The role of Padma Basic®, a Tibetan-based herbal formula, in circulatory and cardiovascular disease
Isaac Eliaz
Introduction
Padma Basic is a mixture of 20 botanical ingredients that are based on a Tibetan formulation known to reduce inflammation and oxidative stress. Extensive in vitro and in vivo research over the last 30 years has demonstrated that this unique herbal preparation can play an important role in the prevention and treatment of arteriosclerosis. It may also be a safe adjunct to conventional coronary artery disease procedures such as drug therapy, angioplasty, bypass surgery, and chelation therapy. The antioxidative, (1,2) anti-inflammatory, (2-4) antiproteolytic, immunomodulatory and fribrinolytic (5) properties of this Tibetan botanical preparation support its use in a variety of inflammatory related diseases, including arteriosclerosis. In accordance with its broad spectrum of activity, the preparation has shown significant benefits in various clinical trials designed to assess its effectiveness in the treatment of angina and peripheral vascular disease. (6-10)
Atherosclerosis: The Inflammatory Connection
Coronary heart disease is the single largest killer of American men and women today. (11) Approximately every 29 seconds an American will suffer a coronary event. Coronary heart disease was responsible for over 459,000 deaths in 1998, or one out of every 5 deaths. The lifetime risk for developing coronary heart disease after the age of 40 is 49% for men and 32% for women. Atherosclerosis is the primary cause of heart disease and stroke. The etiology of arteriosclerosis is very complex and is marked by the thickening and narrowing of the artery walls. (12,13)
Atherosclerosis is a multi-factorial process which may involve the following mechanisms: inflammation, infection, and autoimmunity. (14) Recent data indicates that approximately 40% of subjects having a serious incidence of myocardial infarction are not exposed to any of the classical risk factors for atherosclerosis. (15,16) Two main hypotheses have been proposed to explain the pathogenesis of atherosclerosis: chronic endothelial injury and dyslipidemia. (13) Both of these appear to be interrelated and are associated with increased oxidative stress and inflammation. According to the injury theory, atherosclerosis is caused by damage to the vascular endothelium, leading to adhesion of blood platelets to the sub-endothelium, chemotaxis of monocytes, and migration of smooth muscle cells into the intima, ultimately promoting the formation of fibrous plaques. (12) A major cause of this damage is inflammation, which generates oxidative stress. (17,18)
The lipid hypothesis involves an elevation in plasma low-density lipoproteins (LDL), which may oxidize and contribute to the penetration of LDL into arterial walls. (18) LDL-ox is now believed to be the prime candidate for an auto-antigen that leads to a chain of autoimmune reactions. Scavenger receptor sites on the surface of macrophages facilitate the entry of LDL-ox into the macrophages, transferring them into lipid-laden “foam cells.” The foamy macrophages adhere to the endothelial lining, trap smooth muscle cells and contribute to the thickening and narrowing of blood vessel. (19)
Another important component in the formation of atherosclerosis, coronary artery disease and pulmonary artery disease is an innate tendency of certain individuals to hyper-coagulate. Hypercoaguability can manifest itself through the following blood parameters: elevated LP(a) (Lipoprotein a), increased plasminogen activator inhibitor-1 (PAI-1), elevated homocystine, increased fibrinogen and decreased fibrinolysis. (20,21) It is important to note, that while a patient can have a number of these abnormalities, their PT/PTT can still be normal as their system is moved towards deposition of fibrin monomers and not to the formation of clots. (22) However, stress and trauma caused by infections, inflammation or auto-immune processes can stimulate the formation of occlusive blood clots. (23,24)
Free radicals, the by-products of an inflammatory reaction, can damage the endothelium of blood vessels. (25) These oxygen radicals are produced by oxidative bursts from neutrophils via secretion of NO and proteases such as elastase (26) and by oxidized metal ions of iron and copper. (27,28) Recent data (29,30) suggests that C-reactive protein is involved in the atherosclerotic process by inducing the expression of adhesion molecules and chemokines in arterial endothelial cells, with the subsequent
recruitment of monocytes to the arterial wall. There is also growing evidence as to the role of infectious agents as inflammatory triggers of atherosclerosis. The progression of atherosclerosis is accelerated in several autoimmune conditions, including SLE and APS (anti-phospholipid process), supporting the view that the immune system may play an important role in the causation of arteriosclerosis. (14)
History of Formula
Formal Tibetan medicine was founded in the eighth century AD from a composite of the four most prominent Asian medical systems of the time: Ayurveda, Chinese, Unani (which inherited Greek medicine) and BonShamanic medicine. (31,33) Padma, a traditional Tibetan herbal formula, was handed down from the Tibetan monasteries of Transbaikalia (Siberia) to the Tsar’s court of Russia in 1850. The present formula has remained unchanged for more than 30 years and is essentially the formula used in Poland in the first half of the 20th century by a descendent of the Tibetan medical dynasty of Buryatiya.
