Platinum – Red Label Supplement Packs

Multi Without Iron

Balanced Profile Vitamins and minerals work synergistically and cooperatively when present in proper amounts. However, imbalances between micronutrients can disrupt this synergistic relationship, possibly leading to instances of competitive intestinal absorption or displacement at the metabolic/cellular level, which can produce relative excesses and insufficiencies. For this reason, Multi Without Iron formulas feature a balanced nutrient profile that includes calcium and magnesium, zinc and copper, vitamins C and E, bioactive folate, vitamin B12, B vitamin complex, beta-carotene, and trace elements.*

Bioavailability- The micronutrients are provided in bioavailable forms so that they can be better absorbed and utilized. Multi Without Iron formulas contain a full complement of Albion® patented mineral chelates and complexes. Albion is a recognized world leader in mineral amino acid chelate nutrition and manufactures highly bioavailable nutritional mineral forms that are validated by third party research and clinical studies. Not only do these formulas contain natural vitamin E, which has been proven to be up to 100% more bioavailable than synthetic dl-alpha-tocopherol, but it is also provides mixed tocopherols to more closely approximate how one might consume vitamin E in healthful foods.[9,10] Folate is provided as 5-methyltetrahydrofolate (5-MTHF)—the most bioactive form of folate.[11] Multi Without Iron formulas feature 5-MTHF as Quatrefolic®, which is proven to have greater stability, solubility, and bioavailability over calcium salt forms of 5-MTHF. Vitamin B12 is provided as MecobalActive™. This patented form of methylcobalamin has very high purity; no harmful solvents are used in its production.[12] Vitamins B2 and B6 are also provided in activated forms.*

Energy Production Multi Without Iron formulas provide generous levels of B vitamins, which serve as prime coenzymes in glycolysis and oxidative phosphorylation and as cofactors in amino acid and lipid metabolism. The balanced presence of B vitamins is essential to their cooperative functioning and excellent for those with stressful lifestyles.* Antioxidant Protection Vitamins E and C, selenium, zinc, beta carotene, and trace elements provide broad-spectrum antioxidant activity. Their combined presence supports their ability to regenerate each other and maintain consistent levels of antioxidant activity both intra- and extracellularly.* Detoxification Support Xenobiotics, including environmental pollutants and medications, must undergo biotransformation into molecules that can be easily excreted from the body. There are significant levels of bioavailable riboflavin, niacin, folate, and B12 present in these formulas to support phase I detoxification. Beta carotene, vitamin C, tocopherols, selenium, copper, zinc, and manganese are present to protect tissues from reactive intermediates formed between phase I and phase II detoxification.*

This high-quality, hypoallergenic, multivitamin/mineral blend includes activated vitamins; folate as Quatrefolic® (5-MTHF) for optimal utilization; and patented Albion® TRAACS® chelated mineral complexes in vegetarian capsules. The comprehensive nutrient profile in Multi Without Iron® supports foundational wellness; antioxidant activity with vitamins C and E, selenium, and beta-carotene; and phase I detoxification.*

MCHC plus Mag

Numerous published studies support the safety, tolerability, and bone health-related effectiveness of MCHC supplementation.[1,2] Studies suggest that the bioavailability of calcium from MCHC supplements may be as good as or better than the bioavailability of calcium from calcium gluconate supplements.[3,4]

PRx Products utilize standardized, safe, bovine-sourced MCHC from New Zealand, a country with stringent standards. Its production features a proprietary technique that preserves the bioactive contents of bone. This process creates a naturally balanced formula because whole bone extract provides all of the nutrients found in healthy bone.* Unlike other calcium supplements on the market, MCHC plus Mag consists of collagenous and non-collagenous proteins and peptides. These compounds include insulin-like growth factors I and II (IGF-I, IGF-II), transforming growth factor beta (TGF-beta), and osteocalcin, factors that stimulate alkaline phosphatase activity and support metabolism in human bone cells.[5] Removal of the protein fraction appears to reduce the positive effects of the formula, highlighting the importance of its presence.*[6] A study suggested that the occurrence of positive and statistically significant changes in forearm bone integrity were the result of daily supplementation with 3000 mg of microcrystalline hydroxyapatite.[7]

Earlier studies compared MCHC plus Mag to other forms of calcium with regard to the support of normal bone turnover and bone mineral integrity. In one 20-month, double-blind study, women were given 1400 mg of elemental calcium (equivalent to approximately 5000 mg MCHC) as either calcium carbonate or MCHC plus Mag. At the end of the study, the presence of bone integrity was statistically significant in the MCHC plus Mag group.*[8] Clinical trials suggested that MCHC plus Mag supplementation was well tolerated and yielded a positive outcome for dental status, bone integrity, and healthy bone metabolism.[9,10] A randomized, controlled study indicated that the addition of MCHC plus Mag to exogenously administered hormones provided statistically significant support (4.7%, P<0.1) to vertebral bone mass.[10] Another study of 60 subjects suggested that bone mass was maintained while on MCHC plus Mag.*[11] MCHC plus Mag is high-quality MCHC from New Zealand.

