1 to 2 ounces a day; for arthritis, asthma, chronic fatigue syndrome, 2 ounces 1 to 2 times a day; for breast cancer, 2 ounces 3 times a day " . Willix says that " it appears there are no adverse side effects to Essiac. I’m sure it contains dozens of useful phytochemicals, and a few immune boosters. Remember, we might not want to boost the immune system in auto-immune rheumatics. (Essiac’s oxalic acid might be undesirable in some conditions). Chamomile (Chamomilla recutita): Even in a book with an ominous title like Adverse Effects of Herbal Drugs (De Smet, et al. 1992) we read that chamomile is reportedly anti-convulsant, anti- fungal, anti-herpetic, anti-inflammatory, antiseptic, anti-viral (herpes, polio), immunostimulant, sedative and spasmolytic. If true, that means it could serve in dermatology, ear-nose-throat disease, gastroenterology, gynecology, pediatrics, pulmonology, and stomatology as an anthelmintic, anti-spasmodic, carminative, diuretic, expectorant, sedative, stimulant, and tonic. Externally it is applied as a counter-irritant liniment for bruises, hemorrhoids, inflammation and sores. Local anti-inflammatory activity is considered due to apigenin, apigenin-7-D-glucoside, luteolin and quercetin. Hydroalcoholic extracts of dried chamomile flowers have repeatedly demonstrated mild but significant anti-inflammatory activity (AIA), while extracts from fresh flowers were found to be 40% more active. The AIA for isolated apigenin was 10 times greater than that of matricin, which was in turn 10 times greater than that of chamazulene. Essential oils are not as active as the hydroalcoholic extracts. Matricin is characteristic of extracts from fresh chamomile, and differences in the content of this constituent may account for variable AIA results (Bingol and Sener 1995 CLB). Reports of asthmatic and contact allergenic problems may be exaggerated or due in many cases to misidentifications. Neither apigenin, apigenin-D- glucoside, bisabolol, cis-en-yn-dicycloether, farnesene, luteolin, nor matricin had any allergenic potency in the absence of anthecotulide. (De Smet 1992). A topical compress of chamomile or arnica is worth the try, if you’re not having any luck with a pepper or peppermint (or spearmint) compress. Cayenne (Capsicum annuum): Capsaicin, the hot principle of the hot pepper, was the only herbal approach mentioned (barely), besides steroids (once herbally derived), in Newsweek’s, " Living with Arthritis " (March 20, 1989). Here again we were reminded of iatrogenic perils: " Nearly 9 million arthritis sufferers take large doses of such " NSAIDs " daily. Some 10,000 of them die every year from gastrointestinal complications - many of them " silent ulcers " that show no symptoms until they become life threatening. " Arthritic rats have been injected with capsaicin " that blocks pain-transmitting neurons and succeeded in reducing the inflammation in their joints. " So Dr. Levine, of whom Newsweek spoke, was injecting the active ingredient from hot peppers, seeking " a whole new class of drugs to combat rheumatoid arthritis. " ... Numerous studies (some dramatically, some slightly encouraging) report the success of capsaicin, the hot ingredient in red pepper, for pains. Substance P, thought to be the mediator of peripheral pain pulses, is apparently depleted by capsaicin. (Cordell and Araujo, 1993) Researchers are also finding significant pain relief applying a capsaicin cream externally to painful arthritic knees four times daily. For rheumatoid arthritis, the treatment reduced pain by more than half while osteoarthritis pain was reduced some one-third. Deal et al. (1991) conclude " Capsaicin cream is a safe and effective treatment for arthritis. " Not only reducing pain, capsaicin also increases the production of the enzyme collagenase and prostaglandins, reducing both pain and inflammation (pages from Herbalgram No. 27, 1992). If you’re not having any luck with capsaicin pepper or the Jamu capsicum pads (pepper pain pads or PPP), then you might try peppermint (or spearmint) compresses. Celery Seed (Apium graveolens): The maker of one celery seed extract got into the business because it had done his arthritis so much good. When I saw his ad claiming that celery seed was also hypouricemic, I didn’t believe it. So I replaced