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.*

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.*

5-HTP CR100

5-HTP CR100 has a delivery system that releases 5-HTP slowly and steadily over a period of time. 5-HTP is a drug-free amino acid derived from a plant that naturally increases the body’s level of serotonin, the chemical messenger that affects emotions, behavior, appetite, and sleep. Today’s stress-filled lifestyles and dietary practices may negatively affect how the body handles serotonin. Regular use of PRx 5-HTP CR100 helps promote a more positive outlook and greater appetite control.*

5-hydroxytryptophan (5-HTP) is a precursor to serotonin. In the body, the essential amino acid tryptophan (when acted upon by the enzyme tryptophan hydroxylase) converts to 5-HTP. The compound is subsequently decarboxylated to serotonin, thereby elevating extracellular serum serotonin levels. Supplementing with 5-HTP bypasses the somewhat limiting conversion of tryptophan to 5-HTP. [1,2] Oral 5-HTP is well-absorbed in the intestine without the need for a transporter; other amino acids do not compete with it for absorption. It easily crosses the blood-brain barrier, is not degraded by the enzymes that degrade tryptophan, and it is excreted through the kidneys.*[1,3] Mood and Comfort Serotonin regulates many normal brain activities, increases norepinephrine and dopamine, and is important in regulating mood and behavior. Adequate levels of serotonin are associated with normal calmness and relaxation.*[1-5] Several studies have demonstrated that 5-HTP supports a healthy frame of mind, good energy levels, ease of movement, and restful sleep.[1,6,7] Published studies (dose~100-600 mg/day) have also demonstrated the effectiveness of 5-HTP supplementation in supporting cerebral comfort.*[8-10] Appetite Used in a high dose (i.e., 300 mg/three times a day), 5-HTP decreased food consumption and reduced weight. This result may relate to the effect of 5-HTP in supporting normal hypothalamic regulation, which includes appetite homeostasis.[11] However, nausea at this relatively high dose was a common complaint.[12,13] In other research, sublingual 5-HTP administered five times per day for eight weeks in adult overweight women significantly supported feelings of post-meal hunger satisfaction.*[14] Hormones and Sleep 5-HTP is thought to effect the HPA axis, as it has the ability to raise plasma cortisol levels, to cause transient increase in growth hormone (at 150 mg dose), and in men only, to support healthy levels of thyroid stimulating hormone.[15,16] Serotonin is also converted to melatonin; thus, supplementation has similar effects. Support of sleep quality is likely related to 5-HTP’s ability to increase the length of rapid eye movement (REM).[3,17] In children, supplementation with 5-HTP may help modulate arousal level and support peaceful sleep.*[18]

Liver Support

Liver Support™ contains the amino acid N-acetyl-L-cysteine, a key component of glutathione—a tripeptide that plays a significant role in detoxification and antioxidant support. Liver Support also contains a combination of alpha-lipoic acid, silymarin from milk thistle, and selenium for support of antioxidant activity, regeneration of other antioxidants, and promotion of healthy immune function.*

The liver is the body’s major metabolic organ. It processes, packages, stores, and ships out carbohydrates, fats, proteins, and micronutrients. It is responsible for the breakdown and elimination of alcohol, toxins, hormones, and medications, as well as for the synthesis of vital proteins, such as albumin, prealbumin, and clotting factors. It may be stated that the health of the body depends on the health of the liver.

Research suggests that providing targeted nutrition supplementation may help support liver function and health.*[1] N-Acetyl-Cysteine (NAC) An acetylated derivative of the sulfurcontaining amino acid L-cysteine, NAC promotes the synthesis of glutathione—a tripeptide that is active in detoxification and antioxidant systems. Glutathione also supports a healthy defense against hepatotoxic environmental pollutants, gamma-radiation, and other potential toxins.*[1,2] Alpha-Lipoic Acid Sometimes referred to as thioctic acid, alpha-lipoic acid is both water- and fat-soluble. It supports glutathione, helps regenerate antioxidant vitamins C and E, helps maintain the ratio of reduced to oxidized CoQ10 in the mitochondria, and helps support healthy levels of nitric oxide in the liver and kidney.[3]

