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RESEARCH

Our Story

We are a focused, disciplined and dedicated company with the best business associates and the best product in the industry. We will never lose focus on the basics of our business, and the key to our success -- delivering clean, safe, and effective total body nourishment products to our doctors and their patients. Our educational seminars are designed to educate doctors and the general public regarding Nature's recipe for the highest quality nutrition. We support organic farming and are dedicated to making living forms of Synbiotic-foodgrownTM nutrition of the highest degree of quality and integrity available to our customers. To this end, we have proudly associated ourselves with organic farms and manufacturing facilities that produce the proprietary ingredients for our products.

THE WISDOM OF COMMENSAL-PROBIOTIC CELLS

When the research data came in, leading scientists were amazed. How could one type of natural food supplement be so superior to any others they've ever tested before? Here are the answers... these extraordinary nutrients were created by nature's timeless wisdom and by friendly, commensal-probiotic cells in a way that harnessed the healing power of life-sustaining whole foods. They found what the world cultures have known for thousands of years. Food fermentation enriched the nutritive content by formatting thousands of nutrients with co-proteins and ligands (large complexes of nutrients). Nobel prizewinners found that ligands actually provide the "key" that unlocks the cells "lock", allowing cells to get nourished about 30 times faster then eating whole foods or taking ordinary supplements

We define these ligands as Synbiotic-foodgrownTM nutrients. They unique, miraculous healing compounds loaded with superior nourishment and harmonic polarities that are in tune with the organizing brilliance of life itself. Created in a proprietary natural fermentation process, they open the lock and thereby take the place of the natural key that is missing in synthetic USP vitamins. Nature choreographs these wonderfully elegant and extremely complex catalytic nutrients, making man-made USP laboratory-made vitamins look clunky.

TrinisolTM spent years studying ways to mimic the molecular dances of these commensal bacteria and to toughen their molecular architecture so, like a fine wine, they could remain bioactive and unspoiled for many years. These nutrients provide a foundation of wellness created by Mother Nature. Since no nutrient in nature is ever isolated or separated from other nutrients, it makes no sense to take synthetic nutrition in USP milligram doses.

The unique difference in our fermentation process is that our Synbiotic-foodgrownTM food concentrates contain tiny nutrient complexes: the molecular weight is about 250 daltons (a dalton is equal to one twelfth the mass of carbon 12, the most abundant isotope of carbon). Since whole foods are 60,000 daltons, it becomes obvious why the versatility and reactivity of this form of human nutritive is superior to eating raw foods or taking other forms of nutritional support. The use of co-proteins and ligands as carrier agents has been researched extensively by the pharmaceutical industry and by Nobel prizewinners as a way to deliver drugs more efficiently to cell receptor sites (Science 291:5501: 48-49, 2001; Trends in Pharmacologcial Sciences, 20:9, 370-75; 1999; Cellular Signaling. 14:4; 297-309, 2002).

The healing wisdom of nature is primarily found in the genes of commensal cells. Genetically speaking, the human body has 90% more commensal cells than human cells. Commensal cells collectively contain about 100 times more genes that human cells. This rich genetic endowment by nature gives them the remarkable ability to "heighten one's disease fighting capacity" (Scientific American, Aug 1992). Commensal cells produce co-enzymes, proteins, essential fatty acids, vitamins, and compounds that heal and repair the body (Science, 2006; 312:1355-9). New laboratory evidence reveals how commensal cells produce acids, bacteriocins and hydrogen peroxide to kill harmful yeast and bacteria in the gut and interfere with their ability to produce harmful toxins that cause pain and inflammation in our bodies (Gut, 2003; 52:827-33).

As researchers are discovering, the genetics of these cells can transform us into a "super-organism" with an ability to do things far in excess of our innate healing abilities. They powerful cells don't just complete us; they offer us the ability to improve the quality our lives dramatically. Dr. Shanahan calls them "a virtual organ with a metabolic activity in excess of the liver" (Best Pract Res Clin Gastroenterol, 2002;16: 915-31).

Our commensal cell ferments of Spirulina and Green Barley utilize genes to manufacture the most nutrient-dense food supplements on the planet, making them ideal for fighting stress and fatigue, increasing energy and endurance, enhancing memory and concentration, and boosting the energy levels of all systems of the body.**

Why Supplement with Synbiotic-FoodgrownTM Nutrients and Probiotic-type Commensal Cells?

Antibiotics, synthetic vitamins, and processed "calorie-condensed" foods are the main culprits that kill human commensal cells. Scientists know that the relationship between commensal and human cells is mutually beneficial (Anaerobe, 2005;11:247-51) and critical to the proper functioning of the immune system (J Soc Biol 2006, 200:113-20). Researchers found that 48% of us lack L. plantarum, 74% lack L. rhamnosus and 86% have no L. paracasei (J Appl Microbiol, 1998; 85: 88-94). Our research shows that 75% of all chronically ill patients are depleted in Bifidobacterium strains, Lactobacillus strains, and the pre- and synbiotic nutrients that allow them to gain a strong foothold in the gut.