The World Organization for Animal Health (the OIE) has classified New Zealand as a “negligible BSE risk country,” the most favorable official classification a country can be given.[12] MCHC plus Mag is manufactured under proprietary processes that meet FDA, USDA, and EU regulatory requirements. Gentle processing is used to retain the delicate protein matrix and organic factors. X-ray-diffraction analysis confirms the microcrystalline structure. The MCHC is assayed for hydroxyproline content. The collagen content is greater than 22% with the majority being type l, the predominant collagen occurring in bone. Frequent heavy metal assays assure purity. MCHC plus Mag 1100™ delivers 1100 mg of MCHC plus Mag per capsule. MCHC plus Mag MD™ delivers 500 mg of MCHC plus Mag per capsule along with vitamin D, magnesium, and additional calcium. Vitamin D is provided as cholecalciferol, which stimulates intestinal calcium absorption and helps support calcium and phosphorus homeostasis in the body. Calcium is provided as MCHC and DimaCal® dicalcium malate, and magnesium is provided as Albion dimagnesium malate and TRAACS® magnesium bisglycinate chelate. The buffering malate forms of calcium and magnesium do not react with stomach acid and are less likely than carbonates to cause discomfort and acid rebound.*[13

N-ACETYL CYSTEINE

N-Acetyl-L-Cysteine (NAC) is a source of the conditionally essential amino acid L-cysteine and a precursor to the tripeptide glutathione. NAC and glutathione support antioxidant and detoxification activity in the body.*

NAC (N-acetyl-cysteine) NAC, a sulfur-containing derivative of the amino acid L-cysteine, supports antioxidant and detoxification mechanisms in the body. NAC supports antioxidant activity by neutralizing hydrogen peroxide, hypochlorous acid, and the highly reactive hydroxyl radical and also serves as a source of sulfhydryl groups. In addition, NAC enhances production of the tripeptide glutathione—a key component of both antioxidant and detoxification enzymes.*[1] NAC is recognized for its support of normal mucous production and may positively support respiratory function and eye health, especially when consumed over a prolonged period.[1-3] Research suggests that NAC may protect cell and tissue health by supporting normal metal status in the body.*[1,4,5]

Glutathione –  While the absorption of oral glutathione may be limited,[6] supplementation with NAC may significantly increase circulating levels of glutathione in the body.[7,8] Once NAC promotes production of glutathione, glutathione is incorporated into crucial antioxidant enzymes (e.g., glutathione peroxidase and glutathione reductase) and detoxification enzymes (glutathione S-transferases). Through the activity of these enzymes, glutathione directly supports antioxidant activity, phase II detoxification, and the normal breakdown of metabolites, toxins, and other compounds in the body. Glutathione also participates in fatty acid synthesis and amino acid transport across the cell membrane.*[1] A variety of factors may determine glutathione requirements, including level of exposure to toxins, increased phase I detoxification activity, and overall need for antioxidant support. Maintaining glutathione levels may be important to maintaining the health of the respiratory, hepatic, and immune systems, as well as supporting antioxidant protection of lipids and proteins and supporting the normal response to inflammation.[7-13] Levels of endogenous antioxidants, including glutathione, may decrease with age.[14] It is important to maintain adequate levels of glutathione in the body to support overall health and well-being throughout the lifespan.*

Vitamin D3 5000

While vitamin D3 (cholecalciferol) is made in the skin when 7-dehydrocholesterol reacts with sunlight, many things affect the degree to which this biosynthesis occurs, including time of day, seasons, location, smog/pollution, clothing, shade of skin (darker skin requires more sun), and sunscreen use. Low-cholesterol diets and certain cholesterol therapies can also affect vitamin D formation. By some estimates, one billion people worldwide have vitamin D deficiency or insufficiency.[1]

Reversing deficiency and maintaining optimal serum vitamin D levels beneficially impacts biochemistry and numerous body systems; this is largely because calcitriol—the metabolic product of vitamin D—is a secosteroid hormone that targets over 200 genes in a wide variety of tissues.[2,3] As the research demonstrates, vitamin D is clearly imperative for the development, growth, and maintenance of a healthy body from gestation to senescence.* Bone Health The body needs vitamin D to absorb calcium, and the importance of vitamin D in skeletal health and bone density is well established. Although bone density is most often associated with calcium intakes, insufficient vitamin D negatively affects calcium absorption.[3] Without adequate absorption, the body must take calcium from its stores in the skeleton, which weakens existing bone and prevents the formation of strong, new bone.

Clinical research shows that taking vitamin D orally with calcium supplements can support healthy bone turnover[4-6], and adequate calcium and vitamin D throughout life—as part of a well-balanced diet—may reduce the risk of osteoporosis.* The Expanding Roles of Vitamin D The role of vitamin D in good health continues to expand as the knowledge of this vitamin’s effects on different body systems grows. Research now suggests that optimal serum levels of vitamin D support normal cell differentiation,[3,7] cardiovascular health,[2,3] normal immune function,[8] good balance,[2] healthy mood,[9] normal fetal development,[10] neuronal growth and neurodevelopment,[2,3,10,11] healthy glucose metabolism,[2,3] musculoskeletal comfort,[2,3] periodontal health,[12] and normal intestinal immune responses.[8]

Areas of research that have gained momentum over the past several years concern the relationship of vitamin D deficiency or insufficiency to changes in cellular proliferation, changes in fetal brain development, and mental health. [7,10,13-15] Evidence is also mounting that vitamin D supplementation may provide key immune support.*[16-19] D2, D3, and Metabolites As previously stated, D3 is the form of vitamin D produced in the skin. D2 (ergocalciferol) is derived from fungal sources by activating ergosterol with ultraviolet light. It is not naturally present in the human body. After vitamin D is formed in the skin or taken orally, it is metabolized into two different substances within the body: calcidiol (25-hydroxyvitamin D) and calcitriol (1,25-dihydroxyvitamin D). Calcidiol is the body’s main storage form of vitamin D, while calcitriol (made from calcidoil) is “activated” vitamin D. Although D2 and D3 are similar biochemically, a recent study reported D3 to be approximately 87% more potent in raising and maintaining serum calcidiol concentrations and in producing two- to threefold greater storage of vitamin D than did equimolar D2.*[20