The redox couple of lipoic acid and dihydrolipoic stabilizes NF-kappaB transcription and may help support healthy immune functions in the body.*[4,5] Milk Thistle Seed Extract Silymarin, the active component in milk thistle, has a history of use in promoting liver health. It supports antioxidant activity, neutralizes toxins, and also may protect hepatocytes’ genetic material. Like alpha-lipoic acid, silymarin supports production of cellular glutathione. Its actions in the liver include maintaining normal levels of fat peroxidation and fibrous tissue formation; supporting a healthy immune response and the natural response to inflammation; and promoting protein synthesis and normal regeneration of liver tissue.[6]

A randomized placebo-controlled study of 103 individuals suggested that silymarin yielded statistically positive results and was well tolerated.*[7] Selenium (as selenomethionine) An important coenzyme for the glutathione peroxidase detoxification system, selenium also appears to support the endogenous antioxidant defenses of hepatocytes by upregulating their manganese superoxide dismutase (MnSOD) expression. At the same time, selenium appears to support healthy cytokine balance by affecting interleukin-6 (IL-6) transcription in Kupffer cells (liver-based macrophages).[8]

Kupffer cells play a crucial role in maintaining normal structure and function in the liver. Supporting their function and the body’s normal inflammatory response in turn supports liver health overall.*[9] Upon studying targeted nutrition support for liver health, physician and researcher Dr. Burton M. Berkson chose to combine alpha-lipoic acid, silymarin, and selenium to obtain a balanced and low-cost approach to liver support.[10] These three ingredients plus NAC are all present in Liver Support™ to support liver health, antioxidant activity, and the body’s natural immune defenses.*

GI Max Caps

GI Max Caps™ features L-glutamine, zinc and pantothenic acid to nutritionally support the gastrointestinal mucosa and the prebiotic inulin to provide nourishment of the gastrointestinal mucosa cells. It also features aloe leaf extract, which has traditionally been used for optimal GI function.*

Pantothenic Acid (as calcium d-pantothenate), a component of Coenzyme A, has various essential roles that sustain life. Among these is maintenance of muscle tone of the gastrointestinal tract. Pantothenic acid supports the synthesis of serotonin and acetylcholine and therefore, may be beneficial in combating stress, often a component of gastrointestinal disorders.*

Zinc (as bis-glycinate chelate) has so many important roles in the body, including the quenching of free radicals possibly present in gastrointestinal disorders. Individuals with inflammatory bowel disorders or any diarrhea-related condition are at risk for zinc deficiency. Zinc deficiency may potentiate the effect of toxins produced by E.coli. A deficiency may also impair the absorption of water and electrolytes and perpetuate the diarrhea. Chronic low zinc impairs nitric oxide production, a substance that plays an important part in triggering diarrheal disease.*[1]

Inulin is a prebiotic fermented by intestinal flora to produce short chain fatty acids, including butyrate. Butyrate acts as “fuel” for colonocytes and enhances expression of biotransformation genes that induce glutathione Stransferase, protecting colonocytes from carcinogens.*[2]

L-Glutamine, a conditionally essential amino acid, is most important for intestinal energy supply; regeneration of the gastrointestinal mucosa is dependent upon its utilization. Supplementation has been shown to decrease inflammatory tissue damage in patients with conditions that generally result in low glutamine levels.[3] L- Glutamine is considered an immunonutrient and is particularly important for the body under stress-related conditions.*

Aloe (Leaf Extract), used for thousands of years, is perhaps most well-known for healing of damaged epithelial tissue, including the bowel lining. Despite the lack of scientific published studies there is anecdotal evidence to suggest that aloe vera helps inflammatory conditions of the gastrointestinal tract. In some individuals it may increase G.I. transit time, improve protein digestion and absorption, increase stool bulk and normalize stool bacteria where high levels of yeasts previously existed.*[4]

Mood Support ES

Mood Support ES™ combines key B vitamins, including 5-MTHF as Quatrefolic® and Albion® di-magnesium malate, with critical amino acids to support overall central nervous system health, calmness, and a positive mood.*

B Vitamins – Due to their involvement in the synthesis of chemicals crucial to brain function, B vitamins are essential to mental and emotional well-being. Because B vitamins are water soluble and not stored by the body, dietary or supplementary sources are critical to maintaining optimal levels. In addition, B vitamins can be destroyed or used at a higher rate with consumption of alcohol, refined sugars, nicotine, and caffeine.