Consumers spend billions of dollars each year on probiotic supplements, yet none of these address the health and ability of the commensal cells to stay in the body and influence the body on a grand scale. Further compounding the problem is the fact that these supplements do not know how to activate commensals with mineral-ligands that allow them to find a happy home in our gut. One survey found that one-third of these supplements "contained no living bacteria whatsoever" (Amer Soc Microbiol 2001). Another reported "half the products have got the wrong bacteria in them, the wrong amount, or are completely sterile" (FSA Project ref G01022, 2006).

An imbalance of gut commensal organisms or dysbiosis has been linked to learning difficulties, poor coordination, and autism (J Clin Immunol, 2004; 24:664-73). Probiotics boost immune function (J Med Food, 20069:321-7); can overcome "superbugs" or treatment-resistant infections (Ann Intern Med, 2006; 145: 758-64); and help diarrhea (Lancet Infect Dis 2006; 6:374-82) or constipation (Best Pract Res Clin Gastroenterol, 2006; 20: 575-87). And, a deficiency of commensal cells has been linked to ulcerative colitis, irritable bowel syndrome, Crohn's disease, and stomach disorders (J Clin Gastroenterol, 2006; 40:264-9).

Since commensals carry a huge toolbox for making nutrients, TrinisolTM uses select strains of these cells with appropriate mineral-ligand activators to culture foods into synbiotic-foodgrownTM nutrients. Research at Yale University found that the ability of commensals to make these nutrients depended riboswitches (switches that regulate the ability of commensals to make nutrients). This research explained why most probiotics are transient and do not increase the body's commensal cell population and the body's nutritional status. Borrowing further from nature's design, we discovered a unique way to use mineral-ligands to turn these toggle-like switches "on" for a whopping 300 times more bioactivity. As scientists discovered, commensals could turn the switch off and literally starve unwanted microbes to death (Nature 419:952-56, 2002; RNA 9:6; 644-47, 2003; Nature Biotechnology in press, 2007).

Making synbiotic nutrients from whole food concentrates was not easy. It required a painstaking four-step design process that allowed ligands and co-proteins to bond to the nutrients at extremely low molecular weights. In fact, it took almost a decade of research to find ways to inhibit mold overgrowth (common in cultured and fermented food concentrates) and to stabilize the nutrients so they would have a much longer shelf life that fresh foods.

Looking at these mineral-ligand complexes under a microscope revealed that nature had choreographed some wonderfully elegant and extremely complex catalytic nutrients. Scientists were telling us that it could take decades to define and name them all. The good news is that these known and unknown nutrients could be put to work to benefit those with a weak digestive system, supplying them with nourishment thousands of times faster then eating whole foods or taking other forms of nutrition. This rapid uptake of nourishment seemed to make the body super-resilient to stress.** Plus, these 250 dalton catalysts boosted chemical reaction rates a billion fold. And, unlike USP vitamins, these mineral-ligand catalysts could breakdown a variety of toxic environmental compounds.

Let's face it-with longer work hours, rush hour traffic, and escalating pollution, and stress being our number one health enemy, finding the time to take handfuls of supplements or eat right is difficult. Yet, when nutrients are chaperoned to our cells in a synbiotic-foodgrownTM format, our body is nourished instantly.**

The TrinisolTM Philosophy

We take nutrition very seriously and have deep respect for the wisdom in nature. Our products are made using nature's recipe for prolonging the shelf life and reformatting nutrition so it's easy to assimilate and utilize at the cell level. Our products are of the highest quality and are guaranteed to be free of solvents and common toxins found in the majority of other supplements.

Using advanced principles of quantum physics and Quantum MedicineTM we harmonize the nutrients so that they maintain the quantic harmonic states of innate intelligence. This results in long-lasting winning formulas that nourish innate intelligence and support the bi-polar polarities of the human energy system. It is our opinion that this homeopathic-like effect makes a major difference in how the body re-balances itself energetically following a stressful event. People notice immediate changes in their energy levels, moods, emotions, concentration, physical appearance, endurance, and strength.

It took almost three decades of testing sick people energetically to determine the exact ratios and doses of ingredients necessary to nourish the body's self-healing mechanisms.**

Nobel Laureates Dr. Casmir Funk and Dr. Albert Szent-Gyorgyi were awarded he Nobel Prize for identifying vitamins in foods. They always advised the general public to get their nutrients from whole foods and not isolated USP vitamins. TrinisolTM embraced these scientific concepts and refused to accept the central dogma around which the entire nutritional industry was being built. We understand the importance of getting complete nutrition from fermented food sources and have blazed trails in understanding how to maintain these nutrients in fresh vibrant states for long periods of time (without any decay, loss of nutrients or mold).

