Organic Golden Flax Seeds
Flax seeds are thought to have originated in the ancient Middle East during biblical times. They are an important source of polyunsatured fatty acids, including Omega-3, plus Magnesium, Zinc and dietary fiber. Flax oil from flax seeds is the richest known source of linolenic acid. It contains protein, mucilage, phytosterols and lignans, which are naturally included at 100 times the level of the next best source, wheat bran.
Suggested Use: Grind your own seeds on a daily basis for the freshest and healthiest seed oil. Add to cereals, salads and blender drinks. Take with plenty of fluids
L-Arginine is a conditionally essential basic amino acid involved primarily in urea metabolism and excretion as well as DNA synthesis.
NOW L-Arginine Powder is a 100% pure, free form, pharmaceutical grade amino acid.
Double Strength - 400 mg Complex Providing 200 mg SAMe Active Ions
SAMe is a supplement formed in the body by an enzymatic reaction between adenosine-triphosphate (ATP) and methionine. It was discovered in 1952 in Italy and has been researched and manufactured there. SAMe works closely with folic acid and vitamin B-12
SAMe appears to raise levels of dopamine, an important neurotransmitter in mood regulation. SAMe also possesses anti-inflammatory, pain-relieving, and tissue-healing properties that may support healthy joints.
Saw Palmetto Standardized Extract
Saw Palmetto Berries come from a small palm tree which grows in the southeastern US. It has been used by Native Americans and researched in Europe and Japan, where it is widely consumed
Supports a healthy prostate.
Standardized to contain between 85-95% fatty acids and biologically active sterol compounds
High Potency Multiple with Green Superfood Concentrates
Details: Note: natural color variations may occur in this product. Vegetarian Formula
Suggested Use: Adults: take 2 tablets daily, preferably with meals.
Warnings: Accidental overdose of iron-containing products is a leading cause of fatal poisoning in children under 6. Keep this product out of reach of children. In case of accidental overdose, call a doctor or Poison Control Center immediately.
Free Of: yeast, soy, milk, corn, wheat, preservatives.
Other Ingredients: Alfalfa, Rose Hips, Dicalcium Phosphate, Cellulose, Stearic Acid, Croscarmellose Sodium, Magnesium Stearate, Silica, Vegetable Protein Coating
S u p p l e m e n t F a c t s
Serving Size: 2 tablets
Servings Per Container: 90
Per Serving % Daily
Vitamin A (100% as Beta-Carotene) 10,000 IU 200%
Vitamin C (from Calcium Ascorbate) 500 MG 833%
Vitamin D (as Cholecalciferol) 200 IU 50%
Vitamin E (as d-alpha Tocopheryl Succinate) 200 IU 667%
Vitamin K (from Green Foods) 25 MCG 31%
Thiamine (Vitamin B-1) 50 MG 3333%
Riboflavin (Vitamin B-2) 50 MG 2941%
Niacin (as Niacinamide) 50 MG 250%
Vitamin B-6 (as Pyridoxine HCI) 50 MG 2500%
Folate (Folic Acid) 400 MCG 100%
Vitamin B-12 (as Cyanocobalamin) 100 MCG 1667%
Biotin 100 MCG 33%
Pantothenic Acid 50 MG 500%
Calcium (from Calcium Carbonate and Calcium Ascorbate) 100 MG 10%
Iron (from Amino Acid Chelate) 10 MG 55%
Iodine (from Kelp) 150 MCG 100%
Magnesium (from Magnesium Oxide and Amino Acid Chelate) 50 MG 13%
Zinc (from Amino Acid Chelate) 15 MG 100%
Selenium (from Amino Acid Chelate) 50 MCG 71%
Copper (from Amino Acid Chelate) 1 MG 50%
Manganese (from Amino Acid Chelate) 5 MG 250%
Chromium (from Yeast-free GTF) 100 MCG 83%
Molybdenum (from Amino Acid Chelate) 50 MCG 67%
Potassium (from Amino Acid Chelate) 50 MG 1%
Boron (from Amino Acid Chelate) 1 MG
Vanadium (from Amino Acid Chelate) 50 MCG
Choline Bitartrate 50 MG
Inositol 50 MG
PABA 30 MG
Spirulina 250 MG
Chlorella (Broken Cell Wall) 250 MG
Barley Grass (Organic) 250 MG
Alfalfa Juice Concentrate 100 MG
Octocosanol (Wheat Free) 100 MCG
Eleutherococcus senticosus (Siberian Ginseng Root) 50 MG
Citrus Bioflavonoids (37% Total Bioflavonoids as Hesperidin) 50 MG
Rutin 25 MG
Psyllium Husk Fiber 50 MG
Echinacea purpurea (root) 50 MG
Apple Pectin 25 MG
Betaine HCI 25 MG
Glutamic Acid 25 MG
Papain (Papaya) 25 MG
Lipase 10 MG
Amylase 10 MG
Chlorophyll 9 MG
Amino Acids 17 380 MG
* Percent Daily Values are based on 2,000 calorie diet.
