* Please Note: This information is based partly on Traditional Medicine which uses natural materials to support health. This information has not been evaluated or approved by the FDA. These statements have not been evaluated by the Food and Drug Administration (FDA). These products are intended to support general well being and are not intended to treat, diagnose, mitigate, prevent, or cure any condition or disease. If conditions persist, please seek advice from your medical doctor.
Description
The Diabetex Multivitamin & Mineral Formula has been designed to address the special nutritional needs of those with prediabetes or type 2 diabetes, and type 1 diabetes. Vitamins and minerals play facilitating roles in all phases of metabolism. Along with diligence in specific protocols of natural medicine and pharmaceutical medications, optimal nutritional support should be emphasized in all diabetic states. Sugar, fat, and protein are the obvious nutrients that overshadow our discussions about diabetic states, but key micronutrients are critical managers in the challenged metabolism of diabetes. These are discussed below.
Key Minerals
Chromium is one of the central nutrients involved in diabetic states. Chromium supplementation presents the possibility for making profound improvements in the diabetic condition. Chromium is required in the prevention and control of diabetes as an essential nutrient involved in the metabolism of glucose, insulin, and blood lipids and suboptimal dietary intake of chromium is associated with increased risk factors relating to diabetic states and cardiovascular diseases.(13) Chromium plays a critical dose-related role in stabilizing the beta-subunit conformational change that accounts for tyrosine kinase activity for mediating insulin signaling.(14) Since the mid 1990s, chromium has been shown to improve glucose and related variables in subjects with glucose intolerance, type 1, type 2, gestational, and steroid-induced diabetes.(13)
Its past recommended daily amount has been generally 200 mcg, but the research on chromium has consistently demonstrated that a very safe yet more effective range is 200 to 1000 mcg/day. In the recommended daily amount of 2 tablets BID, this product supplies 400 mcg of organic chromium, covalently bound to rice protein (hydrolyzed vegetable protein, HVP) for enhanced absorption.
Magnesium is also emphasized because it too is a central nutrient mineral in diabetes management, and very often ignored. Magnesium deficiency is a factor in the emergence of Syndrome X with its elevated triglycerides, obesity, and insulin resistance.(16,17) Magnesium deficiency occurs in up to 40 percent of diabetic patients and it is not obvious who these people are.(18,19) A protracted magnesium deficiency increases the risk for cardiovascular disease, retinopathy, and neuropathy, while routinely supplementing magnesium lowers risks for these complications.(19-22) In the recommended daily amount of 2 tablets BID, this product supplies 400 mg, an excellent amount for consistent daily exposure.
Zinc plays a key role in the synthesis and action of insulin, both physiologically and in diabetes, and seems to stimulate insulin action and insulin receptor tyrosine kinase activity enhancing glucose disposal and utilization.(23) Increased urinary zinc excretion appears to contribute to the marginal zinc nutritional status that has been observed in diabetics.(24)
Furthermore, zinc plays an important role in anti-oxidation, making it a player in reducing the extent of diabetic complications relating to oxidative stress.(25) Thus zinc is a key nutrient for supporting optimal glucose and insulin metabolism in diabetic states. This product at 2 tablets BID supplies 30 mg.
Key B Vitamins
The B vitamins are so intimately involved in metabolism as coenzymes that their optimal tissue levels help to maintain effective robust metabolism. Full-blown deficiencies are rare. However, marginal deficiencies can exist, impeding optimal glucose and fat metabolism. Since all of the B vitamins are water soluble and at risk of urinary loss in diabetes that is not tightly controlled, this product supplies them in higher concentrations than seen in general multivitamin products.
A major concern in diabetes management is risk reduction for vascular complications. One factor in adverse vascular changes is the accumulation of homocysteine in the blood. Hyperhomocysteinemia is positively correlated with coronary heart disease, cerebrovascular disease, and peripheral vascular disease.(26,27) Furthermore, hyperhomocysteinemia is a significant independent risk factor for overall mortality in type 2 diabetic patients.(28) This product specifically addresses the homocysteine diabetic risk with optimal strengths of the three B vitamins required to reduce homocysteine levels, B6, B12, and folic acid.