Safe, effective and loaded with nutrition, we take pride in our products and the superior nutrition they deliver. Based on science....supported by clinical evidence, you can now experience the amazing effects of optimal nutrient utilization formulas and benefit from optimal nourishment at the cellular level.**


Facts you need to know:

Uncompensated stress depletes nutrients about 30 times faster than the body can extract (digest) nutrition from foods;
 
Stress inhibits digestion dramatically causing chronic nutritional deficiencies and maldigestion;
 
Common nutritional supplements rarely nourish the cells or compensate for the ill effects of stress;
 
Over 97% of supplements are toxic, ineffective or offer no protective effects from stress or environmental pollutants (university research supported claim).
 

Discover the Most Advanced Nutrient Delivery System in the World: SYNBIOTIC-FoodGrownTM Nourishment

Today, many individuals are confused about what the body needs for nourishment. Millions of Americans consume synthetic fractionated USP (United States Pharmacopoeia) chemical vitamins, inorganic "hard rock" minerals, isolated starches or sugars, amino acids and toxic mold in the name of nutrition. Hard rock minerals dug up in mines and synthetic "man-made" vitamins are in many fortified breakfast cereals and daily multivitamins. Research shows these supplements can be harmful to the body and actually increase stress and pollutant-induced damage to the body.

Every now and then a truly rare nutritional breakthrough appears...a breakthrough that changes nutrient delivery as we know it and gives us a way to correct nutritional deficiencies by bypassing the GI Tract. Living Synbiotic-FoodgrownTM nutrient organized in ligand formats by probiotic-commensal cells are immeasurably beneficial in keeping us healthy.** At very small doses, they have superior potency and bioactivity compared with megavitamins that work adversely to accelerate stress reactions.

Synbiotic-FoodgrownTM nutrients--made in a similar fashion to yogurt, miso, kefir, or wine--are easy-to-assimilate and fast-acting against the ravages of stress. Rather than rely on common USP isolated chemical vitamins, we put our trust in nature's timeless wisdom and probiotic cells to nourish cells dramatically faster than whole foods or ordinary supplements.** Plus, to insure these nutrients have the correct polarity we use a proprietary homeopathic-like process to maintains quantic harmonic states of innate healing in the body.**

Don't be...FOOLED Cell Utilization of Nutrients = Optimal Health

Synbiotic-foodgrownTM living nutrients help to mend our stress-damaged bodies. Our unique bacterial culturing-fermentation process generates huge amounts of natural ligands and detoxifying compounds like GSH, GPx and SOD. In addition, there are huge amounts of mineral-ligand and mineral-protein complexes formats like selenoproteins and zinc-taurate complexes to detoxify the body and insure cellular health.**

Proteins are the wheels, cogs, chutes and conveyor belts that transport the synbiotic nutrients to cells. Complex vitamins, known as co-enzymes are small, "nano" sized molecules that cooperate with protein enzymes to ignite powerful biochemistry in the body.

Epic metabolic pathways are activated in the construction of these nutrients which can occur in the fermentation tank or in the body as commensals construct nutrients from synbiotics and strictly control nutrient levels by shutting synthesis down when nutrients are ample and the cells infrastructure is adequate.

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Studies on Pre- and Synbiotic Nutrition

1. Yanick, P. "Biomolecular Nutrition and the GI Tract." Townsend Letter for Doctors (Dec. 1993):1248-1250.

2. Yanick, P 2006 Gastrointestinal Rejuvenation via Synbiotic Nourishment to Upregulate Prebiotic Butyrate, IGFs and HGH Townsend Letter for Doctors & Patients.

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65. Frame LT et al: 1998. Caloric Restriction as a Mechanism Mediating Resistance to Environmental Disease. Environ Health Perspectives 106:313-324

66. Truswell AS. 2002 Cereal grains and coronary heart disease. European Journal of Clinical Nutrition. 56(1):1-14.

67. Yang JL, et al: 2003. Barley beta-glucan lowers serum cholesterol based on the up-regulation of cholesterol 7alpha-hydroxylase activity and mRNA abundance in cholesterol-fed rats. Journal of Nutritional Science and Vitaminology (Tokyo) 49(6):381-387.

68. McIntosh GH et al: 1991. Barley and wheat foods: influence on plasma cholesterol concentrations in hypercholesterolemic men. American Journal of Clinical Nutrition. 53(5):1205-1209.