my allopurinol with celery seed extract. Six months later, after several traumatic injuries, and a couple of minor overdoses of ethanol, any of which normally would have triggered a gout crisis, I was still gout free. I would not have believed this anecdote if anyone told it but me. After the second month on celery seed, I then tried celery stalks, whole or juiced, for a couple weeks with the same results, a little messier and more trouble but food farmacy at its best. Bisset (1994) says only that " Celery seed is now only occasionally used in folk medicine, chiefly as a diuretic in bladder and kidney complaints, and an adjuvant in arthritic and rheumatic conditions. The effect is ascribed primarily to the essential oil. . . described as having sedative activity. Extensive animal experiments have demonstrated that the at most very slightly toxic alkaloid fraction has depressant, tranquilizing effects on the CNS. . .The drug is contraindicated in inflammation of the kidneys, since the essential oil (like other apiaceous oils) may increase the inflammation as a result of epithelial irritation. " Still in the UK, celery seed is found in some 60 anti-inflammatory preparations. And in my database, I found at least 25 anti-inflammatory compounds including: alpha-pinene, apigenin, ascorbic-acid, bergapten, butylidene-phthalide, caffeic-acid, chlorogenic-acid, cnidilide, copper, coumarin, eugenol, ferulic-acid, gentisic-acid, isopimpinellin, linoleic-acid, luteolin, magnesium, mannitol, myristicin, protocatechuic-acid, quercetin-3-galactoside, rutin, scopoletin, thymol, umbelliferone, and xanthotoxin. Is this combination of natural chemicals synergetically preventing my gout as well as my allopurinol? Stay tuned. Evening Primrose (Oenothera biennis): Horrobin (1992), advocate of evening primrose oil (EPO) and gamma-linolenic-acid (GLA), has an interesting point or two about PGE1 (prostaglandin E1). GLA can be administered, orally, as a precursor of PGE1, dihomogammalinolenic-acid (DGLA) and 15-hydroxy-dihomogamma-linolenic acid (15-OH-DGLA) which can block the arachidonic cascade and production of inflammatory compounds. This has been shown effective, in in vivo and in vitro models of arthritis. Horrobin concludes that anyone reviewing this literature should be convinced that GLA is a potent treatment for experimental inflammatory and auto-immune disorders. (Horrobin, 1992). Leventhal et al. (1993) worked with 37 rheumatoid arthritic patients giving them 1.4 gm GLA/day (from borage oil) or placebo. GLA patients had a 36 to 45% reduction in tenderness and 28 to 41% reduction in swollen joints. Patients given a placebo showed no improvement. There was significant reduction in synovitis in as early as 6 weeks. Nutritionists advise me that the balance between omega-3’s and omega-6’s is important, one suggested ratio being 1 part EPO with one part flaxseed oil and one part fish oil. Fenugreek (Trigonella foenum-graecum): I had doubted that wild yam would be effective as a transdermal estrogenic without spiking with progesterone. However, several clinically practicing herbalists (such as Susan Weed) argued that point with me at the 1995 fall outings in the Catskills. They said that they, themselves, had made salves out of wild yam, adding no progesterone, and that their clients were having the desired progesteronic effects. If they are right, I speculate that fenugreek would have similar effects, because the seed can contain more diosgenin (to 1.9%) than the roots of many wild yams (0.45% in Dioscorea bulbifera). Diosgenin itself is said to be useful in inflammation. Fenugreek seed contains two steroidal saponins which on hydrolysis give diosgenin and gitogenin, with traces of neotigogenin, tigogenin and yamogenin. Steroid hormones derived from diosgenin have many applications. Lydia Pinkham’s Compound contained 12 ounces fenugreek seed, 8 ounces unicorn root (Aletris), and 6 ounces each of life root (Senecio), black cohosh (Cimicifuga), and pleurisy root (Asclepias) in enough alcohol to make 100 pints of compound. The fenugreek and cohosh both contain diosgenin, the precursor for steroids. I have to agree with the author who suggests that Lydia Pinkham was a few years ahead of ERT (Estrogen Replacement Therapy). I might even try it for sciatica. Even