After its introduction to Eastern Europe, this Tibetan herbal formula became well known throughout Russia, Poland and later Switzerland. The preparation (table 1) is based on a traditional Tibetan medical longevity formula and is considered “cooling.” As such, it is used in the treatment of “hot” conditions. Translated into Western terms, the Tibetan medicine concept of heat would correspond to such Western conditions as arteriosclerosis, heart disease, and other acute and chronic inflammatory conditions. Padma was registered with the Swiss drug regulatory authority (IOCM) in 1978 after demonstrating clinical effectiveness in the treatment of intermittent claudication.
The Swiss pharmaceutical company, PADMA AG, has manufactured the herbal preparation under the name of Padma 28[R] since 1969. The properties and benefits of this preparation have been extensively researched for the past 25 years. In Denmark, Poland, Lithuania and Switzerland, this formula is registered as a drug for peripheral artery disease. In other European countries (i.e. United Kingdom, Italy, Austria, and the Netherlands), Padma 28 is sold as a food supplement. The same food supplement is sold in the United States and Canada under the name Padma Basic.
Mechanisms of Action
The mechanism of action of the preparation may help to explain its remedial effects on arteriosclerosis. Laboratory and clinical studies have demonstrated that this herbal formulation demonstrates anti-oxidative and anti-inflammatory activities that protect normal cells and tissue from the inflammatory process. These include: the inhibition of the “oxidative burst” in neutrophils and monocytes, (2,4,5) inhibition of cytolysis from free radicals and proteases, (4) inhibition of lipid peroxidation (formation of LDL-ox), (1,2) protection of DNA from oxidative stress, (1) inhibition of NO-synthase (iNOS) in macrophages, (3) reduction of oxidized enzymes (1) and increased fibrinolytic activity including the reduction of the clot lysis time and PAI-1. (5) (see Table 2: Mechanisms of Action of Padma and its Physiological Effects).
The herbal preparation’s inhibitory effect on oxidative stress damage of proteins and DNA is related to its antioxidant activity and the ability to chelate heavy metal ions such as iron and copper. (1) Herbal extracts of the preparation contain reducing compounds as shown by the reduction of ferricytochrome c to ferrocytochrome c and the reduction of [Fe.sup.3+] to [Fe.sup.2+], indicating a strong inhibitory effect on Fenton-type chemical reactions (1) (Figure 1). The importance of iron chelation as a major antioxidant effect of flavonoids has been well documented (34) and may explain the inhibitory activity of this herbal extract on oxidative stress. The herbal preparation contains a complicated mixture of plant constituents including polyphenols, bioflavonoids, steroidal saponins, glycosides, glycyrrhizin, valepotriates, di and tri-terpenoids, alkaloids and other phyto-chemicals demonstrating both anti-oxidant and anti-inflammatory activity. (35-41)
[FIGURE 1 OMITTED]
The Effects on Circulatory Disease
Numerous published studies from Switzerland, Poland, Israel and Denmark have confirmed the preparation’s ability to help reduce the severity of pain and increase walking distance in patients with intermittent claudication. Schrader (9) in a placebocontrolled double-blind study measured the effects of the preparation in patients with intermittent claudication. After 14 days without vasoactive therapy, 23 patients were treated with Padma and 20 patients with placebo. After just 16 weeks of supplementation patients treated with Padma had a significant increase in maximum and pain-free walking distance.
