What is Arborium Plus?
Arborium Plus is an Oral Natural Herbal Solution for Non-Invasive Cardiac (Heart) and Stroke Management. This is a Proprietary Herbal extract manufactured by Redhill Herbal Company, Dehradun, Uttranchal, India.

What are the ingredients of Arborium Plus?
Arborium Plus is a mixture of Rhododendron Arborium flower juice and Seabuckthorn (Hippophae rhamnoides) fruit juice blended with suitable preservative. The Herbal formulation is rich in Anti-oxidants, Beta-carotenes, Flavonoids, Vitamins including C & E and Essential Minerals in natural form.

What is the history of ingredients?
The medicinal value of Rhododendron and Seabuckthorn were mentioned in ancient Indian, Tibetan, Chinese and Russian Medical scriptures.

Who can use Arborium Plus?
a) Persons suffering with / prone to Coronary Heart Disease (CHD)
b) Persons suffering with / prone to High Blood Cholesterol and Triglyceride levels
c) Persons suffering with / prone to Atherosclerosis of Blood vessels
d) Persons suffering with / prone to Cerebro Vascular Disease (CVD) - Stroke
e) Persons suffering with / prone to ageing problems including arthritis and depression.
f) Can be used as Free radical scavenger to counter act pollution problems

What is the dosage of Arborium plus?
a) Therapeutic dosage - 10ml per day in the morning after breakfast for sixty days followed by maintenance dosage of 5ml per day for sixty days.
b) Preventive dosage - 5ml per day in the morning after breakfast for sixty days.

What is the interaction with other Allopathic, Homeopathic, Ayurvedic, Sidha and Unani Medicines?
Arborium Plus can be taken safely with other drugs mentioned above. Only about 15 minutes gap is to be maintained between Arborium plus and other drugs.

What are the side effects of Arborium Plus?
Being a flower and fruit juice, there are no known side affects for this product as on today.

What is Coronary Heart Disease (CHD)?
Coronary heart disease (CHD) (also known as atherosclerotic coronary artery disease or ischemic heart disease) is caused by atherosclerosis, the build-up of plaque on the insides of the coronary arteries, which supply blood to the heart. Over time, this causes these blood vessels to become narrow. Since not as much blood can pass through, the blood supply to heart muscle is reduced. The clinical symptoms of CHD can be angina pectoris, myocardial infarction, or simply, sudden death. By far the most common cause of CHD is coronary artery atherosclerosis, a patchy nodular type of arteriosclerosis (a general term for hardening and thickening of the artery wall), which causes reduced perfusion and increased susceptibility to occlusion.

What are the High risk factors for Coronary heart disease and stroke?
The well established risk factors are High Blood pressure, Cigarette smoking, Stress, High blood Cholesterol, Physical inactivity, Obesity and Diabetes.

What is Atherosclerosis?
The initial lesion in atherosclerosis, the fatty streak, is usually asymptomatic and consists mostly of accumulated foam cells. Foam cells develop from monocyte/ macrophages and contain large quantities of cholesterol ester and free cholesterol in cytoplasmic lipid droplets. The fatty streak can develop into a fibrous plaque, which consists of a fibrous cap of smooth muscle cells and dense connective tissue, a cellular layer, and a core of dead tissue. A complex lesion involving calcification, necrosis, ulceration, hemorrhage, and thrombosis of the fibrous plaque can also occur and cause the clinical symptoms of CHD.

What is the role of Low Density Lipoproteins (LDL) in Atherosclerosis?
LDL is considered to be the major atherogenic lipoprotein in the blood; serum concentration of LDL has been shown to be directly related to risk for CHD (serum concentration of HDL, on the other hand, has been shown to be inversely related to risk for CHD). Chronic high cholesterol, in the form of LDL, could be considered a form of metabolic stress; however, much evidence suggests that it is oxidized LDL and not unmodified LDL that plays a key role in the formation of at least the initial atherosclerotic plaque. Oxidation seems to be the most likely modification of LDL in vivo, because endothelial cells, smooth muscle cells, and macrophages in vitro are able to oxidize LDL. In addition to being a legend for the scavenger receptor, oxidized LDL also seems to have other biological effects: cytotoxicity, stimulation of endothelial-leukocyte adhesion, chemoattraction of monocytes, inhibition of macrophage migration, inhibition of NO (endothelium derived relaxation factor), and increased tissue factor expression. All of which may be involved in the formation of the initial lesion. Preventing oxidation of LDL could lead to a reduction in fatty streak formation and possibly prevention of the more advanced lesions involved in CHD.