Commission E approves fenugreek externally as a poultice for inflammation. Garlic (Allium sativum): As a gout sufferer I was interested to read that the enzyme xanthine oxidase from the liver was inhibited by garlic; more so with boiled garlic than with fresh garlic juice, showing that something other than allicin is responsible. Anti-arthritic activity was found for steam-distilled garlic oil fed at 2.5 mg/kg in rats, decreasing the arthritis 26%. Garlic’s effects were synergistically increased by dietary boron (Koch & Lawson, 1996), well represented in stinging nettle (also recommended for arthritis). The effects of aqueous extracts of raw and boiled garlic on cyclooxygenase (CO) activity were studied in rabbit platelets, lung, and aortic tissues. Raw garlic inhibited CO by 50% in these tissues at 0.35, 1.10, and 0.90 mg respectively. Boiled garlic extract had little effect on CO in these tissues as compared to raw. Platelets in particular were very sensitive to the effect of raw garlic extract, and therefore raw garlic preparations may be required in order to exert significant anti-thrombotic effects. (Ali, 1995 CLB) That’s why there are two cloves of garlic in the celery juice I am taking today in lieu of allopurinol. And one in my celery soup. Ginger (Zingiber officinale): Srivastava and Mustafa (1992) gave 3-7 gm powdered ginger a day to 56 patients with rheumatoid arthritis (n=2, osteoarthritis (n=1 or myalgia (n=10). More than 75% of the arthritics experienced varying degrees of relief from pain and swelling. None reported adverse effects from the high levels of ginger, from 3 to 30 months. Perhaps that’s why Jean Carper drinks ginger tea for her own osteoarthritis as reported in Parade Magazine (July 31, 1994. p. 4). If 10 gm ginger gives some relief to more than 75% of arthritics, naive arthritics should give ginger a try. Ginkgo (Ginkgo biloba): Recently ginkgo extracts have been promoted as a topical agent (or cosmetic) to improve peripheral circulation, hence useful as slimming and moisturizing agents due to their microvasculokinetic activity. Della Loggia et al. (1996) demonstrated anti- inflammatory activity of some Ginkgo biloba constituents and their phospholipid complexes. Ginkgolides, bilobalides, a bioflavonic fraction, and some pure bioflavonones (especially when mixed synergistically) were comparable to indomethacin as anti-inflammatories. Ginkgolides inhibit the pro-inflammatory PAF (platelet aggregating factor). Its bioflavones inhibit histamine release from mast cells and cAMP phosphodiesterases. The extract also reduces production of oxygen species by activated neutrophils. Complexes with distearoylphosphatidylcholine, more soluble in non-polar solvents than the parent compounds, are still even more strongly lipophilic, resulting in increased bioavailability and activity. For example the complex shows some 5 times more anti-edemic activity than the free compounds. The complex of a mix of ginkgolides A and B was more potent than indomethacin while the free mixture was not quite as effective. But phospholipid itself, alone, was inactive, merely increasing the activity of ginkgolides by making them more bioavailable. Of pure bioflavones, amentoflavone was strongest with anti-edemic (IC45=2 æM/ear), followed by ginkgetin (IC25=2 æM/ear) and sciadopitysin (IC19=2 æM/ear) as compared with an IC60=2 æM/ear for indomethacin. The mix of the bioflavonic fraction (corresponding to ca 0.2æM of bioflavones) inhibited 73% of the edema, compared with 45% for amentoflavone, the strongest competitor. Thus the pure flavones exhibit additive or even synergetic activity when mixed. (Della Loggia, R., et al. 1996) Horse Chestnut (Aesculus hippocastanum): Borrowing data from Chang et al. (1996) on Fraxinus bungeana DC, I see good rationale also for the horse chestnut. Containing esculetin, esculin, fraxetin and fraxin, bunge’s ash has been used folklorically as an anti-inflammatory analgesic uricosuric for gout and rheumatism, and as an anti-aggregant, anti-bronchitic, anti-diarrheal, and antipyretic, as well as a screen. Chang et al. (1996) speculate that these chemicals act synergistically for treatment of these diseases, and the glucosides esculin and fraxin are hydrolized in the body to the aglycones esculetin and fraxetin, the