Mood Support ES provides vitamin B6 in its principal coenzyme form, pyridoxal 5’-phosphate (P5P); vitamin B12 in its readily bioavailable form, methylcobalamin; and folate in the form of 50% calcium folinate and 50% Quatrefolic®. Quatrefolic is a form of 5-MTHF (5-methyltetrahydrofolate) that is proven to have greater stability, solubility, and bioavailability than calcium salt forms.* Folate and vitamins B6 and B12 are needed for proper methylation, a vital and fundamental process involved in many biochemical pathways such as the conversion of homocysteine back to methionine or to cysteine. Adequate intakes of these B vitamins plus a healthy metabolic conversion of folate to 5-MTHF support the maintenance of homocysteine levels within the normal range. Moreover, healthy homocysteine levels, as well as healthy serum B-vitamin levels, have a role in nerve health and have been associated with normal psychological function, mood, and cognition.[1-3]

Because 5-MTHF can cross the blood-brain barrier and may be better utilized by those with genetic variations in folate metabolism, 5-MTHF may be particularly well-suited to supporting healthy neurotransmission and promoting healthy homocysteine levels already within the normal range.* Pyridoxine nutritional status selectively modulates central production of both serotonin and GABA.[4]

Other neurotransmitters such as dopamine and norepinephrine are also synthesized using P5Pdependent enzymes.* Magnesium As a cofactor for over 325 enzymes in the body, magnesium has a multitude of actions, including a calming effect on the nervous system. Laboratory, animal, and epidemiological research suggests a link between magnesium sufficiency and a healthy mood and calm demeanor.[5,6] A suboptimal intake of magnesium could potentially cause intraneuronal magnesium deficits that affect neuronal integrity and function.*

GABA (Gamma-aminobutyric acid) GABA is an inhibitory neurotransmitter found in 30%-40% of the brain synapses. It helps calm the brain by neutralizing the excitatory effects of glutamate. It is thought that either low GABA levels or decreased GABA function in the brain may have an adverse impact on neurological health. Optimal levels of GABA support normal delta (deep) sleep and have been associated with healthy mood.*[7]

5-HTP (5-hydroxytryptophan) 5-HTP is a precursor to serotonin, a neurotransmitter that regulates many normal brain activities, supports healthy production of norepinephrine and dopamine, and assists with supporting healthy mood and behavior. In addition, a review of studies investigating serotonergic neurotransmission suggests that increasing serotonin availability may assist in weight management as it relates to periodic carbohydrate cravings.*[8] In the synthesis of serotonin, tryptophan is converted into 5-HTP by the enzyme tryptophan hydroxylase. Supplementation with 5-HTP bypasses this rate-limiting conversion. Oral 5-HTP is well-absorbed in the intestine without the need for a transporter; other amino acids do not compete with it for absorption. It easily crosses the blood-brain barrier, is not degraded by the enzymes that degrade tryptophan, and it is excreted through the kidneys.*[9,10]

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]

Vitamin D3 5000

While vitamin D3 5000(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]

Insulin Support Caps

Insulin Support Caps™ is an extraordinary combination of herbal and nutrient support for healthy glucose metabolism. It features concentrates of fenugreek, gymnema and bitter gourd, the addition of high levels of vanadium along with select B vitamins and the mineral, chromium. This formula provides nutritional support for glucose and insulin metabolism and supports healthy blood lipid levels already within the normal range*

Thiamin activates glyceraldehyde phosphate dehydrogenase (GAPDH). Decreased availability of this enzyme has been implicated in diabetes complications such as blindness, nerve damage, kidney failure, stroke and cardiovascular disease.[1] Thiamin repletion in the case of a six year-old girl with diabetes caused by a genetic mutation effecting thiamine transport demonstrated its benefits.[2] Thiamin deficiency may cause diabetic neuropathy by decreasing transketolase, needed for normal myelinization and thiamine monophasphatase, needed for primary sensory neuron function.*[3]

Niacin is required for lipid metabolism, tissue respiration and glycogenolysis. It may preserve and protect Beta cells.[4] Niacinamide improved insulin secretion in lean diabetics who had failed drug treatment.*[5]

Chromium and Biotin synergistically improve glucose tolerance.[6,7] Biotin, in large doses (5-15 mgs) enhances the effects of enzymes involved in glucose metabolism. One small study demonstrated reversal of diabetic neuropathy.[8] Chromium polynicotinate, preferred for its bioavailability and biological activity may increase insulin receptor sensitivity and enhance glucose transport. Anderson, et al. showed 1000 mcgs of chromium stabilized blood sugar in two months along with insulin and cholesterol level improvement.*[9]