Tyrosine NAC

Each Tyrosine NAC capsule contains 400 mg of L-tyrosine, a conditionally essential amino acid the body can convert to the neurotransmitters dopamine, epinephrine, and norepinephrine. These neurotransmitters are found to increase mental alertness and focus and also preserve normal memory under stressful conditions. N-acetyl-Lcysteine is present to support glutathione production, antioxidant activity, and neuronal protection.*

Tyrosine, or 4-hydroxyphenylalanine, a proteogenic, non-essential amino acid that can be synthesized in the body from phenylalanine, is converted into dopamine, epinephrine, and norepinephrine. Although present in foods such as dairy, eggs, soy, peanuts, sesame, seaweed, avocados, bananas, poultry, lima beans, and others, tyrosine, when consumed in food, must compete for absorption with the other amino acids present. Taken as a supplement, tyrosine does not have to compete with other amino acids and, therefore, its full benefits can be realized.*

Stress conditions, such as a cold environment, psychological stress, sleep deprivation, and strenuous, prolonged athletic activity, appear to reduce the body’s ability to convert phenylalanine to tyrosine. This underproduction may manifest itself as poor memory and performance. Tyrosine, as a precursor for catecholamine synthesis, presumably augments brain catecholamine levels and improves working memory under stress. Tyrosine also supports adrenal and pituitary function, and may increase thyroid hormone. Additionally, it is necessary for production of the skin pigment, melanin. Oral contraceptives may cause a decline in tyrosine plasma levels, possibly because estrogen can increase glucocorticoid levels. This, in turn, elevates levels of tyrosine aminotransferase, which degrades tyrosine in the liver.*

Although increased dopamine may be beneficial in some circumstances, excessive synthesis of this neurotransmitter generates hydoxy radicals that stress glutathione levels. N-acetyl cysteine (NAC), a derivative of the amino acid, L-cysteine, is the precursor to glutathione and helps augment the body’s reserve of this important antioxidant. It has been included in this formula primarily to protect the neurons against dopamine toxicity. However, NAC also lessens the load on the methylation cycle, thereby decreasing the load on the THB cycle and promoting the conversion of tyrosine to dopamine.* Only a percentage of the tyrosine consumed will make it into the brain for conversion to catecholamines. The rest will be picked up for structural protein usage, etc. The only component that needs to be balanced with a glutathione precursor is the portion of tyrosine that is converted into catecholamines. For this reason, less NAC than tyrosine is present.*

Adrenal Booster

Adrenal Booster™ pairs glandulars with targeted nutrients to support the body’s response to everyday stressors. Among the comprehensive blend of nutrients are high-potency pantothenic acid and vitamin C, activated B vitamins, and mineral amino acid chelates. Gland and organ tissues are derived from an Argentinian bovine source that ensures safety and purity.*

Stress is caused by physiological, psychological, or emotional triggers (stressors) that cause a disturbance in the homeostasis of an organism. How we respond to those stressors (physiologically and psychologically) influences how well we cope with change and with ongoing stress. Structural or physical trauma, distress, poor diet, infection, toxic exposure, leaky gut, births, deaths, lack of sleep, temperature changes, electromagnetic radiation, and allergies or food sensitivities are all potential stressors. Combined, they amount to a total stress level and can ultimately disrupt homeostasis with direct effects on the autonomic nervous system, the hypothalamic-pituitaryadrenal (HPA) axis, and the cardiovascular, metabolic, and immune systems.[1]

Specifically, research reveals that prolonged stress has a profound effect on the adrenal glands, lymph nodes, thymus gland, and gastrointestinal system.[2] Endocrinologist Hans Selye identified the various stages of the stress response (alarm, resistance, and exhaustion) and described the entire phenomenon as the general adaptation syndrome (GAS). Micronutrients, such as vitamins, minerals, and antioxidants, are involved in the majority of metabolic functions in the body. B vitamins are especially important to energy generation within the cellular mitochondria, and a deficiency of any B vitamin can compromise mitochondrial function.[3,4] Riboflavin supports the respiratory chain, niacin supplies protons for oxidative phosphorylation, and pantothenic acid is required for coenzyme A production, metabolic enzyme complex formation, and fatty acid oxidation. Stressors can increase metabolic demand, energy expenditure, and micronutrient needs.[5]

Micronutrient sufficiency and balance have been established as crucial to helping maintain a healthy psychological and physiological response to stress.[6] Unfortunately, experts estimate that a significant proportion of the general population does not consume adequate dietary levels of several micronutrients. Experts suggest that exogenous supplementation can improve micronutrient status and sufficiency and help support a healthy response to stress.*[7] Clinical research supports the premise that micronutrient supplementation can favorably support the stress response in a variety of circumstances.[7]