Daily Value not established.
Stevia Extract Packets
Stevia Rebaudiana is a small plant native to Paraguay and Brazil. It was discovered in 1887 by a South American scientist named Antonio Bertoni who learned of the herb from the Guarani Paraguayan Indians. Stevia was known locally as Caa'-ehe or Kaa'-he-e wh
A good quality Stevia leaf is estimated to be 300 times sweeter than cane sugar, or sucrose. Also known as 'honey leaf' and yerba dulce, stevia is not absorbed through the digestive tract, and is therefore non-caloric. Although stevia adds sweetness to foods, it cannot be sold as a sweetener because the FDA considers it an unapproved food additive. However, under the provisions of the Dietary Supplement Health and Education Act (DSHEA) passed in 1994, stevia can be sold as a dietary supplement.
100% Natural Mixed Tocopherols
Vitamin E is a major antioxidant and the primary defense against lipid peroxidation. It is particularly important in protecting the body's cells from free radical/oxidative damage. These protective benefits are achievable with supplemental intakes higher than what is normally consumed in the average diet.
Mixed tocopherols may be superior at inhibiting lipid peroxidation than alpha-tocopherol alone, according to an in vitro study printed in the May 2002 issue of the Journal of Cardiovascular Pharmacology (39, 5:714-21, 2002).
For more information about Vitamin E, read THE VALUE OF ANTIOXIDANTS: Vitamin E by Dr. Michael G. Kurilla, M.D.
THE VALUE OF ANTIOXIDANTS: Vitamin E
By Dr. Michael G. Kurilla, M.D.
Oxidation is a chemical process where something reacts with oxygen. For example, rusted metal and a slice of an apple that turns brown if left out are common results of the oxidation process. In the human body, oxidation is a frequent occurrence because we rely on oxygen (which is carried throughout our bodies by blood) for life. To combat the unwanted effects of oxidation, nature has evolved a diverse array of antioxidants (agents that either prevent or repair unwanted oxidation) to counteract the adverse effects of oxidation.
With an increasing appreciation of the involvement of oxidation in the initial stages and progression of several major disease processes, particularly cardiovascular disease, the use of dietary antioxidants is being more critically evaluated. While not definitively proven at this time, the evidence accumulated to date is showing vitamin E to play a significant role in slowing or even reversing major disease processes. Investigators in this area are encouraged by the findings that the presumed mechanisms underlying the action of vitamin E are reasonably well understood as well as results of human studies in general, supporting predictions based on these presumed mechanisms. Equally encouraging to potential users of vitamin E is the extremely low toxicity. This article discusses the functions of vitamin E and the results of various studies that suggest its role in disease reduction, particularly cardiovascular diseases. Finally, some general guidelines for supplementation with vitamin E are presented.
VITAMIN E BASICS
The recognition of vitamin E's requirement in our diet goes back 75 years, when Evan and Bishop identified this substance as required for reproduction in the rat3. The name tocopherol was applied with tokos (for childbirth) and pherein (to bring forth) combined with ol (to denote its phenolic chemical nature). What is referred to as vitamin E is in reality a mixture of at least 8 related substances that can be divided into two groups, the tocopherols (alpha, beta, gamma, and delta forms) and the tocotrienols (alpha, beta, gamma, and delta forms)6. The two groups have different sources. The tocopherols are most plentiful in oil seeds, leaves, and other green parts of plants, while the tocotrienols are found mainly in the bran and germ portions of seeds and cereals. In humans, alpha-tocopherol appears to be the most important due to its high biological activity, or usability within the human body.