Niacinamide is supplied at 100 mg/day in the recommended daily amount because at that strength it has been shown to enhance chromium action.(15) Niacin/Niacinamide therapy for high cholesterol has been shown to cause insulin resistance, but the required amount for this effect is 2 or more grams per day.
Key Anti-oxidation Constituents
Antioxidant efforts should be a major focus in order to preserve as much as possible the health of the vascular endothelium and other tissues adversely affected in diabetes. Diabetic complications are driven by oxidative stress due to hyperglycemic conditions, and few diabetic patients can avoid accumulative lapses in tight glycemic control.
The antioxidant vitamins C and E are well provided when using the recommended daily amount. These vitamins play an integral part in the antioxidant network. The concept of an antioxidant defense network developed from experimental observations of a dynamic interplay between vitamins C and E, coenzyme Q10, glutathione, and alpha-lipoic acid.
These five antioxidants are now understood to coalesce into a functional network because each remains redox-sensitive, meaning that they can be regenerated into their active antioxidant form through redox reduction by a network member with sufficient reduction potential. This network of antioxidants comprises a pool of shared redox reducing power. Not all antioxidants undergo endogenous reduction to be regenerated in the body. Such a dynamic defensive network serves as a renewable electron-donating system for neutralizing the destructive metabolic ebb and flow of free-radicals, reactive oxygen species (ROS), and reactive nitrogen species (RNS).(29)
Part of the normal daily influx of dietary reducing power that feeds into the antioxidant network comes from plants that provide powerful reducing agents. The plant ingredients listed under Additional Ingredients of this product comprise a source of potent antioxidant polyphenols, carotenoids, and curcuminoids. Consumed at the recommended daily amount, essentially 55 mg/day of actual antioxidant mass is delivered as part of the total antioxidant defense against diabetic complications.
Vitamin D and Diabetes
In a Diabetes Care 2006 Cardiovascular and Metabolic Risk Brief Report,(30) Cigolini et.al. stated that there is a growing body of evidence that low 25-hydroxyvitamin D3 concentrations may be inversely associated with type 2 diabetes,(31,32,33) metabolic syndrome,(34,35) insulin resistance,(36) and cardiovascular disease.(37) A number of other researchers have also made the connection between low vitamin D3 and type 1 and type 2 diabetes. Accordingly, this formula provides vitamin D3 at 400 IU in the recommended daily intake of 2 tablets BID.
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Directions
Use 2 tablets BID with meals, or as directed by a physician. (Meal time fat/oil is required for fat-soluble vitamins.) The ingesting of this product should be separated by at least two hours from the dosing of any antibiotic medication that can complex with mineral nutrients.
Cautions
Adverse Side Effects
Adverse side effects are generally not associated with the nutrients comprising this product and the other constituents when consumed at the recommended amount. There is the possibility of an idiosyncratic to any constituent.
Taking tablets on an empty stomach may cause nausea.
The recommended daily intake of 100 mg of niacinamide may be able to cause flushing in more sensitive people, with sensations of burning, tingling, and itching, as well as erythema on the face, arm and chest and headache.(1)
Precaution / Cautions
Type 1 diabetic patients, and type 2 patients on oral hypoglycemic medications and/or insulin, should be advised of the potential for enhanced glucose clearance and reactive hypoglycemia when initiating this product.
Chromium, magnesium, and zinc each contribute significantly to blood glucose clearance, and particularly if these nutrients were low when medication dose adjustments were finalized.
People with compromised kidney function may develop inappropriate levels of the mineral nutrients in this product and should be guided by their physician before using.
This product should not be considered appropriate prenatal or postnatal nutritional support since it is designed specifically to address supportive nutrition in diabetic states.
This product contains vitamin E at 200 IU/day when using the recommended amount. There may be a risk for potentiating anticoagulation medications.
Interactions
The information in this section under the various nutrient headings only identifies common drugs, conditions, or natural substances that are known to directly or indirectly reduce tissue levels, or inhibit activation of, or the action of the respective nutrients.
This information is primarily developed from the Natural Medicines Comprehensive Database, which can be consulted for greater details, and fuller information on potential adverse drug interactions.(1) Information contained in this section should not be considered exhaustive.
Since the goal of vitamin and mineral supplementation in diabetes care is to optimize the availability of nutrients that affect metabolic pathways important in diabetes management, interactions that compromise nutrient levels may interfere with good diabetes management. Accordingly, using this product at the recommended daily amount of 2 tablets BID should be encouraged in people with prediabetes or diabetes, and especially if the potential for nutrient depletion exists due to a medication profile.