In a randomized, double-blind, placebo-controlled (RDBPC) trial, high-potency doses of B vitamins and vitamin C along with an array of minerals were studied for their effects on perceived stress scores (measuring one’s self perception of stress) in 215 males aged 30 to 55 years. Results revealed significant improvements on the perceived stress scale (PSS), the profile of mood states (POMS), and the general health questionnaire (GHQ-12) for those taking the multivitamin/mineral supplement.[8] Another RDBPC study of 80 males revealed consistent and statistically significant modulation in anxiety and perceived stress in the men who took a high-potency multivitamin/mineral supplement compared to those who took the placebo. Participants taking the supplement also reported feeling less tired and better able to concentrate compared to their placebotaking counterparts.[9] Similar results were achieved in a double-blind, placebo-controlled, double-center study of 300 subjects taking a multivitamin/mineral supplement, with significant improvement in baseline stress scores.[6] The levels of vitamin C, riboflavin, B6, pantothenic acid, and zinc provided in the recommended dose of two Adrenal Booster capsules twice daily meets or exceeds the levels used in these clinical studies. The recommended daily dose of four capsules also provides 30 mg of niacin (compared to 50 mg used in studies) and 90 mg of magnesium (compared to 100 mg used in studies).*

Adrenal Booster also contains a blend of complementary nutrients and purified glandulars. Rhodiola rosea, chlorella, grape seed extract, magnesium, zinc, chromium, bioflavonoids, and L-tyrosine are present at levels that allow for additional supplementation to round out their profile. Activated B vitamins and Albion® TRAACS® (the real amino acid chelate system) mineral amino acid chelates, along with other chelated minerals, are key features of the formula. Adrenal, parotid, thymus, and spleen glandulars are extracted from an Argentinian bovine source that ensures safety and purity.*

Niacin 750

Niacin 750 is one of the most studied and documented nutrients for support of lipid levels already within the normal range, especially high-density lipoprotein cholesterol (HDL-C) levels. Sustained release niacin, as found in Niacin 750, has a lesser flushing effect compared with instant-release niacin. Use of a proprietary, wax-coated technology permits release that is complete in seven to eight hours, the time that is considered ideal for a time release form of niacin.*

The cardiovascular benefits of niacin (vitamin B3) were introduced in the June 1956 issue of Mayo Clinic Proceedings. [1] More than 20 years later, the Framingham Heart Study touted the benefits of niacin on lipid metabolism. A decade later, as the study continued, researchers labeled niacin “front-line” cardiovascular support.[2] This status was further reinforced in 1988 when the National Cholesterol Education Program (NCEP) panel designated niacin a “first-line therapy” for support of specific parameters related to cardiovascular health.*[3] Mechanisms of Action Several mechanisms of action have been proposed for niacin. Various experimental models suggest niacin can modulate lipoprotein biosynthesis in the liver, inhibit the release of free fatty acids from adipocytes, inhibit synthesis of apo B, induce lipoprotein lipase, and help maintain the structure and function of HDL (high-density lipoprotein) by reducing the amount of apo A-1 broken down from HDL during hepatic processing.[4,5]

In addition, when niacin is used with resins, it can stimulate bile flow and may therefore affect lipid biosynthesis.*[6] Human Trials Since the late 1970s, studies and clinical trials, lasting from four weeks to five years with daily doses of extended-release (also known as sustained/prolonged/slow-release) niacin up to 3000 mg/day, have consistently demonstrated niacin’s efficacy and safety. [6] In 2004, the ARBITER 6-HALTS trial clearly demonstrated that niacin offers targeted support of cardiovascular health.[7] Final results of this trial, published in 2010, further demonstrated that niacin supports healthy carotid intima-media thickness (CIMT).[8] While the supportive effect niacin has on blood lipids is well documented, there has been a recent focus by NCEP and other researchers on how niacin’s effect on HDL may influence cardiovascular events.[9] More well-designed studies that address innate limitations and are carried to completion are needed.*

Why Isn’t Niacin More Widely Used? The two common concerns are cutaneous flushing and increased liver enzymes. Cutaneous flushing is harmless, although it can be a nuisance. Flushing is most often seen with the use of immediate/instant-release forms of niacin and can occur with doses as low as 30 mg/day, but it is more likely to occur with the much higher doses used to support healthy blood lipids. Flushing may last 10 to 15 minutes and rarely, but possibly, up to two hours. The proprietary wax-coated technology used in Niacin 750 tablets allows a gradual, sustained release of niacin over a seven-to-eight hour period. This delivery dramatically reduces the flushing associated with immediate-release forms. Adherence to a regimen with the special wax-coated form of niacin, as found in Niacin 750, ranged from 88-97% in four human clinical trials.[10,11] Flushing, itching, tingling, and upper gastrointestinal side effects were minimal, but did increase when dosing was increased to 2000 mg/day.

It is important to note that Niacin 750 should not be confused with “no-flush” niacin, which is inositol hexanicotinate (IHN), a supplement that does not contain any free niacin and may not be as supportive of cardiovascular health as those providing nicotinic acid.*[12,13] The second concern with regard to liver enzyme elevation was first elucidated by the results of McKenney’s study, published in 1994 in the Journal of the American Medical Association (JAMA), wherein subjects received 3000 mg/day of niacin over an extended period of time.[14] In April 2004, McKenney retracted his earlier warnings about the harmful effects of niacin and publicly supported its unique benefits.[15] Although they generally do not enter an unhealthy range, liver enzymes may increase when initiating niacin therapy, especially in amounts greater than 1000 mg/day. Enzyme levels return to normal promptly after cessation of niacin.*[15]

References

Multi w/o iron

1. Ames BN. A role for supplements in optimizing health: the metabolic tune-up. Arch Biochem Biophys. 2004 Mar 1;423(1):227-34. [PMID: 14989256]