A study by Drabaeck et al., (7) tested the clinical effects of the herbal preparation on patients with intermittent claudication. Thirty-six patients were randomized in a doubleblind study and received either two tablets of herbal preparation or placebo twice a day. At the end of the four-month study, subjects who took the preparation exhibited improvements in both pain-free and maximum walking distance, with increases of 100% and 60% respectively. The placebo group did not demonstrate any improvement in either of the above parameters.
Further studies on the benefits of the preparation in intermittent claudication were conducted at the Hadassah University Hospital in Jerusalem. (6) This study reported on the positive benefits of the preparation on circulation using non-invasive techniques for vascular testing. Of the 60 patients who completed this six-month double blind, randomized trial, 50% of the Padma supplemented group exhibited a significant drop in blood pressure (>15%) compared to only 25% of the patients taking placebo. Calculated blood flow deficit in the limbs (42) (ischemic window) was also improved in over 50% of the treatment group, while only 15% of the control group showed improvement. This study clearly demonstrated a marked improvement in blood circulation due to the supplementation with this Tibetan herbal preparation.
Other studies have indicated that the herbal preparation can improve chronic ischemia in patients with atherosclerosis. Smulski et al. (8) showed the herbal preparation to significantly increase walking distance in intermittent claudication, decrease blood platelet aggregation, increase alpha-lipoproteins and reduce the level of cholesterol, triglycerides, total lipids and beta lipoproteins over a 16 week period. This randomized, double blind trial showed no significant improvement in any of the patients who took the placebo. The authors concluded that the herbal preparation might be a useful therapeutic adjunct for chronic ischemia of the lower extremities. Samochowiec (43) and Hurliman (44) also demonstrated the significant benefits of the herbal preparation in improving both pain-free and maximum walking distance in patients with intermittent claudication.
The Effects on Angina Pectoris
A clinical study by Wojcicki et al. (10) measured the effect of the preparation on the frequency and severity of angina pectoris. The study was designed to evaluate the herbal preparation on fifty patients in a double blind, placebo controlled trial. The clinical response to therapy was good or excellent in 80% of the treated patients with a 69% reduction of angina episodes. There was also a significant increase in the amount of work performed before angina occurred and platelet aggregation and total lipids were reduced in patients receiving the preparation.
Potential Benefits in Inflammatory Related Conditions
The inflammatory processes involved in the development of arteriosclerosis are quite similar to other forms of chronic inflammation that result in persistent oxidative stress and permanent activation of the immune system. As Gutteridge (25) pointed out, more than 200 different diseases may be caused by oxidative stress. Because of its anti-inflammatory abilities, the preparation has consistently shown favorable effects in a variety of health issues that have chronic inflammation as a key component in their development including: multiple sclerosis, (45) chronic hepatitis, (46,47) cirrhosis of the liver, (48) rheumatoid arthritis (49) and recurrent respiratory tract infections in children. (50,51) The active substances in the herbal formulation act synergistically in their anti-oxidative, fibrinolytic and immune-regulating properties.
Recommended Usage
The recommended dosage depends on the health status of the individual. In some of the studies that evaluated the effect of the preparation on circulatory conditions, only 4 tablets per day (two, twice daily) were sufficient to achieve a therapeutic effect. In most cases it is advisable to start with a dosage of six tablets per day. The use of the herbal preparation may cause significant clinical improvement within 2-4 months. For patients with immune disorders, chronic infections and inflammatory-related degenerative conditions, 2 tablets, three times per day are recommended. Controlled studies and extensive clinical experience have shown that once the patient’s condition has been improved only 1-2 tablets per day may be necessary as a maintenance dose. No detrimental effects of using Padma have been documented, even with long-term use.
Padma Basic is packaged in a blister form to ensure long shelf life and prevent loss of volatile components. It is recommended to take the tablets on an empty stomach. During the last 30 years more than 2 billion tablets have been used in Europe without any major side effects or complaints. A small percentage of patients may experience mild epigastric discomfort, which is usually resolved by taking the preparation with a meal. The preparation does not seem to interact adversely with the metabolism of other drugs including Coumadin. There is no data available on the safety of the herbal supplement during pregnancy.