Vanadyl Sulfate may reduce hepatic gluconeogenesis and “mimic” insulin’s effect.[10] In rats, vanadyl sulfate was also shown to alter the expression of genes dysregulated in diabetes.*[11] Fenugreek Seed and its constituent, 4-isoleucine appear to directly stimulate insulin.[12] The combination of fenugreek with vanadium appeared to normalize altered membrane linked functions and GLUT4 distribution.[13] Fenugreek also lowered high serum cholesterol and triglycerides.*[14]

Bitter Gourd (aka. bitter melon) contains an insulin-like polypeptide shown to exhibit hypoglycemic effects[15] with an onset of action between 30-60 minutes and a peak effect at about 4 hours.[16] It is approved as an antidiabetic drug in China.*[17] Gymnema sylvestre reduced fasting blood sugars, glycosylated hemoglobin (HbA1c) and glycosylated plasma protein levels and thus insulin requirements in Type 1 diabetics by reducing glucose absorption in the intestine, stimulating pancreatic beta cell growth and possibly increasing endogenous insulin secretion as suggested by an increase in C-peptide levels. Gymnema was shown to also reduce serum triglycerides, total cholesterol, VLDL and LDL.*[18]

L-Glutamine (Add on product)

L-Glutamine (glutamine) is the most abundant amino acid in the body and is necessary for the maintenance of many metabolic functions. Under situations of stress, physiological demands increase, triggering a need for glutamine supplementation. For ease of dosing, PRx’s L-Glutamine provides 4 grams of this amino acid per scoop to help replenish the body’s stores and support glutamine’s many functional roles.*

Glutamine is the most abundant free amino acid in the body and is an energy substrate for most cells—especially enterocytes (intestinal epithelial cells) and immune cells. It is also an essential component for numerous metabolic functions, including acid-base (pH) homeostasis; nitrogen supply; neurotransmitter production; and synthesis of glutathione, glucose, proteins, and nucleic acids.[1,2] Glutamine is primarily synthesized and stored in skeletal muscle. It is considered a conditionally essential amino acid because, under normal circumstances, the body can manufacture enough to sustain physiological demands. However, under metabolic stress—such as illness/disease, injury, infection, surgery, chemotherapy, prolonged exercise, or environmental stress—glutamine is released from body stores into the bloodstream and transported to tissues in deficit. Increased demands make exogenous glutamine sources (food, supplements) a necessity.*[2]

Support During and Recovery After Stress States During stress states, the body’s glutamine requirement exceeds supply, severely reducing both plasma and skeletal muscle pools of free glutamine.[1] Without adequate glutamine to meet the needs of the intestine, immune system, and vital organs, a negative nitrogen balance and catabolism can result.[3]

Nitrogen is necessary to repair wounds and keep the vital organs functioning; approximately one third of this nitrogen comes from glutamine. Adequate nutrition, which includes glutamine, can help spare host energy reserves and impede recovery complications.[4] In fact, it has been recommended that patients preparing for elective surgery ready themselves nutritionally, in part through glutamine supplementation, to optimize recovery.[5]

Research also suggests glutamine may help diminish risks associated with conventional therapeutics—such as high-dose chemotherapy and radiation—by supporting mucosal integrity, immune competence, and glutathione biosynthesis.*[4,6,7] Intestinal Health and Barrier Function The greatest amount of glutamine is used by enterocytes. As their preferred fuel source, glutamine is necessary for their maintenance and healthy turnover. Supplementation may therefore enhance mucosal health.[1,8]

A healthy intestinal mucosa not only supports optimal nutrient absorption, but it also supports mucosal immune function and provides a barrier between bacteria and their products in the intestines and the bloodstream.[1,9,10] Disruption of intestinal barrier function can lead to decreases in mucosal immune activity and increases in escaping toxins and bacteria, resulting in infections, illness, allergic reactions, skin conditions, and more. In various experimental models, glutamine administration has been shown to reduce epithelial cell death and preserve or improve barrier function.[11-13] For instance, in an animal model of chemotherapy-induced intestinal damage, glutamine decreased the severity of intestinal injury perhaps through improved intestinal cell turnover and enhanced antioxidant activity.*[14]