much more potent superoxide scavengers. Since these scavengers are implicated in many clinical disorders, scavengers can reasonably be expected to increase the span of health in preventive and therapeutic medicine. Licorice (Glycyrrhiza glabra): Your doctor might recommend a steroid. Some herbal alternatives to the steroids (which themselves contain steroids or steroid precursors), are fenugreek (Trigonella), licorice (Glycyrrhiza), sarsaparilla (Smilax), and wild yam (Disocorea). The licorice has a lot going for it, including ulcer prevention, but it can raise the blood pressure and lower potassium levels. In their survey of anti-inflammatory phytochemicals, Handa et al. (1992) state that glycyrrhizin potentiates the anti-arthritic activity of hydrocortisone in rats. The aglycone is about 1/8th as effective as cortisol in some tests. Derivatives of these and the flavonoids liquiritogenin, liquiritin, quercetin and rutin have also demonstrated anti-inflammatory activity. Duwiejua and Zeitlin (1993) enumerate several triterpenes with significant anti-inflammatory activities, one licorice compound equaling in intensity alpha, beta-boswellic acid (from Boswellia serrata) which completely inhibits the complement pathway (100% at 0.1 æM). Moreover glycyrrhetinic acid mimics corticosteroid activity. Licorice needs be watched, but for me, with moderate blood pressure and potassium levels, the licorice looks good. Diabetics might prefer the fenugreek, which has at least 5 hypoglycemic compounds. Pineapple (Ananas comosus): Naturopaths now suggest a dose of 150-450 mg bromelain, thrice daily, on an empty stomach. Early studies had been on enteric-coated pills of only 20 mg. Bromelain, a proteolytic enzyme, at low levels in pineapple, is suggested to help inflammation in several ways: inhibiting the formation of an inflammatory prostaglandin (E-2) while selectively stimulating the production of an anti-inflammatory prostaglandin (E-1); reducing edema and inflammation by inhibiting kinin formation, and activating the production of plasmin from plasminogen. In one study (Lotz-Winter, 1990), bromelain lowered kininogen and bradykinin levels up to 60%, decreased prostaglandin E-2 and thromboxane B-2 levels, and reduced the symptoms of inflammation. Bromelain can reduce inflammation in arthritis, sports injury or trauma, and can be useful in thrombophlebitis (Taussig and Batkin, 1988). Nonetheless, Commisson E suggests bromelain at 80-320 mg (in 2 or 3 doses) only for " acute postoperative and post-traumatic conditions of swelling, especially of the nasal and paranasal sinuses. " Bromelain has both proteolytic and lipolytic attributes, and is fairly well endowed with glutamine, reportedly catabolic. Lipolytic and catabolic activities might help you lose weight, almost always useful in arthritis. One might mix the pineapple with richer sources of glutamine for a lipolytic. I had assumed that the bromelain, if ingested, would itself be digested. But Boik (1995) says that a substantial percentage appears to be absorbed into the blood, up to 40% absorbed unchanged in animal models. Stinging Nettle (Urtica dioica): If I had arthritis, I might replace some nightshade foods with non-nightshade foods that have folk reputations for arthritis, like dandelion and nettle (more promising in gout than in rheumatoid arthritis). Analyses of my stinging nettle provided me by USDA scientists showed that on a dry weight basis it contained 47 ppm boron. A hundred gm serving would then contain more than the 3 mg boron the USDA scientists suggested could help in osteoporosis. According to Alternative Medicine, the Definitive Guide, (Goldberg, 1993) the Rheumatoid Disease Foundation suggests the use of boron to treat osteoarthritis and rheumatoid arthritis. " Boron apparently plays a role in the retention of calcium and also positively stimulates hormonal factors for both men and women, contributing to healthy bones. " (Goldberg, 1993) Stinging nettle can give you numbing microinjections, presumably of acetylcholine, histamine and 5-hydroxytryptamine, as well as a histamine-liberating enzyme (according to the Wealth of India). One M.D. told me that injections like these might stimulate the production of mast cells which might cause anti-inflammatory reactions elsewhere in