Thiamine (B1)
Alpha-lipoic acid supplementation even in lower doses may present competition for thiamine absorption, especially in alcoholic people who are expected to already be low in thiamine.(2,3)
Thiamine absorption is reduced in conditions of alcoholism, cirrhosis, and malabsorption syndromes.(1)
Long-term use of diuretics may result in reduced thiamine levels, especially when using furosemide at greater than 80 mg/day, and in those who are 60 years old or older.(1)
Riboflavin (B2)
Chlorpromazine has structural similarities to riboflavin and can interfere with its conversion to the active form, flavin adenine dinucleotide (FAD).(1,4)
Doxorubicin forms complexes with riboflavin, competes for tissue binding sites, reduces conversion to flavin adenine dinucleotide, and increases urinary excretion.(1,5)
Oral contraceptives may interfere with the absorption of riboflavin, or its conversion to active coenzyme forms.(1,6)
Niacinamide (B3)
Based on two case reports, azathioprine may induce symptomatic niacin deficiency where marginal niacin status exists, through the inhibition of nicotinamide adenine dinucleotide (NAD) synthesis.(1) NAD levels play an important role in managing type 2 diabetes.
Prolonged use of chloramphenicol may interfere with the activity of NAD and has been reported to cause pellagra.(1)
Cycloserine can lower vitamin B6 levels, inhibiting the conversion of tryptophan to niacin,(7) and cause niacin deficiency.(1) Encephalopathy responsive to niacinamide has occurred occasionally in people taking cycloserine.(1)
Ethionamide is similar enough to niacinamide to interfere with its activity,(1) possibly affecting its role in managing diabetes.
Isoniazid can reduce the levels of vitamin B6, resulting in a reduced conversion of tryptophan to niacin,(1) possibly resulting in an adverse niacin deficiency in diabetes cases. Isoniazid also has structural similarities to niacin and might interfere with niacin's conversion to nicotinamide adenine dinucleotide (NAD)(1,8) that is otherwise required in diabetes management.
Dopa decarboxylase inhibitors such as carbidopa inhibit an enzyme involved in the conversion of tryptophan to niacin,(1) possibly affecting NAD levels in diabetic cases.
Mercaptopurine has structural similarities to adenine and interferes with synthesis of nicotinamide adenine dinucleotide (NAD), especially after prolonged therapy with high doses (e.g., 250 mg/day for 4 years).(1)
Phenytoin may be able to induce niacinamide deficiency,(1) possibly adversely affecting NAD levels in diabetes management.
Pyrazinamide is structurally similar to niacinamide and may interfere with its activity, evidenced by the fact that it can induce Pellagra.(1)
Valproic acid may be able to induce niacinamide deficiency,(1) possibly adversely affecting NAD levels in diabetes management.
Pyridoxine (B6)
Cycloserine increases pyridoxine excretion in the urine.(1)
Estrogen replacement therapy can lower vitamin B6 plasma levels.(1)
Hydralazine can cause pyridoxine deficiency in some patients through increased excretion.(1)
Isoniazid interacts with pyridoxine, increasing urinary excretion and depletion.(1)
Theophylline tends to reduce plasma pyridoxal-5-phosphate levels, the active form of pyridoxine (vitamin B6).(1) Pyridoxine supplements of 10-300 mg/day have been tried in people taking theophylline, but results are conflicting.(1)
Biotin
Biotin action may be frustrated in those using more than 100 mg of alpha-lipoic acid per day. Alpha-lipoic acid has a similar enough structure to that of biotin so that it can theoretically interfere with biotin's metabolic role as an enzyme cofactor.(9)
Carbamazepine, phenobarbital, primidone, and phenytoin can each reduce plasma biotin levels, and in one study each drug was able to reduce biotin plasma levels by 50% compared to controls.(1)
Raw egg white contains avidin, a protein which binds biotin in the intestine, preventing biotin absorption. Two or more raw egg whites daily for several months may lead to symptomatic biotin deficiency.(1)
Pantothenic acid (B5)
None
Folic acid
Aminosalicylic acid can reduce dietary folate absorption.(1)
Carbamazepine can reduce serum folate levels, but megaloblastic anemia has not been reported.(1) (Folic acid supplements have worsened seizure control in some people, physician guidance is recommended. This product supplies 800 mcg/day when using the recommended 2 tables BID.)