Muscle Tissue Preservation –  Of the 20 amino acids required for protein synthesis, glutamine is the most abundant. It makes up 50% of all amino acids in the blood and 60% of those in the body. Not only is glutamine necessary to maintain positive nitrogen balance and protein synthesis, but also it has recently been shown to prevent muscle loss by influencing myostatin levels.[15] Myostatin is a protein that inhibits muscle differentiation and growth. Its increased bioactivity has been observed in glucocorticoid-induced hypercatabolism and is associated with several pathologies characterized by marked skeletal muscle depletion.*[15] Glutamine is thought to have ergogenic effects through its influences on fluid and electrolyte uptake, glutamine pool repletion after intense training, stimulation of muscle glycogen synthesis, and ability to increase growth hormone levels.[16-18] While ergogenic effects are supported from a biochemical standpoint, more definitive studies are needed.*

References

Multi w/o iron

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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

NAC

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

5-HTP CR100

1. Juhl JH. Fibromyalgia and the serotonin pathway. Altern Med Rev. 1998 Oct;3(5):367-75. [PMID: 9802912]

2. Gutknecht L, Jacob C, Strobel A, et al. Tryptophan hydroxylase-2 gene variation influences personality traits and disorders related to emotional dysregulation. Int J Neuropsychopharmacol. 2007 Jun;10(3):309-20. [PMID: 17176492]

3. Birdsall TC. 5-Hydroxytryptophan: a clinically-effective serotonin precursor. Altern Med Rev. 1998 Aug;3(4):271-80. [PMID: 9727088]

4. Agren H, Reibring L, Hartvig P, et al. Low brain uptake of L-[11C]5- hydroxytryptophan in major depression: a positron emission tomography study on patients and healthy volunteers. Acta Psychiatr Scand. 1991;83(6):449-55. [PMID: 1882697]

5. Zmilacher K, Battegay R, Gastpar M. L-5-hydroxytryptophan alone and in combination with a peripheral decarboxylase inhibitor in the treatment of depression. Neuropsychobiology. 1988;20(1):28-35. [PMID: 3265988]

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7. Puttini S, Caruso I. Primary fibromyalgia syndrome and 5-hydroxy-L-tryptophan: a 90-day open study. J Int Med Res. 1992 Apr;20(2):182-89. [PMID: 1521674]

8. Ribeiro CA. L-5-hydroxytryptophan in the prophylaxis of chronic tension-type headache: a double-blind, randomized, placebo controlled study. Headache. 2000 Jun;40(6):451-56. [PMID: 10849040]

9. Nagata E, Shibata M, Hamada J, et al. Plasma 5-hydroxytryptamine (5-HT) in migraine during an attack-free period. Headache. 2006 Apr;46(4):592-96. [PMID: 16643553]

10. Nicolodi M, Sicuteri F. L-5-hydroxytryptophan can prevent nociceptive disorders in man. Adv Exp Med Biol. 1999;467:177-82. [PMID: 10721054]

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12. Cangiano C, Ceci F, Cascino A, et al. Eating behavior and adherence to dietary prescriptions in obese adult subjects treated with 5-hydroxytryptophan. Am J Clin Nutr. 1992 Nov;56:863-67. [PMID: 1384305] Cangiano C, Laviano A, Del Ben M, et al. Effects of oral 5-hydroxy-tryptophan on energy intake and macronutrient selection in non-insulin dependent diabetic patients. Int J Obes Relat Metab Disord. 1998 Jul;22(7):648-54. [PMID: 9705024]

13. Rondanelli M, Klersy C, Iadarola P, et al. Satiety and amino-acid profile in overweight women after a new treatment using a natural plant extract sublingual spray formulation. Int J Obes (Lond). 2009 Oct;33(10):1174-82. [PMID: 19752879]

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15. Mashchak CA, Kletzky OA, Spencer C, et al. Transient effect of L-5- hydroxytryptophan on pituitary function in men and women. J Clin Endocrinol Metab. 1983 Jan;56(1):170-76. [PMID:6600170]

16. Wyatt RJ, Zarcone V, Engelman K, et al. Effects of 5-hydroxytryptophan on the sleep of normal human subjects. Electroencephalogr Clin Neurophysiol. 1971 Jun;30(6):505-09. [PMID: 4105646]

17. Bruni O, Ferri R, Miano S, et al. L -5-hydroxytryptophan treatment of sleep terrors in children. Eur J Pediatr. 2004 Jul;163(7):402-07. [PMID:15146330]

Liver Support

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

2. Hu C, Jiang L, Geng C, et al. Possible involvement of oxidative stress in trichloroethylene-induced genotoxicity in human HepG2 cells. Mutat Res. 2008 Jan 18. [PMID: 18289923]