The major activity of vitamin E is the ability to function as an antioxidant, particularly for the preservation of polyunsaturated fats14; it is this group of fatty acids that is most susceptible to oxidative damage. In addition, there is an increasing recognition among cardiovascular disease investigators that lipid (fat) oxidation, especially the lipid contained in LDL (low density lipoprotein), accelerates the process of atherosclerosis13. Since vitamin E dissolves in fat, and is therefore said to be fat soluble, it is uniquely suited to functioning as an antioxidant in this environment. In addition, there is some evidence that other antioxidants may work with vitamin E to potentiate, or increase the effectiveness of, its antioxidant activity15.
VITAMIN E AND CARDIOVASCULAR DISEASE
Several lines of evidence have accumulated over the last two decades that suggest cholesterol levels are crucial for the progression of atherosclerosis9. Atherosclerosis is a disease process whereby cholesterol is deposited into the walls of blood vessels resulting in a gradual narrowing of the vessel along with reduced flexibility ("hardening of the arteries"). The reduction in the vessel's diameter not only reduces blood flow, but also makes a blood clot formation more common, and more likely to completely obstruct blood flow to downstream tissues. In the heart, where alternate blood flow is limited, this occurrence can precipitate a myocardial infarction ("heart attack").
LDL cholesterol (known as "bad" cholesterol), rather than total cholesterol appears to be the major source of cholesterol for starting this process. Experiments in animals have demonstrated that providing additional LDL to the blood accelerates this process13. Those same studies have shown that prior oxidation of LDL (which damages the LDL) increases the rate that cholesterol gets deposited in vessel walls. Studies in humans have also revealed that individuals can make antibodies against their own oxidized LDL and that levels of these antibodies correlate with risk for myocardial infarction10.
LDL is a tiny particle consisting of cholesterol, proteins, fatty acids, triglycerides, and an assortment of several types of antioxidants with alpha-tocopherol being dominant. Therefore, vitamin E is uniquely suited for the job of preventing LDL from becoming oxidized. To evaluate this possibility, various lines of investigations have been initiated to study this possibility15.
A number of studies have reported an inverse correlation between plasma concentrations of vitamin E and coronary mortality (death due to coronary artery disease), although this has not been consistently found. What these studies reveal is that the lowest risk for cardiovascular disease is found in those people with the highest levels of vitamin E in their blood The best studies to date have been prospective ones that have followed individuals who begin the study without cardiac disease and compared disease incidence with vitamin E intake. The Health Professionals Follow-up Study has followed nearly 40,000 men age 40 - 75 who started without cardiac disease11. During the study period, the group with the highest intake of vitamin E had a 40% reduction in cardiovascular disease incidence compared to the lowest group. This risk reduction held up even after controlling for a wide array of other known risk factors. The study was also able to separate contributions from dietary sources and supplements. Only vitamin E supplements (>100 IU/day) had a significant effect.
The Nurses' Health Study followed over 87,000 women, age 34 - 59 for eight years and correlated vitamin E intake with cardiovascular disease incidence12. A similar reduction in cardiac disease was noted at 34%. In addition, the investigators were able to show that only supplementation of greater than 100 IU/day of vitamin E was associated with the reduced risk. Another key finding was that at least 2 years of supplementation was necessary before risk reduction was found. This is particularly relevant because the proposed way that vitamin E works is by preventing LDL oxidation. Since the oxidized LDL deposit process is slow and gradual, occurring over many years, a reduction in oxidized LDL would be expected to only show up after some period of time of vitamin E use.