69. Behall KM et al: 2004 Lipids significantly reduced by diets containing barley in moderately hypercholesterolemic men. Journal of the American College of Nutrition. 23(1):55-62.

70. Bourdon L et al: 1999. Postprandial lipid, glucose, insulin, and cholecystokinin responses in men fed barley pasta enriched with beta-glucan. American Journal of Clinical Nutrition. 69(1):55-63.

71. Burger WC et al: 1984 Suppression of cholesterol biosynthesis by constituents of barley kernel. Atherosclerosis. 51(1):75-87.

72. Delaney B et al: 2003. Beta-glucan fractions from barley and oats are similarly antiatherogenic in hypercholesterolemic Syrian golden hamsters. Journal of Nutrition. 133(2):468-475.

73. Keogh GF et al: 2003. Randomized controlled crossover study of the effect of a highly beta-glucan-enriched barley on cardiovascular disease risk factors in mildly hypercholesterolemic men. American Journal of Clinical Nutrition.78(4):711-718.

74. Li J, Kaneko T et al; 2003 Long-term effects of high dietary fiber intake on glucose tolerance and lipid metabolism in GK rats: comparison among barley, rice, and cornstarch. Metabolism. 52(9):1206-1210.

75. Li J, Kaneko T et al: 2003 Effects of barley intake on glucose tolerance, lipid metabolism, bowel function... Nutrition. 9(11-12):926-929.

76. Liljeberg HG et al. 1996 Products based on a high fiber barley genotype, but not on common barley or oats, lower postprandial glucose and insulin responses in healthy humans. Journal of Nutrition. 126(2):458-466.

77. Lupton JR et al: 1993 Barley bran flour accelerates gastrointestinal transit time. Journal of the American Dietetic Association. 93(8):881-885.

78. Lupton JR et al: 1994. Cholesterol-lowering effect of barley bran flour and oil. Journal of the American Dietetic Association. 94(1):65-70.

79. Qureshi AA et al: 1986. The structure of an inhibitor of cholesterol biosynthesis isolated from barley. Journal of Biological Chemistry.261(23):1544-1550.

80. McIntosh GH et al 1991. Barley and wheat foods: influence on plasma cholesterol concentrations in hypercholesterolemic men. American Journal of Clinical Nutrition. 53(5):1205-1209.

81. Bamba T et al 2002. A new prebiotic from germinated barley for nutraceutical treatment of ulcerative colitis. Journal of Gastroenterology and Hepatology. 17(8):818-824.

82. Fukuda M et al: 2002. Prebiotic treatment of experimental colitis with germinated barley foodstuff: a comparison with probiotic or antibiotic treatment. International Journal of Molecular Medicine. 9(1):65-70.

83. Hanai H et al: 2004 Germinated barley foodstuff prolongs remission in patients with ulcerative colitis. International Journal of Molecular Medicine. 13(5):643-647.

84. Kanauchi O et al 2003:. Treatment of ulcerative colitis patients by long-term administration of germinated barley foodstuff: multi-center open trial. International Journal of Molecular Medicine. 12(5):701-704.

85. Kanauchi O et al: 2003. Germinated barley foodstuff, a prebiotic product, ameliorates inflammation of colitis through modulation of the enteric environment. Journal of Gastroenterology. 38(2):134-141.

86. Rath, H C et al: 1996. Normal luminal bacteria, especially Bacteroides species, mediate chronic colitis, gastritis, and arthritis in HLA-B27/human beta 2 microglobulin transgenic rats. J. Clin. Invest. 98: 945-953.

87. Kanauchi O et al. 2002 Treatment of ulcerative colitis by feeding with germinated barley foodstuff: first report of a multicenter open control trial. Journal of Gastroenterology. 37(Suppl 14):67-72.

88. Kamm MA & Senapati A 1992 Drug management of ulcerative colitis. British Medical Journal, 305: 35-38.

89. Roediger WEW 1980 The colonic epithelium in ulcerative colitis: an energy deficiency disease. Lancet, 2: 712-715.

90. Roediger WEW et al 1982 Trophic effect of SCFAs on mucosal handling of ions by the defunctioned colon. Brit Jf Surgery, 69: 23-25.

91. Roediger WEW 1980 The role of anaerobic bacteria in the metabolic welfare of the colonic mucosa in man. Gut, 21: 793-798.

Cummings JH 1981 Short chain fatty acids in the human colon. Gut, 22: 763-779.

92. Clausen MR et al: 1995 Kinetic studies on colonocyte metabolism of short chain fatty acids and glucose in ulcerative colitis. Gut, 37: 684-689.

93. Mortensen FV et al: 1990 Short chain fatty acids dilate isolated human colonic resistance arteries. Gut, 31: 1391-1394.

94. Harig JM et al: 1989 Treatment of diversion colitis with short-chain-fatty acid irrigation. New England Journal of Medicine, 320: 23-28.