3. Abdel-Zaher AO, Abdel-Hady RH, Mahmoud MM, et al. The potential protective role of alpha-lipoic acid against acetaminophen-induced hepatic and renal damage. Toxicology. 2008 Jan 20;243(3):261-70. [PMID: 18068886]

4. Suzuki YJ, Aggarwal BB, Packer L. Alpha-lipoic acid is a potent inhibitor of NFkappa B activation in human T cells. Biochem Biophys Res Commun. 1992 Dec 30;189(3):1709-15. [PMID: 1482376]

5. Baur A, Harrer T, Peukert M, et al. Alpha-lipoic acid is an effective inhibitor of human immuno-deficiency virus (HIV-1) replication. Klin Wochenschr. 1991 Oct 2;69(15):722-4. [PMID: 1724477]

6. Pradhan SC, Girish C. Hepatoprotective herbal drug, silymarin from experimental pharmacology to clinical medicine. Indian J Med Res. 2006 Nov;124(5):491- 504. [PMID: 17213517]

7. El-Kamary SS, Shardell MD, Abdel-Hamid M, et al. A randomized controlled trial to assess the safety and efficacy of silymarin on symptoms, signs and biomarkers of acute hepatitis. Phytomedicine. 2009 May;16(5):391-400. [PMID: 19303273]

8. Shilo S, Pardo M, Aharoni-Simon M, et al. Selenium supplementation increases liver MnSOD expression: molecular mechanism for hepato-protection. J Inorg Biochem. 2008 Jan;102(1):110-8. [PMID: 17804075] Roberts RA, Ganey PE, Ju C, et al. Role of the Kupffer cell in mediating hepatic toxicity and carcinogenesis. Toxicol Sci. 2007 Mar;96(1):2-15. Review. [PMID: 17122412]

9. Berkson BM. A conservative triple antioxidant approach to the treatment of hepatitis C. Combination of alpha lipoic acid (thioctic acid), silymarin, and selenium: three case histo

GI Max Caps

1. Wapnir RA. J Nutr. 2000 May; 130 (5S Suppl): 1388S-92S Zinc deficiency, malnutrition and the gastrointestinal tract. [PMID: 10801949]

2. Sauer J, Richter KK, Pool-Zobel BL. Products formed during fermentation of the prebiotic inulin with human gut flora enhance expression of biotransformation genes in human primary colon cells. Br J Nutr. 2007 Mar 7;:1-11 [PMID: 17381985]

3. Sido B. Low intestinal glutamine level and low glutaminase activity in Crohn’s disease: a rationale for glutamine supplementation? Dig Dis Sci. 2006 Dec;51(12):2170-9. [PMID: 17078002]

4. Davis K, et. al. Randomised double-blind placebo-controlled trial of aloe vera for irritable bowel syndrome. Int J Clin Pract. 2006 Sep;60(9):1080-6 [PMID: 16749917]

5. Bland, J. Ph.D. (1985), Linus Pauling Institute of Science and Medicine, Palo Alto, C.A., Prevention Magazine, Effect of Orally Consumed Aloe Vera Juice in Gastrointestinal Fun

Mood Support ES

1. Coppen A, Bolander-Gouaille C. Treatment of depression: time to consider folic acid and vitamin B12. J Psychopharmacol. 2005 Jan;19(1):59-65. [PMID: 15671130]

2. Lewis SJ, Lawlor DA, Davey Smith G, et al. The thermolabile variant of MTHFR is associated with depression in the British Women’s Heart and Health Study and a meta-analysis. Mol Psychiatry. 2006 Apr;11(4):352-60. [PMID: 16402130]

3. Selhub J, Bagley LC, Miller J, et al. B vitamins, homocysteine, and neurocognitive function in the elderly. Am J Clin Nutr. 2000;71(2):614S-20S. [PMID: 10681269]

4. McCarty MF. High-dose pyridoxine as an ‘anti-stress’ strategy. Med Hypotheses. 2000 May;54(5):803-07. [PMID: 10859691]

5. Whittle N, Li L, Chen WQ, et al. Changes in brain protein expression are linked to magnesium restriction-induced depression-like behavior. Amino Acids. 2011 Apr;40(4):1231-48. [PMID: 21312047]

6. Sartori SB, Whittle N, Hetzenauer A, et al. Magnesium deficiency induces anxiety and HPA axis dysregulation: modulation by therapeutic drug treatment. Neuropharmacology. 2012 Jan;62(1):304-12. [PMID: 21835188]