Conclusion
Padma Basic/28 is a Tibetan herbal preparation that has been marketed in Europe for several decades and contains a complex mixture of bioflavonoids, polyphenols, nutrients and phytochemicals that may act synergistically. The preparation has been shown to elicit anti-inflammatory, antioxidant, and immuno-modulating abilities that confer positive benefits when administered to patients with peripheral vascular disease (intermittent claudication), angina, and chronic inflammatory disorders. Based on oxidative stress as a basic pathological process for atherosclerosis, the anti-oxidative, anti-inflammatory, anti-proteolytic, immunomodulatory and fibrinolytic properties of this Tibetan-based herbal preparation make it possible to justify its use in a variety of diseases. The preparation has demonstrated favorable effects in the treatment of multiple sclerosis, chronic infections in children, hepatitis B, rheumatoid arthritis and cirrhosis of the liver as well as circulatory disease. Based on extensive research over the last 25 years, Padma is an important addition to the management strategies of peripheral circulatory and coronary artery disease.
Table 1: Ingredients in PADMA BASIC[R] *
Cetraria islandica, Iceland Moss
Saussurea lappa, Costus root
Azadirachta indica, Margosa fruit
Elettaria cardamomum, Cardamom fruit
Pterocarpus santalinus, Red Sandalwood
Terminalia chebula, Tropical Almond fruit
Pimenta dioica, Allspice fruit
Aegle marmelos, Bengal Quince
Gypsum, Calcium Sulfate
Aquilegia vulgaris, Columbine aerial part
Plantago lanceolate, Plantain aerial part
Glycyrrhiza glabra, Licorice root
Polygonum aviculare, Knotgrass aerial part
Potentilla aurea, Golden Cinquefoil aerial part
Syzygium aromaticum, Clove flower bud
Hedychium spicatum, Gingerlily rhizome
Sida cordifolia, Heart-leaved Sida aerial part
Valeriana officinalis, Valerian root
Lactuca sativa, Lettuce leaf
Calendula officinalis, Marigold flower
Cinnamomum camphora, Natural Camphor
* When sold in Switzerland, Poland, and Lithuania the formula
also includes aconite.
Table 2 Mechanisms of action for PADMA 28/Basic and its
physiological effects
Study Results Mechanism of Action
Anti- Anti- Anti-
oxidative proteolytic thrombogenic
Regeneration of x
protective enzymes
(horse-radish
peroxidases) in immune
cells [1], in vitro
Attenuation of excessive x
NO production of
inducible nitric oxide
synthase (iNOS) in
macrophages at the
level of the gene
expression, but no
direct scavenging
of NO [3], in vitro
Inhibition of the x
<<oxidative burst
response>> in human
neutrophils by
trapping of the free
and/or inhibition of the
production of the same
[2,4], in vitro
Reduction of the x
<<oxidative burst
response>> of the
monocytes from
PADMA 28-treated
patients [5], in vivo
Inhibition of the x x
cytolysis triggered by a
<> of free
radicals ([H.sub.2]
[O.sub.2] generated from
glucose oxidase), membrane-
penetrating substances
(streptolysins SLS and
SLO) and proteases
(trypsin) [2], in vitro
Inhibition of the oxidation x
of intralipid (lipid
oxidation) [2], in vitro
Prophylaxis and protection x
from oxidative stress
on DNA: scavenging
of peroxynitrate
(ONOO-) and hydroxyl
radicals (OH+) [1],
in vitro
Chelating of heavy metals x
([Fe.sup.2+]), i.e.