the body. (Remember that the urtication for arthritis is often done remote from the site). Like bee stings, nettle stings have evolved in the antiarthritic folklore of every continent where they occur. Maybe both, like acupuncture and capsaicin, induce tingling and endorphins. Commission E suggests internal and external application as supportive therapy for rheumatic ailments (Blumenthal et al., 1997). In a letter to a medical journal, C. F. Randall (1994) recounts the story of an 81-year-old male osteoarthritic (with radiographically confirmed unilateral hip osteoarthritis) who found great relief from topical nettle where ibuprofen had offered none. (He had to apply the leaves (sting himself only once every few days to maintain the effect). Randall also mentioned an elderly woman who had used it to help her inflamed arthritic fingers. (Randall, 1994). One German study (Obertreis et al. 1996), undertaken to study the anti-rheumatic activities of Urtica dioica, showed that nettle extracts inhibit both detrimental eicosanoid and cytokine metabolism. Tumor necrosis factor-a and interleukin-1B are cytokines both suspect in pathogenesis of osteo- and rheumatoid arthritis. Concentrations of nettle extracts from 1.25-5 mg/ml inhibited their secretion dose-dependently and significantly, 5 mg/ml 51% and 100% respectively, after 24 hours. Since none of the flavonoids tested alone inhibited, other factors or synergy must be involved. The nettle extract also stimulated the production of interleukin-6, potentially useful for inhibiting interleukin-1B’s deleterious effects. Turmeric (Curcuma longa): Curcumin is used widely in India and Indonesia for inflammation. A pleiotropic cytokine, Tumor Necrosis Factor-alpha (TNF), induces production of beta- Interleukin-1 (Il-1). Together they cause both acute and chronic inflammation, and have been implicated in auto-immune disorders. At 5 æM, curcumin inhibits lipopolysaccharide-induced production of TNF and Il-1. Could that be good for arthritics yet bad for oncophobes? (Chan, 1995). Turmeric’s curcumin inhibits prostaglandin synthesis (weaker than ibuprofen). At high doses, it stimulates the adrenals leading to the release of endogenous cortisone. (Srivastava and Srimal, 1985) A relatively non-toxic nutraceutical, curcumin inhibits inflammation as well as cortisone or phenylbutazone in acute models, but only half as well in chronic models. (Srimal and Dhawan, 1973) Patacchini et al (1990) say that both curcumin and capsaicin deplete nerve endings of the neurotransmitter of pain, substance P. In one study, the activity of 1,200 mg/day curcumin was comparable to 300 mg phenylbutazone. But some compounds, perhaps synergetic with curcumin, are more potent. In a survey of anti-inflammatory phytochemicals, Handa, Chawla, and Sharma (1992) ranked them this way for experimental anti-edemic activity: sodium curcuminate > tetrahydrocurcumin > curcumin > phenylbutazone > triethylcurcumin. Still the triethylecurcumin was best at inhibiting granulomatous tissue formation. Two other natural analogues, feruloyl-4-hydroxycinnamoylmethane and bis-(4-hydroxycinnamoyl)-methane were actively anti-inflammatory while diacetylcurcumin and ferulic-acid were inactive. (WARNING: Though it has a lower ulcerogenic index than phenylbutazone, curcumin at 2 x ED50, administered for 6 days, can produce ulceration in rats). (Handa, Chawla, and Sharma, 1992). I now assume that beta-sitosterol occurs in all plants. Handa et al. say that beta-sitosterol (from nutsedge) has potent anti-inflammatory activity against carrageenan and cotton pellet induced edema in rats (comparable to hydrocortisone and phenylbutazone ipr). It showed a wide safety margin with the ipr LD 50 about 3,000 mg/kg in mice and the minimum ulcerogenic dose 500 mg/kg. Anecdotally, a friend of mine was very impressed with the anti-arthritic activity of turmeric (with cayenne) in DMSO, as was I. It was messy though. Willow (Salix spp): Weissmann (1991) says that 4-8 gm aspirin a day can reduce the redness and swelling of the joints in rheumatoid arthritis (but might be ulcerogenic). Raskin notes the effects of salicylic acid (salicin, o-hydroxybenzoic-acid), which is ubiquitous in plants, is the same in plants (and presumably animals) as aspirin, which undergoes spontaneous