Colestipol can interfere with absorption of folic acid, and reduce serum folate levels.(1)
Cycloserine can reduce serum folate levels and rare cases of megaloblastic anemia have been associated with it.(1)
Metformin absorption has been impaired in some people. (CPS)
Methotrexate prevents the conversion of folic acid to its active form, and lowers plasma and red blood cell folate levels. Patients suffering side effects due to reduced active folate can take folic acid at 1 mg/day, but up to 5 mg may be required.(1)
Supplemented pancreatic enzymes can reduce folate levels in some people.(1)
Phenobarbitol, phenytoin, fosphenytoin, and primidone can each reduce serum folate levels and induce megaloblastic anemia. Folic acid supplementation can worsen seizure control, requiring physician guidance.(1)
Sulfasalazine competitively inhibits absorption of folic acid in the intestine, and the breakdown of dietary folate to its absorbable form.(1) Long-term sulfasalazine therapy can cause reduced serum and red blood cell folate levels and hyperhomocysteinemia.
Cyanocobalamin (B12)
Aminosalicylic acid can reduce oral vitamin B12 absorption.(1)
Metformin can reduce serum vitamin B12. (CPS)
Phenytoin, phenobarbitol, and primidone, have been associated with reduced vitamin B12 absorption, and reduced serum and cerebrospinal fluid levels in some patients.(1)
Calcium & Magnesium
Aminoglycosides induced nephrotoxicity may lead to increased urinary losses of magnesium.(1) Magnesium is an important mineral in diabetes management.
Amphotericin-B produces electrolyte disturbances which can result in low serum magnesium levels.(1)
Antibiotics that form complexes with calcium or magnesium prevent their absorption. This product should be taken with meals and separated from antibiotic doses.(1)
Carbamazepine, phenytoin, fosphenytoin, and Phenobarbital decrease calcium absorption by increasing the metabolism of vitamin D.(1)
Cholestyramine may reduce the absorption of calcium, magnesium, and vitamin D.(1)
Corticosteroids interfere with calcium absorption and metabolism, and increases magnesium urinary loss.(1)
Cyclosporine can cause significant loss of magnesium in the urine.(1)
Digoxin decreases renal tubular resorption of magnesium, increasing excretion in the urine.(1)
Digitalis may adversely affect magnesium status. Magnesium depletion is associated with an adverse heart impact, including arrhythmias and coronary spasms.(10,11)
Estrogens, including oral contraceptives, indirectly lower serum magnesium by promoting magnesium uptake in soft tissues and bones.(1)
Foscarnet can cause symptomatic hypomagnesemia and requires monitoring.(1)
Loop diuretics increase urinary calcium and magnesium excretion and may reduce serum calcium and levels.(1)
H2 blockers and Proton Pump inhibitors when used on a long-term basis may adversely affect mineral balances in some people.
Chromium, Copper, Zinc (No depletion interactions for Mn, Se, Mo, V)
Antacids, H2 blockers, and Proton Pump inhibitors might decrease chromium and zinc levels by affecting pH factors in absorption.(1)
Corticosteroids can significantly increase urinary chromium excretion and induce hyperglycemia.(1,12)
Ethambutol and its metabolites chelate copper and zinc, and may produce tissue depletion.(1)
Deferoxamine increases urinary zinc excretion in a dose-dependant manner.(1)
Thiazide diuretics significantly increase urinary zinc excretion and this effect can persist through 3 years of treatment. Zinc monitoring may be necessary.(1)
Beta Carotene
Orlistat decreases absorption of fat soluble beta carotene, and other fat soluble vitamins.(1)
Vitamin C
Aspirin in a dose-related manner reduces tissue and leukocyte uptake of vitamin C, increasing urinary losses.(1)
Proton Pump inhibitors may lower vitamin C levels by pH factors in absorption.(1)
Vitamin D
Carbamazepine increases hepatic metabolism of vitamin D to inactive compounds, with hypocalcemia and osteomalacia being reported, especially with prolonged therapy.(1)
Mineral oil can reduce the absorption of vitamin D.(1)
Orlistat decreases absorption of fat soluble vitamin D, and other fat soluble vitamins.(1)
Phenytoin, fosphenytoin, and phenobarbital promote hepatic metabolism of vitamin D to inactive forms. Long-term use of these drugs can lead to hypocalcemia and osteomalacia.(1)
Rifampin promotes hepatic metabolism of 25-hydroxy-vitamin D, contributing to osteomalacia with long-term use (>1 year).(1)
Sunscreen products used extensively can significantly reduce skin vitamin D synthesis and plasma levels.(1)
Vitamin E
Orlistat may decrease the absorption of vitamin E to a critical extent.(1)
Contraindications
Patients with hyperparathyroidism or cancer should not supplement with calcium unless directed by a physician.