removal of catalytic
metal ions from the
radical-producing Fenton
reaction [1], in vitro
Inhibition of the lysozyme
release in human
neutrophils [4], in vitro
Inhibition of the tissue- x
destroying activity of
elastase and other
proteases (catherpsin G,
trypsin) [2], in vitro
Increase of the x
fibrinolysis
in intermittent
claudication (euglobulin
clot lysis times
shortened, PAI-1 activity
reduced) [5], in vivo
Study Results Physiological effect
Anti- Immuno- Anti-
inflammatory modulating atherogenic
Regeneration of x x x
protective enzymes
(horse-radish
peroxidases) in immune
cells [1], in vitro
Attenuation of excessive x x x
NO production of
inducible nitric oxide
synthase (iNOS) in
macrophages at the
level of the gene
expression, but no
direct scavenging
of NO [3], in vitro
Inhibition of the x x x
<<oxidative burst
response>> in human
neutrophils by
trapping of the free
and/or inhibition of the
production of the same
[2,4], in vitro
Reduction of the x x x
<<oxidative burst
response>> of the
monocytes from
PADMA 28-treated
patients [5], in vivo
Inhibition of the x
cytolysis triggered by a
<> of free
radicals ([H.sub.2]
[O.sub.2] generated from
glucose oxidase), membrane-
penetrating substances
(streptolysins SLS and
SLO) and proteases
(trypsin) [2], in vitro
Inhibition of the oxidation x x
of intralipid (lipid
oxidation) [2], in vitro
Prophylaxis and protection
from oxidative stress
on DNA: scavenging
of peroxynitrate
(ONOO-) and hydroxyl
radicals (OH+) [1],
in vitro
Chelating of heavy metals
([Fe.sup.2+]), i.e.
removal of catalytic
metal ions from the
radical-producing Fenton
reaction [1], in vitro
Inhibition of the lysozyme x x
release in human
neutrophils [4], in vitro
Inhibition of the tissue- x
destroying activity of
elastase and other
proteases (catherpsin G,
trypsin) [2], in vitro
Increase of the x
fibrinolysis
in intermittent
claudication (euglobulin
clot lysis times
shortened, PAI-1 activity
reduced) [5], in vivo
References
(1.) Suter M, Richter CH. Anti and pro-oxidative properties of PADMA 28, a Tibetan herbal formulation. Redox Report. 2000; 5(1):17-22.
(2.) Ginsburg I, Sadovnik M, Sallon S, et al. PADMA 28, a traditional Tibetan herbal preparation inhibits the respiratory burst in human neutrophils, the killing of epithelial cells by mixtures of oxidants and pro-inflammatory agonists and peroxidation of lipids. Inflammopharmacology. 1999; 7(1):47-62.
(3.) Moeslinger T, Friedl R, Volf I, Brunner M, Koller E, Spieckermann PG. Inhibition of inducible nitric oxide synthesis by the herbal preparation PADMA 28 in macrophage cell line. Can J Physiol Pharmacol. 2000; 78(11):861-866.
(4.) Matzner Y, S. Sallon. The effect of Padma-28 a traditional Tibetan herbal preparation, on human neutrophil function. J. Clin Lab Immunol. 1995; 46(21):13-23.
(5.) Winther K, Kharazmi A, Himmelstrup H, Drabaek H, Mehlsen, J. Padma 28, a Botanical compound decreases the oxidative burst reaction of monocytes and improves fibrinolysis in patients with stable intermittent claudication. Fibrinolysis. 1994; 8(2):47-49.
(6.) Sallon S, Beer G, Rosenfeld J, et al. The efficacy of PADMA 28, a herbal preparation, in the treatment of intermittent claudication: A controlled double-blind pilot study with objective assessment of chronic occlusive arterial disease patients. J Vascular Investigation. 1998; 4(3): 129-36.
(7.) Drabaek H, Mehlsen J, Himmelstrup, H, Winther K. A botanical compound, Padma 28, increases walking distance in stable intermittent claudication. Angiology. 1993;44(11): 863-7.
(8.) Smulski HS, Wojcicki J. Placebo-controlled double-blind study to determine the efficacy of the Tibetan plant preparation PADMA 28 with intermittent claudication. Alternative Therapies. 1995; 1:44-49.
(9.) Schrader R, Effects of the Tibetan herbal preparation Padma 28 in intermittent claudication. Schweiz Med Wochenschr. 1985; 115(22):752-756.
(10.) Wojcicki J, Samochowiec L. Controlled double-blind study of Padma 28 in Angina Pectoris. Herba Polonica. 1986;32:107-114.
(11.) American Heart Association. 2001 Heart and Stroke Statistical Update. Dallas, Texas: American Heart Association; 2000.