95. Vernia P et al: 1995 Short-chain fatty acid topical treatment in distal ulcerative colitis. Alimentary Pharmacology and Therapeutics, 9: 309-313.

96. Sanderson, IR et al: 1987 Improvement of abnormal lactulose/rhamnose permeability in active Crohn's disease of the small bowel by an elemental diet Gut 28: 1073-1076.

97. Mahdi GS et al: 1991 Role of chromium in barley in modulating the symptoms of diabetes. Annals of Nutrition and Metabolism. 35(2):65-70.

98. Naismith DJ et al; 1991 Therapeutic value of barley in the management of diabetes. Annals of Nutrition and Metabolism. 1991;35(2):61-64.

99. Peirce A. The American Pharmaceutical Association Practical Guide to Natural Medicines. New York: Stonesong Press; 1999.

100. Shukla K et al: 1991 Glycaemic response to maize, bajra and barley. Indian Journal of Physiology and Pharmacology. 35(4):249-254.

101. Wursch P et al. 1997 The role of viscous soluble fiber in the metabolic control of diabetes... Diabetes Care 20(11):1774-1780.

102. Yu YM et al 2002. Effects of young barley leaf extract and antioxidative vitamins on LDL oxidation and free radical scavenging activities in type 2 diabetes. Diabetes Metabolism 28(2):107-114.

103. Gum, J.R et al: 1987. Effects of sodium butyrate on human colonic adenocarcinoma cells. J. Biol. Chem. 262: 1092-1097.

104. Guo, YS et al: 1993 Insulin-like growth factor-binding protein modulates the growth response to insulin-like growth factor 1 by human gastric cancer cells Gastroenterology 104: 1595-1604.

105. Rouyer-Fessard, CS et al: 1990 Expression of two types of receptor for insulin-like growth factors in human colonic epithelium. Gastroenterology 98: 703-707.

106. Royall, D., B. M. Wolever, and K. N. Jeejeebhoy. Clinical significance of colonic fermentation. 1990; Am. J. Gastroenterol. 85: 1307-1312.

107. Sanderson, I R et al: 1987 Improvement of abnormal lactulose/rhamnose permeability in active Crohn's disease of the small bowel by an elemental diet.Gut 28: 1073-1076.

108. Shimasaki, S., and N. Ling. 1991 Identification and molecular characterization of insulin-like growth factor binding proteins (IGFBP-1, -2, -3, -4, -5 and -6). Prog. Growth Factor Res. 3: 243-266.

109. Souleimani, A., and C. Asselin. 1993 Regulation of C-fos expression by sodium butyrate in the human colon carcinoma cell line Caco-2. Biochem. Biophys. Res. Commun. 193: 330-336.

110. Straus, D. S. 1994. Nutritional regulation of hormones and growth factors that control mammalian growth FASEB J. 8: 6-12.

111. Tapson, V. F. et al: 1988. Structural and functional characterization of the human T lymphocyte receptor for insulin-like growth factor I in vitro. J. Clin. Invest. 82: 950-957.

112. Whitehead, R. H et al: 1986. Effects of short chain fatty acids on a new human colon carcinoma cell line (LIM1215). Gut 27: 1457-1463.

113. Chung, Y. S. et al: 1985. Effect of sodium butyrate on brush border membrane-associated hydrolases in human colorectal cancer cell lines. 1985; Cancer Res. 45: 2976-2982.

114. Clark, R. et al:.1993 Insulin-like growth factor stimulation of lymphocytes. J. Clin. Invest. 92: 540-548.

115. Yoshida, M. et al: 1990 Potent and specific inhibition of mammalian histone deacetylase both in vivo and in vitro by trichostatin A. 1990 J. Biol. Chem. 265: 17174-17179.

116. Montbriand MJ. 2004 Herbs or natural products that protect against cancer growth. Oncol Nurs Forum 31(6): E127-E146.

117. Saito S, Kondo K, Hamada T, et al. 2003; A case of steroid dependent ulcerative colitis (total colitis type) treated by combined use of germinated barley foodstuff. Nippon Shokakibyo Gakkai Zasshi 100(4):426-429.

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Studies on the need for whole food antioxidants

Aviram, M. (1996) Interaction of oxidized low density lipoprotein with macrophages in atherosclerosis, and the antiatherogenicity of antioxidants. Eur. J. Clin. Chem. Clin. Biochem., 34(8):599-608.

Batieha et al. 1993. Serum micronutrients and the subsequent risk of cervical cancer in a population-based nested case-control study. Cancer Epidemiology, Biomarkers and Prevention. 2:335-339.

Behl, C. (1999) Alzheimer's disease and oxidative stress: implications for novel therapeutic approaches. Prog. Neurobiol., 57(3):301-323.