Finally, there have been studies assessing the progression of disease (which is different from disease induction, or cause). One such study was addressing atherosclerosis reversal by cholesterol lowering drugs with antioxidants5. In this case, supplementers who took >100 IU/day of vitamin E had less progression of their vessel narrowing compared to non-supplementers. In the group taking cholesterol lowering therapy and vitamin E, there was even partial regression (an improvement in the degree of narrowing) of the lesions. Other smaller trials have specifically examined vitamin E therapy in the case of angioplasty (surgery to repair obstructed blood vessels) to reduce restenosis (stenosis means obstruction to flow; restenosis is the process whereby the vessel becomes obstructed again in a rapid fashion after repair) rates2. While the trends are in favor of vitamin E, these trials have been too small to detect statistically significant differences.
CO-ANTIOXIDANTS WORKING WITH VITAMIN E
The study of LDL oxidation has led investigators to examine the mechanism of how vitamin E protects polyunsaturated fats. Appreciation of other antioxidants has developed the notion that while vitamin E protects lipid, there must be other antioxidants present to recycle vitamin E. The other major antioxidants with substantial activity are coenzyme Q10 and vitamin C15. The possibility of additional factors (these so called co-antioxidants) may provide an explanation for failing to detect a significant vitamin E effect in earlier studies where the additional antioxidants were not taken into account. This scenario has been evaluated in a study similar to the above designs, but utilizing an elderly population (ages 67 - 105) over a period of nine years7. In this group all the vitamin E users experienced a reduction in cardiac mortality (deaths due to cardiac disease) of 41%, but vitamin E use alone produced only a 31% reduction, whereas a combined vitamin E and C use produced a 48% reduction. This is strong evidence that antioxidants can work together to reduce risk of disease due to oxidative processes.
OTHER USES OF VITAMIN E
Certainly, cardiovascular diseases are by no means the sole province of vitamin E. The role of vitamin E in protecting the skin from UV (by the sun) damage is well appreciated. There are well established uses in specific pediatric diseases and at least one genetic disorder14. Improvement in immune system function is also plausible. There is some interest in possible cancer reduction (possibly related to immune system augmentation). One study has found a 23% reduction in cancer deaths, although the results were too weak to be considered conclusive evidence7.
A number of studies have addressed the safety of oral vitamin E supplementation1,8. In some cases, doses were very high (2000 IU/day). In general, there have been little to no adverse effects reported. Most of the few side effects that appear in the literature are largely either anecdotal reports where vitamin E was presumed to be the cause or they are incidental findings in toxicity studies that have not been replicated by other studies. Also of comfort are animal studies where high doses have been used to look for mutagenic (the ability to damage DNA), carcinogenic (the ability to cause cancer), or teratogenic (the ability to cause birth defects when ingested by pregnant women) effects. None of these effects were found.
LIMITATIONS AND LACK OF PUBLIC POLICY RECOMMENDATIONS
In spite of the above data, there has been no official declaration on the use of supplemental vitamin E. There are several reasons for this situation. In the first place, there are no prospective, randomized, double blind studies that have unequivocally demonstrated the ability of vitamin E for reducing cardiovascular disease. This type of study is regarded as the "gold standard", particularly for public policy. The only study that has come close is the infamous Finnish beta-carotene study which was looking at lung cancer4. Lost in the press reports were the facts that vitamin E was also included and that cardiovascular diseases were also evaluated. No effect of vitamin E was noted; however, this study actually validates earlier studies since only 50 IU/day of vitamin E was supplied and based on the previous studies, at least 100 IU/day are required for an effect.
From a safety standpoint, the doses needed to produce an apparent effect are well within tolerance limits, although a purist might wish to see more long term data. Lack of gold standard studies would appear to be one major reason for reluctance. Another aspect that may be troublesome for public policy officials is the need for supplementation, rather than mere dietary recommendations. The doses that appear beneficial are beyond the range that can be obtained from diet alone. This implies that people will need to buy supplements and this makes public policy officials more reluctant to offer this type of advice.