7. Mombereau C. Genetic and pharmacological evidence of a role for GABA (B) receptors in the modulation of anxiety- and antidepressant-like behavior. Neuropsychopharmacology. 2004 Jun;29(6):1050-62. [PMID: 15039762]

8. Wurtman JJ. Carbohydrate craving. Relationship between carbohydrate intake and disorders of mood. Drugs. 1990;39 Suppl 3:49-52. [PMID: 2197075]

9. Birdsall TC. 5-Hydroxytryptophan: a clinically-effective serotonin precursor. Altern Med Rev. 1998 Aug;3(4):271-80. [PMID: 9727088]

10. Turner EH, Loftis JM, Blackwell AD. Serotonin a la carte: supplementation with the serotonin precursor 5-hydroxytryptophan. Pharmacol Ther. 2006 Mar;109(3):325-38. [PMID: 16023217]

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.

Insulin Support Caps

1. Obrenovich ME, Monnier VM. Vitamin B1 blocks damage caused by hyperglycemia. Sci Aging Knowledge Environ. 2003 Mar 12; 2003 (10): PE6.

2. Viana MB, Carvalho RI. Thiamine- Responsive Megaloblastic Anemia, Sensorineural Deafness, and Diabetes Mellitus: A New Syndrome?, J Pediatrics, August 1978; 93(2): 235-238.

3. Frydl, V., Zavodska, H. Diabetic Polyneuropathy and Vitamin B1, Medwelt,1989;40:1484-6

4. Pozzilli, B. et al. Adjuvant therapy in recent onset type 1 diabetes at diagnosis and insulin requirement after 2 years. Diabete Metab.1995 Feb:21(1): 4709. [PMID: 7781843]

5. Polo, V. Saibene A., Pontiroli AE. Nicotinamide improves insulin secretion and metabolic control in lean type 2 diabetic patients with secondary failure to sulfonylureas. Acta Diabetol 1998;35:61-4

6. McCarty MF. High dose biotin, an inducer of glutokinase expression, may synergize with chromium picolinate to enable a definitive nutritional therapy for type II diabetes. Med Hypothese 1999 May;52(5):401-6

7. Singer GM, Geohas J. The effect of chromium picolinate and biotin supplementation on glycemic control in poorly controlled patients with type 2 diabetes mellitus: a placebo-controlled, double-blinded, randomized trial. Diabetes Technol Ther. 2006 Dec; 8(6): 636-43 [PMID:17109595]

8. Coggeshall JC, et al. Biotin status and plasma glucose in diabetes. Annals New York Academy of Sciences 1985; 447:389-92 9. www.naturaldatabase.com

9. Badmaev V. Vanadium: review of its potential role in the fight against diabetes; J Altern Complement Med, 1999; 5(3): 273-291

10. Willsky GR. Diabetes-altered gene expression in rat skeletal muscle corrected by oral administration of vanadyl sulfate: Physiol Genomics. 2006 Aug 16;26(3):192-201. Epub 2006 May 9. [PMID: 16684804]

11. Sauvaire Y. et al. 4-hydroxisoleucine. A novel amino acid potentiator of insulin secretion. Diabetes 1998; 47: 20610

12. Siddiqui MR et.al. Low doses of vanadate and Trigonella synergistically regulate Na+/K + -ATPase activity and GLUT4 translocation in alloxan-diabetic rats. Cell Biochem. 2006 Apr; 285 (1-2): 17-27. Epub 2006 Apr 19 [PMID: 16622606]

13. Newall CA, Anderson LA, Philpson JD. Herbal Medicine: A Guide for Healthcare Professionals. London, UK The Pharmaceutical Press, 1993

14. Sarkar S, Pranava M, Marita R. Demonstration of the hypoglycemic action of Momordica charantia in validated animal model of diabetes. Pharmacol Res, 1993;33(1)1-4

15. Raman A, et al. Anti-diabetic properties and phytochemistry of Momordica charantia L. (Cucurbitaceae). Phytomedicine 1996; 26

16. Jia W. Gao W, Tang L. Antidiabetic herbal drugs officially approved in China. Phytother Res 2003 Dec; 17(10): 1127-1134

17. Shanmugasundaram, E.R.B., Rajeswari, G., Baskaran K., Rajesh Kumar, B.R., Radha Shanmugasundaram, K., Kizar Ahmath, B. Use of gymnema sylvestre leaf extract in the control of blood glucose in insulin-dependent diabetes mellitus. J Etnopharmacol 1990;30:281-94