Borlongan, C. V., Kanning, K., Poulos, S. G., Freeman, T. B., Cahill, D. W., and Sanberg, P. R. (1996) Free radical damage and oxidative stress in Huntington's disease. J. Fla. Med. Assoc., 83(5):335-341.

Bowry, V. W., Ingold, K. U., and Stocker, R. (1992) Vitamin E in human low-density lipoprotein: when and how this antioxidant becomes a pro-oxidant. Biochem. J., 288(Part 2):341-344.

Carpenter, K. L. H., Van Der Veen, C., Hird, R., Dennis, I. F., Ding, T., Mitchinson, M. J. (1997) The carotenoids beta-carotene, canthaxanthin and zeaxanthin inhibit macrophage-mediated LDL oxidation. FEBS Letters, 401: 262-266.

Clevidence, B. A. and Bieri, J. G. (1993) Association of carotenoids with human plasma lipoproteins. Methods Enzymol., 214:33-46.

Christen, W.G. (1999) Antioxidant vitamins and age-related eye disease. Proc. Assoc. Am. Physicians, 111:16-21.

Copp, R P et al 1999. Localization of alpha-tocopherol transfer protein in the brains of patients with ataxia with vitamin E deficiency and other oxidative stress related neurodegenerative disorders. Brain Res., 822(1-2):80-87.

Cotter, M.A et al 1995 Effects of natural free radical scavengers on peripheral nerve and neurovascular function. Diabetologia, 38(11):1285-1294.

Coyle, J. T. and Puttfarcken, P. (1993) Oxidative stress, glutamate, and neurodegenerative disorders. Science, 262:689-695.

Dawson, V. L. and Dawson, T. M. (1996) Nitric oxide neurotoxicity. J. Chem. Neuroanat., 10(3-4):179-190.

de Rijk, M. C et al 1997 Dietary antioxidants and Parkinson disease: the Rotterdam study. Arch. Neurol., 54(6)762-765.

Ebadi, M., Srinivasan, S. K., and Baxi, M. D. (1996) Oxidative stress and antioxidant therapy in Parkinson's disease. Prog. Neurobiol., 48(1):1-19.

Facchinetti, F., Dawson, V. L., Dawson, T. M.(1998) Free radicals as mediators of neuronal injury. Cell Mol. Neurobiol., 18(6):667-682

Fahn, S. (1991) An open trial of high-dosage antioxidants in early Parkinson's disease. Am J. Clin. Nutr., 53(1 Suppl):380S-382S.

Fahn, S. and Cohen, G. (1992) The oxidant stress hypothesis in Parkinson's disease: evidence supporting it. Ann. Neurol., 32(6):804-812.

Ferrante RJ et al 1997 Evidence of increased oxidative damage in sporadic & familial ALS. J. Neurochem., 69(5):2064-2074.

Frei, B. (1995) Cardiovascular disease and nutrient antioxidants: role of low-density lipoprotein oxidation. Crit. Rev. Food Sci. Nutr., 35(1-2):83-98.

Gerlach, M.et al 1994 Altered brain metabolism of iron as a cause of neurodegenerative diseases? J. Neurochem., 63(3):793-807.

Gerster, H. (1989) Antioxidant vitamins in cataract prevention. Z. Ernahrungswiss., 28:56-75.

Gerster, H. (1991) Antioxidant protection of the ageing macula. Age Ageing, 20:60-69.

Ghadge, GD et al 1997 Mutant SOD-1-linked familial ALS: molecular mechanisms of neuronal death and protection. J. Neurosci., 17(22):8756-8766.

Goulinet, S. and Chapman, M. J. (1997) Plasma LDL and HDL subspecies are heterogeneous in particle content of tocopherols and oxygenated and hydrocarbon carotenoids: relevance to oxidative resistance and atherogenesis. Arterioscler. Thromb. Vasc. Biol., 17:786-796.

Gradelet SP et al. 1996b. Effects of canthaxanthin, lycopene and lutein on liver xenobiotic-metabolizing enzymes in the rat. Xenobiotica. 26:49-63.

Gradelet SP et al 1997. Modulation of aflatoxin B1 carcinogenicity, genotoxicity and metabolism in rat liver by dietary carotenoids: evidence for a protective effect of CYP1A inducers. Cancer Lett. 114(1-2):221-223.

Gradelet S., A.M. Le Bon, R. Berges, M. Suschetet, and P. Astorg. 1998. Dietary carotenoids inhibit aflatoxin B1-induced liver preneoplastic foci and DNA damage in the rat: role of the modulation of aflatoxin B1 metabolism. Carcinogenesis 19(3):403-411.