(12.) Ross R. The pathogenesis of atherosclerosis: a perspective for the 1990’s; Nature. 1993; 362:801-809.
(13.) Berkow R, editor. Chapter 3: Cardiovascular Disorders. In: The Merck Manual of Diagnosis and Therapy. 15th ed. New Jersey: Merck & Co Inc.;1987. p. 386-90
(14.) Shoenfeld S, Sherer Y, Harats D. Atherosclerosis as an infectious, inflammatory and autoimmune disease. Trends in Immunology. 2001; 22(6):293-295.
(15.) Blake GJ, Ridker PM. Novel clinical markers of vascular wall inflammation. Circ Res. 2001; 89(9):763-71.
(16.) Ridker PM. Role of inflammatory biomarkers in prediction of coronary heart disease. Lancet. 2001; 358(9286):946-948.
(17.) Gurr MI. Diet and coronary heart disease. Progress in Lipid Research. 1992; 31: 195-243.
(18.) Ross R. Atherosclerosis: an inflammatory disease. New Eng J Med. 1995; 340:115-126.
(19.) Hiramatsu K et al. Superoixide initiated oxidation of LDL-cholesterol by human macrophages. Atherosclerosis. 1987; 7:55-60.
(20.) Acevedo M, Tagle R, Simpfendorfer C. Non-traditional risk factors for atherosclerosis. Rev Med Chil. 2001; 129(10):1212-1221.
(21.) Isser HS, Purl VK, Narain VS et al. Lipoprotein (a) and lipid levels in young patients with mycocardial infarction and their first-degree relatives. Indian Heart J. 2001; 53(4):463-466.
(22.) Bajaj SP, Joist JH. New insights into how blood clots form; implications for the use of APPT and PT as coagulation screening test and in monitoring of anticoagulant therapy. Semin Thromb Hemost. 1999; 25(4):407-418.
(23.) Constans J, Seijneur M, Blann AD et al. Endothelial function, platelet activation and coagulation in lower limb occlusive arterial disease during treadmill exercise: correlation with transcutaneous oxygen pressure. Thromb Res. 2000; 99(6):557-561.
(24.) Katras T, Buttajar V, Colvett K. Radiation-related arterial disease. Am Surg. 1999; 65(12):1176-1179.
(25.) Gutteridge JM. Free radicals in disease processes: a compilation of cause and consequences. Free Radical Res Comm. 1993; 19:141-158.
(26.) Ginsburg I, Kohen R. Cell damage in inflammatory and infectious sites might involve a coordinated cross-talk among oxidants, microbial hemolysins and amphiphiles,cationicproteins, phospholipases, fatty acids, proteinases and cytokines. Free Rad Res. 1995; 22:489-57.
(27.) Rice TM, Clarke RW, Godleski JJ et al. Differential ability of transitional metals to induce pulmonary inflammation. ToxicolApp Pharmocol. 2001; 77(1):46-53.
(28.) Healy H, Reith D, Morgen C. Are metalloproteins and acute phase reactants associated with cardiovascular disease in end-stage renal failure? Ann Clin Lab Sci. 2000; 30(3)295-304.
(29.) Ridker PM, Stampfer MJ, Rifai N. Novel risk factors for systemic atherosclerosis: a comparison of C-reactive protein, fibrinogen, homocysteine, lipoprotein(a), and standard cholesterol screening as predictors of peripheral arterial disease. JAMA. 2001 May 16; 285(19):2481-5.
(30.) Ridker PM. High-sensitivity C-reactive protein: potential adjunct for global risk assessment in the primary prevention of cardiovascular disease. Circulation. 2001; 103(13): 1813-8.
(31.) Prassaad Steiner R. Tibetan medicine. Part 1: Introduction to Tibetan medicine and the (fourth tantra). Am J Chin Med. 1987;15(12):83-88.
(32.) Badmaev P. The fundamentals of medical science of Tibet. Moscow, Russia: Gyushi Publishers; 1991.
(33.) Gerke B. On the history of the two Tibetan medical schools: jungjug and zurlug. Ayur Vijnana. 1999; 6:22-26.