2. Toffanello ED, Inelmen EM, Minicuci N, et al. Ten-year trends in vitamin intake in free-living healthy elderly people: the risk of subclinical malnutrition. J Nutr Health Aging. 2011 Feb;15(2):99-103. [PMID: 21365161]

3. Block G, Jensen CD, Norkus EP, et al. Usage patterns, health, and nutritional status of long-term multiple dietary supplement users: a cross-sectional study. Nutr J. 2007 Oct 24;6:30. [PMID: 17958896]

4. Fletcher RH, Fairfield KM. Vitamins for chronic disease prevention in adults: clinical applications. JAMA. 2002 Jun 19;287(23):3127-29. [PMID: 12069676]

5. Moshfegh AJ, Goldman JD, Ahuja JK, et al. U.S. Department of Agriculture, Agricultural Research Service. What we eat in America, Nhanes 2005-2006. Usual nutrient intakes from food and water compared to 1997 dietary reference intakes for vitamin D, calcium, phosphorus, and magnesium. http://www.ars. usda.gov/SP2UserFiles/Place/12355000/pdf/0506/usual_nutrient_intake_vitD_ ca_phos_mg_2005-06.pdf Published July 2009. Accessed February 22, 2011.

6. What we eat in America. WIN Notes. Weight Control Information Network. http://win.niddk.nih.gov/notes/winter99/artcl6.htm. Accessed July 22, 2011.

7. Milk Processor Education Program. What America’s Missing: A 2011 Report on the Nation’s Nutrient Gap. Why Milk.com. http://www.whymilk.com/pdfs/ what_americas_missing.pdf. Accessed August 3, 2011.

8. Alexy U, Libuda L, Mersmann S, Kersting M. Convenience foods in children’s diet and association with dietary quality and body weight status. Eur J Clin Nutr. 2011 Feb;65(2):160-66. [PMID: 21139631]

9. Kiyose C, Muramatsu R, Kameyama Y, et al. Biodiscrimination of alphatocopherol stereoisomers in humans after oral administration. Am J Clin Nutr. 1997 Mar;65(3):785-89. [PMID: 9062530]

10. Burton GW, Traber MG, Acuff RV, et al. Human plasma and tissue alphatocopherol concentrations in response to supplementation with deuterated natural and synthetic vitamin E. Am J Clin Nutr. 1998 Apr;67(4):669-84. [PMID: 9537614]

11. Venn BJ, Green TJ, Moser R, et al. Comparison of the effect of low-dose supplementation with L-5-methyltetrahydrofolate or folic acid on plasma homocysteine: a randomized placebo-controlled study. Am J Clin Nutr. 2003 Mar;77(3):658-62. [PMID: 12600857]

12. Sallares J, Petschen I, Camps X, inventors; Ferrar Internacional, S.A., applicant. Process for the production of methylcobalamin. International publication number [English] WO 2006100059 A1. September 28, 2006

Adrenal Booster

1. Brame AL, Singer M. Stressing the obvious? An allostatic look at critical illness. Crit Care Med. 2010 Oct;38(10 Suppl):S600-7. [PMID: 21164403]

2. Szabo S, Tache Y, Somogyi A. The legacy of Hans Selye and the origins of stress research: a retrospective 75 years after his landmark brief “letter” to the editor of Nature. Stress. 2012 Sep;15(5):472-8. [PMID: 22845714]

3. Depeint F, Bruce WR, Shangari N, et al. Mitochondrial function and toxicity: role of the B vitamin family on mitochondrial energy metabolism. Chem Biol Interact. 2006 Oct 27;163(1-2):94-112. [PMID: 16765926]

4. Angelo G. What is metabolism? Linus Pauling Institute. http://lpi.oregonstate. edu/ss13/metabolism.html. Accessed October 19, 2013.

5. Askew EW. Environmental and physical stress and nutrient requirements. Am J Clin Nutr. 1995 Mar;61(3 Suppl):631S-637S. Review. [PMID: 7879730]

6. Schlebusch L, Bosch BA, Polglase G, et al. A double-blind, placebo-controlled, double-centre study of the effects of an oral multivitamin-mineral combination on stress. S Afr Med J. 2000 Dec;90(12):1216-23. [PMID: 11234653]

7. Drake V. Micronutrients and Cognitive Function. Linus Pauling Institute. http:// lpi.oregonstate.edu/infocenter/cognition.html. Accessed October 12, 2013

8. Kennedy DO, Veasey R, Watson A, et al. Effects of high-dose B vitamin complex with vitamin C and minerals on subjective mood and performance in healthy males. Psychopharmacology (Berl). 2010 Jul;211(1):55-68. [PMID: 20454891]

9. Carroll D, Ring C, Suter M, et al. The effects of an oral multivitamin combination with calcium, magnesium, and zinc on psychological well-being in healthy young male volunteers: a double-blind placebo-controlled trial. Psychopharmacology (Berl). 2000 Jun;150(2):220-5. [PMID: 10907676]

Tyrosine NAC

1. Growdon JH. Effects of oral L-tyrosine administration on CSF tyrosine and homovanillic acid levels in patients with Parkinson’s disease. Life Sci. 1982 Mar 8;30(10):827-32. [PMID: 6175872]

2. O’Brien C, et al. Dietary tyrosine benefits cognitive and psychomotor performance during body cooling. Physiol Behav. 2007 Feb 28;90(2-3):301-7. Epub 2006 Oct 31. [PMID: 17078981]