Grant, W. B. (1997) Dietary links to Alzheimer's disease. Alzheimer's Disease Rev., 2:42-55.

Hall, E. D., Andrus, P. K., Oostveen, J. A., Fleck, T. J., and Gurney M. E. (1998) Relationship of oxygen radical-induced lipid peroxidative damage to disease onset and progression in a transgenic model of familial ALS. J. Neurosci. Res., 53(1):66-77.

Halliwell, B. (1992) Reactive oxygen species and the central nervous system. J. Neurochem., 59(5):1609-1623.

Hellenbrand, W et al 1996 Diet and Parkinson's disease. II: A possible role for the past intake of specific nutrients. Results from a self-administered food-frequency questionnaire in a case-control study. Neurology, 47(3):644-650.

Jacques, P.F 1999 The potential preventive effects of vitamins: cataract & age-related macular degeneration. Int. J. Vitam. Nutr. Res., 69:198-205.

Jama, J. W., Launer, L. J., Witteman, J. C., Den Breeijen, J. H., Breteler, M. M., Grobbee, D. E., and Hofman, A. (1996) Dietary antioxidants and cognitive function in a population-based sample of older persons: the Rotterdam study. Am. J., Epidemiol., 144(3):275-280.

Jenner, P. (1996) Oxidative stress in Parkinson's disease and other neurodegenerative disorders. Pathol. Biol. (Paris), 44(1):57-64.

Jyonouchi, H et al 1996 Effects of various carotenoids on cloned, effector-stage T-helper cell activity. Nutr Cancer 1996;26(3):313-24

Lyle, B.J. et al 1999 Antioxidant intake and risk of incident age-related nuclear cataracts... Am. J. Epidemiol., 149:801-809.

Markesbery, W. R. and Carney, J. M. (1999) Oxidative stress in Alzheimer's disease. Brain Pathol., 9:133-146.

Mitchell, J. J., Paiva, M., and Heaton, M. B. (1999) Vitamin E and beta-carotene protect against ethanol combined with ischemia in an embryonic rat hippocampal culture model of fetal alcohol syndrome. Neurosci. Lett., 263(2-3):189-192.

Olanow, C. W. and Arendash, G. W. (1994) Metals and free radicals in neurodegeneration. Curr. Opin. Neurol., 7(6):548-558.

Oshima, S. et al 1997 Accumulation, clearance of capsanthin in blood plasma after the ingestion of paprika juice in men. J. Nutr., 127:1475-1479.

Pappert, EJ et al 1996 Alpha-tocopherol in the ventricular cerebrospinal fluid of Parkinson's disease patients. Neurology, 47(4):1037-1042.

Rao et al. 1999. Serum, tissue lycopene and biomarkers of oxidation in prostate cancer patients: a case-control study. Nutr. Cancer. 33(2):159-164.

Retz, W., Gsell, W., M�nch, G. R�sler, M., and Riederer, P. (1998) Free radicals in Alzheimer's disease. J. Neural. Transm. Suppl., 54:221-236.

Rumi et al. 1999. Decrease in serum levels of vitamin A, zeaxanthin in patients with colorectal polyp. Eur J Gastroenterol Hepatol 11(3):305-308.

Schmidt R et al 1998 Plasma antioxidants, cognitive performance... Results of the Austrian Stroke Prevention Study. J. Am. Geriat. Soc., 46:1407-1410.

Seddon, JM et al 1994 Dietary carotenoids, vitamins A, C, E, and advanced age-related macular degeneration. J. Am. Med. Assoc., 272:1413-1420.

Snodderly, D.M. (1995) Evidence for protection against age-related macular degeneration by carotenoids... Am. J. Clin. Nutr., 62(suppl):1448S-1461S.

Snow, KK et al 1999 Do age-related macular degeneration-cardiovascular disease share common antecedents? Ophthalmic Epidemiol. 6:125-143.

Simonian, N A et al (1996) Oxidative stress in neurodegenerative diseases. Annu. Rev. Pharmacol. Toxicol., 36:83-116.

Tagami, M et al 1998 Vitamin E prevents apoptosis in cortical neurons during hypoxia and oxygen reperfusion. Lab. Invest., 78(11): 1415-1429.

Vatassery GT et al 1998 Alpha tocopherol in CSF of subjects taking high-dose vitamin E. Neurology, 50(6):1900-1902.

Yl�-Herttuala, S. (1991) Macrophages and oxidized low density lipoproteins in the pathogenesis of atherosclerosis. Ann. Med., 23(5):561-567.

Yu, Z. F., Bruce-Keller, A. J., Goodman, Y., and Mattson, M. P. (1998) Uric acid protects neurons against excitotoxic and metabolic insults in cell culture, and against focal ischemic brain injury in vivo. J. Neurosci. Res., 53(5):613-625.