(34.) Chi-Tang HO et al. Antioxidant effects of polyphenol extracts prepared from various chinese teas. Prevent Med. 1992; 21:520-525.
(35.) Aruoma L, Okezie I, Spencer J, et al. Reaction of plant derived and synthetic antioxidants with trichloromethyl peroxyl radicals. Free Rad Res. 22:187-190.
(36.) Kramer R E. Antioxidants in clove. J Ann Oil Chem Soc. 1996; 62:19-27.
(37.) Robbers J, Speedie M, Tyler V. Phamacognosy and Pharmacobiotechnology. Baltimore, Maryland: Williams and Wilkins; 1996.
(38.) van Acker SA, van Balen GP, van den Berg DJ, Bast A, van der Vijgh WJ. Influences of iron chelation on the antioxidant activity of flavonoids. Biochem Pharmacol. 1998; 56:935-945.
(39.) Lin RC, Hanquet B, Lacaille-Dubois MA. Aferoside A, a steroidal saponin from costus afer. Phytochemistry. 1996; 43(3):665-668.
(40.) Yamarbura J, Liy H, Tamai Y et al. Anti-ulcer effect in rats of bitter cardornan constituents. Chem Pharm Bull (Tokyo). 1990; 38(11):3053-3054.
(41.) Kunovalova GG. Antioxidant activity of parapharmaceutics containing natural inhibitors of free radical processes. Bull Exp Biol Med. 2000; 130(7):658-660.
(42.) Feinberg RL, Gregory RT, Wheeler JR, et al. The ischemic window: a method for the objective quantitation of the training effect in exercise therapy for intermittent claudication. J Vasc Surg. 1992; 16:244-250.
(43.) Samochowiec L. et al. Clinical test of the effectiveness of Padma 28 in the treatment of patients with chronic arterial occlusion (intermittent claudication Fontaine II). Polbiopharm Reports. 1985; 21:3-40.
(44.) Hurliman FA. Lamaistic formula for the treatment of peripheral arterial occlusion (intermittent claudication Fontaine stage II). Swiss medical review. 1978; 38:1407-1409.
(45.) Korvin-Piotrowska T, Nocon D, Stankowska-Chomic A, Starkiewicz A, Wojcicki J, Samochowiec L. Eperience of PADMA 28 in multiple Sclerosis. Phytother Research. 1992; 6:133-136.
(46.) Gladysz A, Janiec W, Wojcicki J. Influence of PADMA 28 on patients with chronic active hepatitis B. Phytother Research. 1993; 7:244-247.
(47.) Brzosko, WJ. Padma 28 in patients with chronic hepatitis B Clinical and Immunological effects. SchweizZschr fur Ganzheits Med. 1992; 7(8):13-14.
(48.) Nefyodov LI, Doroshenko YM, Karavay NL, Brzosko, WJ. Effect of PADMA 28 on impaired amino acid metabolism induced by liver inflammatory pathology. Herba Polonica. 2000; 4 (19):340-345.
(49.) Brzosko WJ, Jankowski A, Prusek W, Ollendiek H. Influence of PADMA 28 and thymus extract on clinical, and laboratory parameters of children with juvenile chronic arthritis. Int J Immunotherapy. 1991; 8(3):143-147.
(50.) Jankowski A, Jankowski R, Brzosko WJ. Treatment of children prone to infection with PADMA 28. SchweizZschr fur Ganzheits Med. 1992; 7(8):13-14.
(51.) Mansfield HJ. Influencing recurring respiratory system infections in children via immunostimulation. Terapeutikon. 1988; 2(12):707-712.
Correspondence:
Isaac Eliaz, MD, LAc, Director
Amitabha Medical Clinic and Healing Center
7064 Corline Ct., Suite A
Sebastopol, California 95472 USA
707-829-5900
Fax 707-829-5282
science@dreliaz.com
www.dreliaz.com
Michael Eli Rosenbaum, MSc, MD,
Director, Orthomolecular Health Medicine (OHM)
Fellow–American Academy of Medical Acupuncture
300 Tamal Plaza, Suite 120
Corte Madera, California 94925 USA
COPYRIGHT 2003 The Townsend Letter Group
COPYRIGHT 2003 Gale Group