hydrolysis to salicylic acid. Exogenously applied, aspirin is " rapidly converted to salicylic acid. " All poplars and willows contain salicylates, in that sense being NSAIDs. The first herbal remedy mentioned by the Time-Life Medical Advisor is a 5 ml tincture made of 2 parts willow and one part each of black cohosh and nettle, taken three times a day. (TMA, 1996) There is a popular anti-arthritic remedy called Phytodolor N, (tincture of Fraxinus excelsior, Populus tremula and Solidago virgaurea). Individual tinctures alone, or combined, exhibit anti-edemic and anti-inflammatory activities, dose-dependently, comparable to diclofenac. (Ghazaly et al. 1992). BOTTOM LINE: I’d rather have high-bromelain pineapple or papaya/pineapple juice fortified with 10 gm ginger and 1 gm turmeric, and spiced up with a bit of licorice and capsaicin, to down after nibbling on sunflower seeds and brazil nuts, and chased with antioxidant tea, than what the doctors are prescribing for osteoarthritis or rheumatoid arthritis. I believe that’s the double " hippocrazic " (Freudian slip for Hippocratic) alternative, doing less harm, and letting food be medicine. I also think Gobo Gumbo might be useful, following exercise, along with some topical capsaicin/curcumin, and ingested proteolade, a mixture of fruits rich in proteolytic enzymes. I’m retired now, and have enough time to concoct these time-consuming " recipes " . But even today, in retirement, I find it easier to take these herbs as standardized extracts and tinctures. And on the road, of course, I won’t be taking my gobo gumbo or my anti-arthritic soups or salads, but I can pack my ABC’s for arthritis: ashwagandha, bromelain, boswellia, cayenne, and my spice capsules like ginger and turmeric. http://www.willner.com/References/webref21.htm REFERENCES Al-Hindawi MK, Al-Khafaji SH, Abdul-Nabi MH, Anti-granuloma activity of Iraqi Withania somnifera, J. Ethnopharm 37, 133, 1992. (CLB) Ali M. Mechanism by which garlic (Allium sativum) inhibits cycloxygenase activity. Effect of raw versus boiled garlic on the synthesis of prostanoids. Prostaglandins Leukotrienes and Essential Fatty Acids 53, 397-400, 1995. (CLB) Ammon HPT, Safayhi H, Mack T, Sabieraj J. Mechanism of anti-inflammatory actions of curcumin and boswellic acids. J. Ethnopharm 1993, 38: 113-119. Ammon, H. P. T., et al, {Tubingen, Germany} Use of preparations of curcuma plant. US patent 5,401,777, issued Mar 28, 1995. Assigned to Steigerwald Arnzmittelwerk, GmbH, Darmstadt, Germany) (as reviewed by Dean, K., 1996. Plant Patents. Herbalgram 37: p. 1. Bing l F. and Sener B, 1995. A review of terrestrial plants and marine organisms having anti- inflammatory action. Int. J. Phamacognosy 33: 81-97 1995. Bisset, N.G., ed. 1994. Herbal Drugs and Phytopharmaceuticals (English translation of Wichtl, 1984, 1989). CRC Press. Boca Raton, FL. 566 pp. Boik, J. 1995. Cancer & Natural Medicine. Oregon Medical Press. Princeton MN. 315 pp. Chan, M. M.-Y. 1995. Inhibition of Tumor Necrosis Factor by Curcumin, a Phytochemical. Biochemical Pharm. 49(11): 1551-6. Chang, W. S. Et al. 1996. Superoxide anion scavenging effect of coumarins. Am. J. Chin. Med. 24(1): 11-17. Cichoke, A. J. 1994. Enzymes and enzyme therapy: How to jump start your way to lifelong good health. Keats Publishing Co., New Canaan CT. 285 pp. Cichoke, A. J. 1996. Arthritis miracle - enzymes fight inflammation and promote joint health. J. Longevity Research 2(6): 40-2, 47. Cordell, G. A. and Araujo, O.E. 1993. Capsaicin: Identification, Nomenclature and Pharmacotherapy. Ann. Pharmacother. 27: 330-6. CSIR (Council of Scientific and Industrial Research). 1948-1976. The Wealth of India. A Dictionary of Indian Raw Materials & Industrial Products. 11 vols. CSIR Hillside Road, New Delhi. (Now in process of second edition; three new volumes published) De Smet, P.A. G. M., Keller, K., Hansel, R. and chandler, R.F., eds. 1993. Adverse Effects of Herbal Drugs 2. Springer-Verlag, Berlin. 348 pp. (often abbreviated as AEHD, 1993) Deal, C. L. et al, 1991. Treatment of Arthritis with Topical Capsaicin: A Double Blind Trial. Clin. Ther. 13(3): 383-95. Della Loggia, R., et al. 1996. Anti-inflammatory activity of some Ginkgo biloba constituents and of their phospholipid complexes. Fitoterapia 67(3):2574.)) Duwiejua, M., and Zeitlin, I.J. 1993. Plants as a source of anti-inflammatory substances, Chap. 11, pp. 152-167. In Harvey et al. 1993, which see. Eisenberg, D. MD et al.. 1993. Unconventional medicine in the United States. New England Journal of Medicine. 