Yanick P 2006. The truth about synthetic vitamins. Unpublished review article.

Zhang LX et al 1991. Carotenoids enhance gap junctional communication and inhibit lipid peroxidation in C3H/10T1/2 cells: relationship to their cancer chemopreventive action. Carcinogenesis (Lond.). 12:2109-2114

Zhang L.X., R.V. Coonery, and J.S. Bartram. 1992. Carotenoids up-regulate Connexin-43 gene expression independent of their provitamin A or antioxidant properties. Cancer Res. 52: 5707-5712.

Research on Synthetic versus Food-Derived Nutrition

1. Yanick, P You Can Feel Better, 1981 Sunshine Press citation of Morgan's 1940 University of California, Berkeley Research report.

2. Sure, B. I., Journal of Biological Chemistry, 74:71-84, 1927.

3. Lee, R. and Stolzoff, J. S.The Special Nutritional Qualities of Natural Foods, Lee Foundation for Nutritional Research, Wisconsin, July, 1942.

4. Alam, S.Q., Alam, B.S., Alvarez, C.J. 1978. Cariogenic effects of excess vitamin E in rats. J. Dent. Res. 57, 244.

5. Aldabergenova, K.U.1979. Hypervitaminosis A state of chromosome apparatus of rat bone marrow cells. Farmakol,Toksikol. 42, 278.

6. Ammann, P.et al: 1986. Vitamin A excess. Helv. Paediatr. Acta 23, 137.

7. Awakura, T., and Morita, T. 1995 Vitamin D toxicosis in cats: natural outbreak and experimental study. J. Vet. Med. Sci. Oct.; 57(5); 831-7.

8. The Alpha-Tocopheral, Beta Carotene Cancer Prevention Study Group. The effect of vitamin E and beta-carotene on the incidence of lung cancer and other cancers in male smokers. NEJM. 1994;330:1029-1035.

9. FDC Reports. Nonprescription pharmaceuticals and nutritionals. The Tan Sheet. 1996;4:4-6.

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11. Hathcock JN et al. Evaluation of vitamin A toxicity. Am J Clin Nutr 1990;52:183-202.

12. Parfitt K (ed) Martindale: the complete drug reference. Pharmaceutical Press. 1999. London.

13. Bendich A et al. Safety of vitamin A. Am J Clin Nutr 1989;49:358-71.

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15. Blank, S. et al 1995 An outbreak of hypervitaminosis D associated with the overfortification of milk. Am. J. Public Health. 85; 656-659.

16. Breslau, R.C. (1957). Hypervitaminosis A: Acute vitamin A toxicity. Arch. Pediat. 74, 178.

17. Briggs,M.H., and Johnson, J. (1973). Dangers of excess vitamin C. Med. J. Aust. 2, 617.

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19. Davies, M, and Adams, P.H. (1978). The continuing risk of vitamin-D intoxication. Lancet. 2, 621.

20. Woodall, A Caution with b-carotene supplements Lancet 347:967, 1996

21. Blot WJ et al. The Linxian trials: mortality rates by vitamin-mineral intervention group. Am J Clin Nutr. 1995;62(6 suppl):14245-14265.

22. Block JB, Evans S.Clinical evidence supporting cancer risk reduction with antioxidants.... JANA. 2000; 3(3); 6-16.

23. Weinberg ED Iron in neoplastic disease. Nutr Cancer. 1983; 4:223-233.

24. Wang Z et al Mammary cancer promotion, MAPK activation with consumption of corn oil-based high fat diet. Nutr Cancer.1999; 34:140-6.

25. Hurston SD et al. Types of dietary fat and the incidence of cancer at five sites. Prev Med. 1990; 9; 242-53.

26. Narisawa T et al. Prevention of n- methylnitrosourea-induced colon carcinogenesis in F344 rats by lycopene and tomatoe juice rich in lycopene. Jpn J Cancer Res. 1998;89:1003-1008

27. Ellithorpe RR Piot Study: 2001. Whole Food Nutritional Supplement Increases Antioxidant Levels in the blood, JANA 4:244-8.

28. Houston MD, Strupp JS. Prevention and treatment of cancer: Is the cure in the produce aisle? JANA. 2000; 3(3); 27-30.

29. Finely, J. et al: Selenium content of foods purchased in North Dakota. Nutr. Res. 1996; 16; 723-28., 1991.

30. Doll, R et al: The causes of cancer. J Nat; Cancer Insti. 1981; 66:1191.

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33. See, D. JANA, 1996, Vol 2:1, 25-41.

34. Yanick, P. New Breakthroughs in Treating IBS. June 2001. Townsend Letter for Doctors & Patients.

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54. Yanick, P. Journal of Applied Nutrition 1988. 40:2, 61-70.

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