3. Palinkas LA. Mental and cognitive performance in the cold. Int J Circumpolar Health. 2001 Aug;60(3):430-9. [PMID: 11590885]

4. Deijen JB, Orlebeke JF. Effect of tyrosine on cognitive function and blood pressure under stress. Brain Res Bull. 1994;33(3):319-23. [PMID: 8293316]

5. Magill RA, et al. Effects of tyrosine, phentermine, caffeine D-amphetamine, and placebo on cognitive and motor performance deficits during sleep deprivation. Nutr Neurosci. 2003 Aug;6(4):237-46. [PMID: 12887140]

6. Rose DP, Cramp DG. Reduction of Plasma Tyrosine by Oral Contraceptives and Oestrogens: A Possible Consequence of Tyrosine Aminotransferase Induction, Clin Chim Acta, 1970;29:49-53. [PMID: 5500691]

7. Lee M, et al. Effects of hydrogen sulfide-releasing L-DOPA derivatives on glial activation: potential for treating Parkinson’s disease. Biol Chem. 2010 Jun 4;285(23):17318-28. Epub 2010 Apr 5. [PMID: 20368333]

8. Clark J, et al. Oral N-acetyl-cysteine attenuates loss of dopaminergic terminals in alpha-synuclein overexpressing mice. PLoS One. 2010 Aug 23;5(8). pii: e12333.[PMID: 20808797]

NAC references

1. Krinsky DL, LaValle JB, Hawkins EB, et al. Natural Therapeutics Pocket Guide. 2nd ed. Hudson (OH): Lexi-Comp; 2003.

2. Grandjean EM, Berthet P, Ruffmann R, Leuenberger P. Efficacy of oral long-term N-acetylcysteine in chronic bronchopulmonary disease: a meta-analysis of published double-blind, placebo-controlled clinical trials. Clin Ther. 2000 Feb 22(2):209-21. [PMID: 10743980]

3. Yalçin E, Altin F, Cinhüseyinoglue F, et al. N-acetylcysteine in chronic blepharitis. Cornea. 2002 Mar;21(2):164-8. [PMID: 11862087]

4. Ottenwalder H, Simon P. Differential effect of N-acetylcysteine on excretion of the metals Hg, Cd, Pb and Au. Arch Toxicol. 1987 Jul;60(5):401-2. [PMID: 3662815]

5. Keogh JP, Steffen B, Siegers CP. Cytotoxicity of heavy metals in the human small intestinal epithelial cell line I-407: the role of glutathione. J Toxicol Environ Health. 1994 Nov;43(3):351-9. [PMID: 7966443]

6. Witschi A, et al. The systemic availability of oral glutathione. Eur J Clin Pharmacol. 1992;43:667-9. [PMID: 1362956]

7. De Rosa SC, et al. N-acetylcysteine replenishes glutathione in HIV infection. Eur J Clin Invest 2000 Oct;30(10):841-2. [PMID: 11029607]

8. Atkuri KR, Mantovani JJ, Herzenberg LA, et al. N-Acetylcysteine—a safe antidote for cysteine/glutathione deficiency. Curr Opin Pharmacol. 2007 Aug;7(4):355-9. Review. [PMID: 17602868]

9. White AC, Thannickal VJ, Fanburg BL. Glutathione deficiency in human disease. J Nutr Biochem. 1994;5:218-26. http://www.sciencedirect.com/ science/article/pii/0955286394900396 Updated January 27, 2003. Accessed February 27, 2012.

10. Pace GW, Leaf CD. The role of oxidative stress in HIV Disease. Free Rad Biol Med. 1995;19:523-8. [PMID: 7590404]

11. Favier A, Sappey C, Leclerc P, et al. Antioxidant status and lipid peroxidation in patients infected with HIV. Chem Biol Interact. 1994 Jun;91(2-3):165-80. Review. [PMID: 8194133].

12. Nakamura H, Masutani H, Yodoi J. Redox imbalance and its control in HIV infection. Antioxid Redox Signal. 2002 Jun;4(3):455-64. [PMID: 12215212]

13. Roberts RL, Aroda VR, Ank BJ. N-acetylcysteine enhances antibody-dependent cellular toxicity in neutrophils and mononuclear cells from healthy adults and human immunodeficiency virus-infected patients. J Infect Dis. 1995 Dec;172(6):1492-502. [PMID: 7594708]

14. Hu HL, Forsey RJ, Blades TJ, et al. Antioxidants may contribute in the fight against ageing: an in vitro model. Mech Ageing Dev. 2000 Dec 20;121(1- 3):217-30. [PMID: 11164475] Additional references

Vitamin D3 5000

1. Tsiaras WG, Weinstock MA. Factors influencing vitamin d status. Acta Derm Venereol. 2011 Mar;91(2):115-24. [PMID: 21384086]

2. Cannell JJ, Hollis BW. Use of vitamin D in clinical practice. Altern Med Rev. 2008 Mar;13(1):6-20. [PMID: 18377099]

3. Heany RP. Vitamin D in health and disease. Clin J Am Soc Nephrol. 2008 Sep;3(5):1535-41. [PMID: 18525006]

4. Dawson-Hughes B, Harris SS, Krall EA, et al. Effect of calcium and vitamin D supplementation on bone density in men and women 65 years of age or older. N Engl J Med. 1997;337:670-76. [PMID: 9278463]