What is the role of hyperhomocysteinemia in atherosclerotic plaques?
Low serum vitamin B12, or genetic defect in uptake or utilization of B12 proteins, such as an intrinsic factor deficiency, can lead to a condition known as hyperhomocysteinemia, a condition in which there is an over-excess of homocysteine in the blood, indicating a problem in sulfur-amino acid metabolism. Hyperhomocysteinemia increases the risk of stroke as it causes an increased formation of a cyclic reactive form of homocysteine that can react with low-density lipoproteins. Such oxidation can lead to atheroma formation, (macrophagocytic lipid aggregations, secondary to increased LDL uptake by these macrophages), as well as intimal injury, oxidation of cholesterol and unsaturated lipids, platelet aggregation, thrombogenic factors, myointimal hyperplasia, deposition of sulfated GAG's, fibrosis, and calcification of atherosclerotic plaques. The chronic effects of the buildup of these toxic thiolactone derivatives of sulfur amino acid metabolites can lead to ongoing vascular stenosis, leading to ischemic diseases of many organs, especially cerebral and cardiac tissues.

What are free radicals and their significance?
Free radicals are molecules with an unpaired electron, which enables them to initiate damaging free radical chain reactions. Normal metabolism produces a small amount of these free radicals. Oxidative phosphorylation, for example involves reduction of molecular oxygen by stepwise addition of electrons. Under normal conditions, ninety-eight percent of the oxygen is reduced to water, but two to five percent of the reduced oxygen enters the univalent pathway which produces by-products called reactive oxygen species (ROS). Most of the ROS are taken care of by superoxide dismutase, catalase, and glutathione peroxidase. The hydroxyl radical is the most dangerous of the ROS. Polyunsaturated fatty acids (PUFAs), due to their carbon-carbon double bonds, are particularly prone to peroxidation by ROS. A significant part of LDL is made up of cholesterol esterified to linoleate, a PUFA. This is another reason to suspect that LDL may be prone to the oxidation that, in keeping with the oxidative modification hypothesis, would be necessary to induce atherogenesis.

What is the use of Antioxidants and beta-carotenes?
Dietary antioxidants, such as vitamins E, C, B-complex, and beta-carotene, have been shown to be important in blocking critical steps in the formation of atherosclerotic plaques. Atherosclerotic plaques have been shown to form from free-radical oxidation of lipids, thereby forming fatty plaques on vessel walls, leading to vascular stenosis. Vitamin C, a water-soluble vitamin has been important in reducing the free-radical formation in aqueous phase. Beta-carotene and vitamin E have been shown to block free radical oxidation in the lipid-phase of LDLs. Studies have shown that low levels of beta-carotene have a higher relative risk for CVA (R.R. = 1.53, p=0.02), as does low levels of vitamin C (R.R. = 1.25, p. = 0.38), and the combined condition with low beta-carotene and vitamin C has an even higher relative risk of 1.96 (p = 0.02). A diet low in both beta-carotene and vitamin C has almost double the risk for having a stroke or ischemic heart disease.

What are the uses of Flavonoids?
Flavonoids are antioxidant compounds that are characterized by their polyphenolic chemical structure. Flavonoids are responsible for primary anti-oxidative effects by attracting oxygen free radicals before these free radicals can cause cellular damage. Over 4,000 flavonoids have been discovered, and they are found in fruit, vegetables, seeds, nuts, flowers, and bark. The best sources of flavonoids in human consumables are red wine, tea, onions, and the ubiquitous agent of health care: APPLES! Flavonoids have also been found to aid in vascular smooth muscle relaxation, which can reduce blood pressure, and thereby reduce the risk of stroke. Flavonoids have been shown to have antibacterial, anti-inflammatory, antiallergic, antimutagenic, antiviral, antineoplastic, anti-thrombotic, and vasodilatory activity. The potent antioxidant activity of flavonoids their ability to scavenge hydroxyl radicals, superoxide anions, and lipid peroxy radicals may be the most important function of flavonoids, and underlies many of the above actions in the body. Oxidative damage is implicated in most disease processes, and epidemiological, clinical, and laboratory research on flavonoids and other antioxidants suggest their use in the prevention and treatment of a number of these. Catechin and its derivatives, oligomeric proanthocyanidins, quercetin and quercetin chalcone, Ginkgo flavone glycosides, silymarin, and others can be utilized in preventative and treatment protocols for cardiovascular disease, cancer, inflammatory conditions, asthma, periodontal disease, liver disease, cataracts and macular degeneration.

How long Arborium Plus is under usage?
Sri KVS Ramasarma formulated Arborium Plus in the year 1999 and all the clinical trials by various Ayurvedic and also Allopathic doctors have been completed by January, 2003. Trial marketing started from April, 2003 and commercial marketing started from September, 2003.

1. Antioxidants and Stoke Prevention Management - By Christopher Komanapali
2. Coronary Heart Disease and Antioxidant Vitamin E - By Steve Hart
3. Antioxidant Flavonoids: Structure, Function and Clinical Usage - Alan L. Miller, MD
4. International Workshop on Seabuckthorn (IWS-2001) New Delhi, India - February 18-21, 2001
5. Rich Nature Natural Health Products
6. Canada Seabuckthorn Enterprises Limited (CSEL)
7. National Institute of Health, United States of America