18. The Review of Natural Products by Facts and Comparisons. St. Louis, MO:Wolters Kluwer Co; 1999

L-Glutamine

1. Oliveira GP, Dias CM, et al. Understanding the mechanisms of glutamine action in critically ill patients. An Acad Bras Cienc. 2010 Jun;82(2):417-30. [PMID: 20563423]

2. Walsh NP, Blannin AK, Robson PJ, et al. Glutamine, exercise and immune function. Links and possible mechanisms. Sports Med. 1998 Sep;26(3):177-91. [PMID: 9802174]

3. Calder PC, Yaqoob P. Glutamine and the immune system. Amino Acids. 1999;17(3):227-41. [PMID: 10582122]

4. Kuhn KS, Muscaritoli M, Wischmeyer P, et al. Glutamine as indispensable nutrient in oncology: experimental and clinical evidence. Eur J Nutr. 2010 Jun;49(4):197-210. [PMID: 19936817]

5. Awad S, Lobo DN. What’s new in perioperative nutritional support? Curr Opin Anaesthesiol. 2011 Mar 30. [Epub ahead of print] [PMID: 21451404]

6. Anderson PM, Schroeder G, Skubitz KM. Oral glutamine reduces the duration and severity of stomatitis after cytotoxic cancer chemotherapy. Cancer. 1998 Oct;83(7):1433-39. [PMID: 9762946]

7. Rocha BR, Gombar FM, Barcellos LM, et al. Glutamine supplementation prevents collagen expression damage in healthy urinary bladder caused by radiotherapy. Nutrition. 2010 Dec 15. [Epub ahead of print] [PMID: 21167680]

8. dos Santos RG, Viana ML, Generoso SV, et al. Glutamine supplementation decreases intestinal permeability and preserves gut mucosa integrity in an experimental mouse model. JPEN J Parenter Enteral Nutr. 2010 JulAug;34(4):408-13. [PMID: 20631386]

9. Nose K, Yang H, Sun X, et al. Glutamine prevents total parenteral nutritionassociated changes to intraepithelial lymphocyte phenotype and function: a potential mechanism for the preservation of epithelial barrier function. J Interferon Cytokine Res. 2010 Feb;30(2):67-80. [PMID: 20028208]

10. Li N, Neu J. Glutamine deprivation alters intestinal tight junctions via a PI3-K/ Akt mediated pathway in Caco-2 cells. J Nutr. 2009 Apr;139(4):710-14. [PMID: 19211824]

11. Tian J, Hao L, Chandra P, et al. Dietary glutamine and oral antibiotics each improve indexes of gut barrier function in rat short bowel syndrome. Am J Physiol Gastrointest Liver Physiol. 2009 Feb;296(2):G348-55. [PMID: 19095767]

12. Vicario M, Amat C, Rivero M, et al. Dietary glutamine affects mucosal functions in rats with mild DSS-induced colitis. J Nutr. 2007 Aug;137(8):1931-37. [PMID: 17634266]

13. Gulgun M, Karaoglu A, Kesik V, et al. Effect of proanthocyanidin, arginine and glutamine supplementation on methotrexate-induced gastrointestinal toxicity in rats. Methods Find Exp Clin Pharmacol. 2010 Nov;32(9):657-61. [PMID: 21225016]

14. Tazuke Y, Maeda K, Wasa M, et al. Protective mechanism of glutamine on the expression of proliferating cell nuclear antigen after cisplatin-induced intestinal mucosal injury. Pediatr Surg Int. 2011 Feb;27(2):151-58. [PMID: 21080177]

15. Bonetto A, Penna F, Minero VG, et al. Glutamine prevents myostatin hyperexpression and protein hypercatabolism induced in C2C12 myotubes by tumor necrosis factor-α. Amino Acids. 2011 Feb;40(2):585-94. [PMID: 20623149]

16. Hoffman JR, Ratamess NA, Kang J, et al. Examination of the efficacy of acute L-alanyl-L-glutamine ingestion during hydration stress in endurance exercise. J Int Soc Sports Nutr. 2010 Feb 3;7:8. [PMID: 20181080]

17. Welbourne TC. Increased plasma bicarbonate and growth hormone after an oral glutamine load. Am J Clin Nutr. 1995 May;61(5):1058-61. [PMID: 7733028]

18. Antonio J, Street C. Glutamine: a potentially useful supplement