5. Papadimitropoulos E, Wells G, Shea B, et al. Meta-analyses of therapies for postmenopausal osteoporosis. VIII: Meta-analysis of the efficacy of vitamin D treatment in preventing osteoporosis in postmenopausal women. Endocr Rev. 2002;23:560-69. [PMID: 12202471]

6. Lips P, Bouillon R, van Schoor NM, et al. Reducing fracture risk with calcium and vitamin D. Clin Endocrinol (Oxf). 2010 Sep;73(3):277-85. [PMID: 20796001]

7. Garland CF, French CB, Baggerly LL, et al. Vitamin d supplement doses and serum 25-hydroxyvitamin d in the range associated with cancer prevention. Anticancer Res. 2011 Feb;31(2):607-11. [PMID: 21378345]

8. Raman M, Milestone AN, Walters JR, et al. Vitamin D and gastrointestinal diseases: inflammatory bowel disease and colorectal cancer. Therap Adv Gastroenterol. 2011 Jan;4(1):49-62. [PMID: 21317994]

9. Humble MB. Vitamin D, light and mental health. J Photochem Photobiol B. 2010 Nov;101(2):142-49. [PMID: 18445674]

10. Grant WB, Soles CM. Epidemiologic evidence supporting the role of maternal vitamin D deficiency as a risk factor for the development of infantile autism. Dermatoendocrinol. 2009 Jul;1(4):223-28. [PMID: 20592795]

11. Currenti SA. Understanding and determining the etiology of autism. Cell Mol Neurobiol. 2010 Mar;30(2):161-71. [PMID: 19774457]

12. Naito M, Miyaki K, Naito T, et al. Association between vitamin D receptor gene haplotypes and chronic periodontitis among Japanese men. Int J Med Sci. 2007 Aug;4(4):216-22. [PMID: 17848979]

13. McGrath JJ, Burne TH, Féron F, et al. Developmental vitamin D deficiency and risk of schizophrenia: a 10-year update. Schizophr Bull. 2010 Nov;36(6):1073- 78. [PMID: 20833696]

14. Gandini S, Boniol M, Haukka J, et al. Meta-analysis of observational studies of serum 25-hydroxyvitamin D levels and colorectal, breast and prostate cancer and colorectal adenoma. Int J Cancer. 2011 Mar;128(6):1414-24. doi: 10.1002/ ijc.25439. [PMID: 20473927]

15. Yin L, Grandi N, Raum E, et al. Meta-analysis: circulating vitamin D and ovarian cancer risk. Gynecol Oncol. 2011 Feb 14. [Epub ahead of print] [PMID: 21324518]

16. Grant WB, Goldstein M, Mascitelli L. Ample evidence exists from human studies that vitamin D reduces the risk of selected bacterial and viral infections. Exp Biol Med (Maywood). 2010 Dec;235(12):1395-96; discussion 1397. [PMID: 21171208]

17. Beard JA, Bearden A, Striker R. Vitamin D and the anti-viral state. J Clin Virol. 2011 Mar;50(3):194-200. [PMID: 21242105]

18. Hertting O, Holm Å, Lüthje P, et al. Vitamin D induction of the human antimicrobial peptide cathelicidin in the urinary bladder. PLoS One. 2010 Dec;5(12):e15580. [PMID: 21179490]

19. Grant WB, Boucher BJ. Requirements for vitamin D across the life span. Biol Res Nurs. 2011 Jan 17. [Epub ahead of print] [PMID: 21242196]

20. Heaney RP, Recker RR, Grote J, et al. Vitamin d3 is more potent than vitamin d2 in humans. J Clin Endocrinol Metab. 2011 Mar;96(3):E447-52. [PMID: 21177785]

MCHC plus Mag

1. Pines A, Raafat H, Lynn AH, et al. Clinical trial of microcrystalline hydroxyapatite compound (‘MCHC plus Mag’) in the prevention of osteoporosis due tocorticosteroid therapy. Curr Med Res Opin. 1984;8(10):734-42. [PMID: 6373153]

2. Stellon A, Davies A, Webb A, et al. Microcrystalline hydroxyapatite compound in prevention of bone loss in corticosteroid-treated patients with chronic active hepatitis. Postgrad Med J. 1985 Sep;61(719):791-6. [PMID: 2997764]

3. Buclin T, Jacquet AF, Burckhardt P. Intestinal absorption of calcium gluconate and oseine-mineral complex: an evaluation by conventional analyses [in French]. Schweiz Med Wochenschr. 1986 Dec 13;116(50):1780-3. [PMID: 3026039]

4. Epstein O, Kato Y, Dick R, et al. Vitamin D, hydroxyapatite, and calcium gluconate in treatment of cortical bone thinning in postmenopausal women with primary biliary cirrhosis. Am J Clin Nutr. 1982 Sep;36(3):426-30. [PMID: 6287835]

5. Stepan JJ, Mohan S, Jennings JC, et al. Quantitation of growth factors in ossein-mineral-compound. Life Sci. 1991;49(13):PL79-84. [PMID: 1653384]

6. Annefeld M, Caviezel R, Schacht E, et al. The influence of ossein-hydroxyapatite compound (‘MCHC plus Mag’) on the healing of a bone defect. Curr Med Res Opin. 1986;10(4):241-50. [PMID: 3022988]

7. Fernández-Pareja A, Hernández-Blanco E, Pérez-Maceda JM, et al. Prevention of osteoporosis: four-year follow-up of a cohort of postmenopausal women treated with an ossein-hydroxyapatite compound. Clin Drug Investig. 2007;27(4):227- 32. [PMID: 17358094]