328:246-252. Ghazaly, M. et al, 1992. Study of the Anti-inflammatory Activity of Populus tremula, Solidago virgaurea and Fraxinus excelsior. Arzn.Forsch. 42(3): 333-6. Goldberg, B (et al.including hundreds of alternative specialists, even Jim Duke). 1993. Alternative Medicine: The Definitive Guide. Future Medicine Publishing, Inc. Puyallup WA. 1068 pp. Gupta, V. N. et al. 1987. Chemistry and pharmacology of gum resin of Boswellia serrata. Indian Drugs 24(5): Handa, S. S. Chawla, A. S. and Sharma, A. K. 1992. Plants with anti-inflammatory activity. Fitoterapia 63(1): 3-31 Horrobin, D.F. 1992. Nutritional and Medical Importance of Gamma-Linolenic Acid. Prog. Lipid Res. 31(2): 163-194. Houghton, P. J., Zarka, R., De Las Heras, B. and Hoult, J.R.S. 1995. Fixed Oil of Nigella sativa and Derived Thymoquinone Inhibit Eicosanoid Generation in Leukocytes and Membrane Lipid Peroxidation. Planta Medica 61(1):33-6. Koch, H. P. and Lawson, L. D., eds. 1996. Garlic- The Science and therapeutic application of Allium sativum L. and related species. Williams & Wilkins, Baltimore. 329 pp. Kulkarni, R. R. et al. 1991. Treatment of osteoarthritis with a herbomineral formula: a double- blind, placebo-controlled, cross-over study. J. Ethnopharm. 33: 91. Lotz-Winter, H. 1990. On the Pharmacology of Bromelain: An Update with Special Regard to Animal Studies and Dose-Dependent Effects. Planta Med. 56: 249-53. Majeed, M. et al. 1996. Boswellin - the Anti-inflammatory Phytonutrient. Nutriscience Publishers, Inc. Piscataway NJ. 78 pp. Obertreis, B et al. 1996. Ex-vivo in-vitro inhibition of lipopolysaccharide-stimulated tumor necrosis factor-a and interleukin-1B, secretion in human whole blood by extractum Urticae dioicae folium. Arzn. Forsch Drug Res 46: 389-94. Pattachini, et al. 1990. Capsaicin-like activity of some natural pungent substances on peripheral ending of visceral primary afferents. Arch. Pharmacol. 342:72-77. Pizzorno, J. E., Jr., 1996. 10 drugs I would never take . . . and the natural alternatives. Natural Health 26(5):82-5, 142-8. Randall, C. F. 1994. Stinging nettles for osteoarthritis pain of the hip. Br. J. Gen. Pract. (Nov.): 533-4. Reddy, C.K., Chandrakasan, C, and Dhar, S.C. 1989. Studies on the Metabolism of Glycosaminoglycans Under the Influence of New Herbal Anti-inflammatory Agents. Biochem. Pharm. 20: 3527-34. Sabinsa Corp. 1995. Personal communication from Dr. M. Majeed, President. Sabinsa Corp., an American company specializing in Ayurvedic herbs. Schwitters , B. and Masquelier, J. 1993. OPC In Practice. Alfa Omega, Rome. 107 pp. Srimal, R.C. and Dhawan, B. 1973. Pharmacology of Diferuloyl Methane (Curcumin), a Non- Steroidal Anti-inflammatory Agent. J. Pharm. Pharmac. 25: 447-52. Srivastava, R. and Srimal, R.C. 1985. Modification of Certain Inflammation-Induced Biochemical Changes by Curcumin. Ind. J. Med. Res. 81: 215-23. Srivastava, K. C. and Mustafa, T. 1992. Ginger (Zingiber officinale) in Rheumatism and Musculoskeletal Disorders. Medical Hypotheses 39(4): 342-8. Stavric, B. 1994. Quercetin in Our Diet: Willner Chemists - The Nutritional Supplement Professionals 100 Park Avenue, New York, NY 10017 & 253 Broadway, New York, NY 10007 2900 Peachtree Rd, NE, Atlanta GA 30305 http://www.geocities.com/mrsjoguest/FreeRadicals.html _________________ JoAnn Guest mrsjoguest DietaryTipsForHBP http://www.geocities.com/mrsjoguest The complete " Whole Body " Health line consists of the " AIM GARDEN TRIO " Ask About Health Professional Support Series: AIM Barleygreen " Wisdom of the Past, Food of the Future " http://www.geocities.com/mrsjoguest/AIM.html PLEASE READ THIS IMPORTANT DISCLAIMER We have made every effort to ensure that the information included in these pages is accurate. However, we make no guarantees nor can we assume any responsibility for the accuracy, completeness, or usefulness of any information, product, or process discussed. Photos: High-quality 4x6 digital prints for 25¢ Quote Link to comment Share on other sites More sharing options...
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