In order to achieve vitamin E levels commensurate with those that appear to afford some beneficial effects, supplementation is necessary; dietary sources of vitamin E are not sufficient to reach these amounts. At least 100 IU/day of vitamin should be taken; levels up to 400 IU/day are well within safety limits and are in the range of what many cardiologists are cautiously recommending now. In terms of what type of vitamin E to take, alpha-tocopherol is the most important form for LDL oxidation. On the other hand, excessive intake of one type may adversely affect other tocopherol species, so a mixed tocopherol is safer. There has been little or no examination of the tocotrienols, but their lower levels suggest that while they may possess some biological activity, the tocopherols are the important players. Since the preparations are standardized to IUs, there is less concern for the specific distribution provided that alpha-tocopherol is the major species. Natural and synthetic tocopherols have the same antioxidation properties, but the biological properties of the different forms vary, so natural is likely better.
Netrition recommends taking 400 IU of natural vitamin E daily for the best antioxidant benefits along with a balanced diet and a complete multi-vitamin and mineral supplement.
1. Bendich A, Machlin LJ: Safety of oral intake of vitamin E. Am J Clin Nutr 48:612-619, 1988
2. DeMaio SJ, King SB, Lembo NJ: Vitamin E supplementation, plasma lipids and incidence of restenosis after percutaneous transluminal coronary angioplasty (PTCA). J Am Coll Nutr 11:68-73, 1992
3. Evans HM, Bishop KS: On the existence of a hitherto unrecognized dietary factor essential for reproduction. Science 56:650-651, 1922
4. Heinonen OP, Albanes D, The Alpha-Tocopherol BC: The effect of vitamin E and beta carotene on the incidence of lung cancer and other cancers in male smokers. N Engl J Med 330:1029-1035, 1994
5. Hodis HN, Mack WJ, LaBree L, et al: Serial coronary angiographic evidence that antioxidant vitamin intake reduces progression of coronary artery atherosclerosis. JAMA 273:1849-1854, 1995
6. Kamaleldin A, Appelqvist LA: The chemistry and antioxidant properties of tocopherols and tocotrienols. Lipids 31:671-701, 1996
7. Losonczy KG, Harris TB, Havlik RJ: Vitamin E and vitamin C supplement use and risk of all-cause and coronary heart disease mortality in older persons: the Established Populations for Epidemiologic Studies of the Elderly. Am J Clin Nutr 64:190-196, 1996
8. Meydani SN, Meydani M, Rall LC, et al: Assessment of the safety of high-dose, short-term supplementation with vitamin E in healthy older adults. Am J Clin Nutr 60:704-709, 1994
9. Mitchinson MJ: The new face of atherosclerosis. Br J Clin Prac 48:149-151, 1994
10. Puurunen M, Manttari M, Manninen V, et al: Antibody against oxidized low-density lipoprotein predicting myocardial infarction. Arch Int Med 154:2605-2609, 1994
11. Rimm EB, Stampfer MJ, Ascherio A, et al: Vitamin E consumption and the risk of coronary heart disease in men. N Engl J Med 328:1450-1456, 1993
12. Stampfer MJ, Hennekens CH, Manson JE, et al: Vitamin E consumption and the risk of coronary disease in women. N Engl J Med 328:1444-1449, 1993
13. Steinberg D, Parthasarathy S, Carew TE, et al: Beyond cholesterol. Modifications of low-density lipoprotein that increase its atherogenicity. N Engl J Med 320:915-924, 1989
14. Thakur ML, Srivastava US: Vitamin-E metabolism and its application. Nutr Res 16:1767-1809, 1996
15. Thomas SR, Neuzil J, Mohr D, et al: Coantioxidants make alpha-tocopherol an efficient antioxidant for low-density lipoprotein. Am J Clin Nutr 62:1357S-1364S, 1995
Dr. Michael G. Kurilla, M.D. has extensive education, work experience, and sound reasoning which shows in his articles. He holds an M.D. and Ph.D. in molecular virology from Duke University. He received Pathology training at the Brigham & Women's Hospital and performed a postdoctoral fellowship at Harvard University with the head of infectious diseases at the Brigham & Women's Hospital. He also worked on the faculty at the University of Virginia in the departments of Pathology and Microbiology - dividing his time between clinical duties at the Clinical Microbiology for the University of Virginia hospital and basic research on viral immunology.
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