8. Rüegsegger P, Keller A, Dambacher MA. Comparison of the treatment effects of ossein-hydroxyapatite compound and calcium carbonate in osteoporotic females. Osteoporos Int. 1995 Jan;5(1):30-4. [PMID: 7703621]

9. Khadzhiev A, Rachev E, Katsarova M, et al. The results of a clinical trial of the preparation MCHC plus Mag [in Bulgarian]. Akush Ginekol (Sofiia). 1990;29(4):85-7. [PMID: 2176437]

10. Castelo-Branco C, Martínez de Osaba MJ, Pons F, et al. Ossein-hydroxyapatite compounds for preventing postmenopausal bone loss. Coadjuvant use with hormone replacement therapy. J Reprod Med. 1999 Mar;44(3):241-6. [PMID: 10202741]

11. Castelo-Branco C, Pons F, Vicente JJ, et al. Preventing postmenopausal bone loss with ossein-hydroxyapatite compounds. Results of a two-year, prospective trial. J Reprod Med. 1999 Jul;44(7):601-5. [PMID: 10442322]

12. Bovine Spongiform Encephalopathy Status of Members. OIE-World Organization for Animal Health Web site. http://www.oie.int/animal-health-in-the-world/ official-disease-status/bse/list-of-bse-risk-status/. Accessed May 9, 2014.

13. Malic acid can be the right ligand for certain applications. Albion® Research Notes. April 2003;12(2). http://www.albionhumannutrition.com/research-notes/ download?start=40. Accessed May 9, 2014.

Niacin 750

1. Parsons WB Jr, Achor RW, Berge KG,et al. Changes in concentration of blood lipids following prolonged administration of large doses of nicotinic acid to persons with hypercholesterolemia: preliminary observations. Mayo Clin Proc. 1956 Jun 27;31(13):377-90. [PMID: 13336128]

2. Kannel WB. Recent findings from the Framingham study—I. Med Times. 1978 Apr;106(4):23-27. [PMID: 642745]

3. Hulley SB. The US National Cholesterol Education Program. Adult treatment guidelines. Drugs. 1988;36 Suppl 3:100-04. [PMID: 3254822]

4. Morgan JM, Carey CM, Lincoff A, et al. The effects of niacin on lipoprotein subclass distribution. Prev Cardiol. 2004 Fall;7(4):182-7; quiz 188. [PMID: 8424822]

5. Holland RE, Rahman K, Morris AI, et al. Effect of niacin on biliary lipid output in the rat. Biochem Pharmacol. 1993 Jan 7;45(1):43-49. [PMID: 8424822]

6. Niacin. http://www.naturalstandard.com/naturalstandard/monographs/ monoframeset.asp?monograph=/monographs/herbs supplements/aux2-niacin. asp&patientVersion=/monographs/herbs supplements/patient-niacin. Accessed August 19, 2010.

7. Taylor AJ, Sullenberger LE, Lee HJ, et al. Biology for the investigation of the treatment effects of reducing cholesterol (ARBITER) 2: a double-blind, placebo controlled study of extended-release niacin on atherosclerosis progression in secondary prevention patients treated with statins. Circulation. 2004 Dec 7;110(23):3512-17. [PMID: 15537681]

8. Villines TC, Stanek EJ, Devine PJ, et al. The ARBITER 6-HALTS Trial (Arterial Biology for the Investigation of the Treatment Effects of Reducing Cholesterol 6-HDL and LDL Treatment Strategies in Atherosclerosis): final results and the impact of medication adherence, dose, and treatment duration. J Am Coll Cardiol. 2010 Jun 15;55(24):2721-67. [PMID: 20399059]

9. Michos ED, Sibley CT, Baer JT, et al. Niacin and statin combination therapy for atherosclerosis regression and prevention of cardiovascular disease events: reconciling the AIM-HIGH (Atherothrombosis intervention in metabolic syndrome with low hdl/high triglycerides: Impact on global health outcomes) trial with previous surrogate endpoint trials. J Am Coll Cardiol. 2012 Apr 4. [Epub ahead of print] [PMID: 22520249]

10. Keenan JM, Fontaine PL, Wenz JB, et al. Niacin revisited. A randomized, controlled trial of wax-matrix sustained-release niacin in hypercholesterolemia. Arch Intern Med. 1991 Jul;151(7):1424-32. [PMID: 2064495]

11. Aronov DM, Keenan JM, Akhmedzhanov NM, et al. Clinical trial of wax-matrix sustained-release niacin in a Russian population with hypercholesterolemia. Arch Fam Med. 1996 Nov-Dec;5(10):567-75. [PMID: 8930228]

12. Backes JM, Padley RJ, Moriarty PM. Important considerations for treatment with dietary supplement versus prescription niacin products. Postgrad Med. 2011 Mar;123(2):70-83. Review. [PMID: 21474895] Norris RB. “Flush-free niacin”: dietary supplement may be “benefit-free”. Prev Cardiol. 2006 Winter;9(1):64-65. [PMID: 16407706]

13. McKenney JM. A comparison of the efficacy and toxic effects of sustained- vs immediate-release niacin in hypercholesterolemic patients. JAMA. 1994 Mar 2;271(9):672-77. [PMID: 8309029]

14. McKenney JM. Pharmacologic options for aggressive low-density lipoprotein cholesterol lowering: benefits versus risks. Am J Cardiol. 2005 Aug 22;96(4A):60E-66E. Review. [PMID: 16098846]