Additional Information
References
1. www.naturaldatabase.com cited June/2007 2. Gal, E.M., Reversal of selective toxicity of (-)-a-lipoic acid in deficient rats, Nature, 205:535, 1965 3. Packer, L., et al, Alpha-Lipoic acid as a biological antioxidant, Free Rad Biol Med, 19:227-250, 1995 4. Pinto, J., et al, Inhibition of riboflavin metabolism in rat tissues by chlorpromazine, imipramine and amitriptyline, J Clin Invest, 67:1500-6, 1981 5. Ogura, R., et al, Riboflavin deficiency caused by treatment with adriamycin, J Nutr Sci Vitaminol, 37:473-477, 1991 6. Newman, L.J., et al, Riboflavin deficiency in women taking oral contraceptive agents, Am J Clin Nutr, 31:247-249, 1978 7. Cervantes-Laurean, N, Gerard McElvaney, and Joel Moses, Niacin, in Modern Nutrition In Health and Disease, Maurice E Shils, James A. Olson, Moshe Shike, A Catharine Ross, editors, ninth edition, Lippincott Williams & Wilkins New York, 1999 8. Darvay, A., et al, Isoniazid induced pellagra despite pyridoxine supplementation, Clin Exp Dermatol, 24:167-169, 1999 9.Packer, Lester and Carol Colman, The Antioxidant Miracle, John Wiley & Sons, New York, 1999 10. Teo, K. K., et al, Role of magnesium in reducing mortality in acute myocardial infarction: A Review of the evidence, Drugs, 46: 347-359, 1993 11. Turlapaty, P., et al, Magnesium deficiency produces spasms of coronary arteries: Relationship to etiology of sudden ischemic heart disease, Science, 208: 199-200,1980 12. Ravina, A., Reversal of corticosteroid-induced diabetes mellitus with supplemental chromium, Diabet Med, 16:164-167, 1999 13. Anderson, A., Chromium, Diabetes Metab, Feb; 26:22-27, 2000 14. Vincent, John B., The Biochemistry of Chromium, J Nutr, 130:715-718, 2000 15. Urgerg, M., Zemel, M.B., Evidence for synergism between chromium and nicotinic acid in the control of glucose tolerance in elderly humans, Metabolism, 36:896-899, 1987 16. Singh, R.B., Association of low plasma concentrations of antioxidant vitamins, magnesium, and zinc with high body fat per cent in Indian men, Magnes Res, 11(1):3-10, 1998 17. Ma, J., et al, Associations of serum and dietary magnesium with cardiovascular disease, hypertension, diabetes, insulin, and carotid arterial wall thickness; the ARIC study, Atherosclerosis Risk in Communities Study, J Clin Epidemiol, 48:927-940, 1995 18. Kao, W.H., et al, Serum and dietary magnesium and the risk for type 2 diabetes mellitus; the Atherosclerosis Risk in Communities Study, Arch Intern Med, 159(18):2151-2159, 1999 19. Merz, C.N., et al, Oral magnesium supplementation inhibits platelet-dependent thrombosis in patients with coronary artery disease, Am J Cardiol, 84:152-156, 1999 20. Lima, M deL, The effect of magnesium supplementation in increasing doses on the control of type 2 diabetes, Diabetes Care, 83(5):682-686, 1998 21. Engelen, W., et al, Are low magnesium levels in type 1 diabetes associated with electromyographical signs of polyneuropathy?, Magnes Res, 13(3):197-203, 2000 22. Rumawas, M.E, et al, Magnesium intake is related to improved insulin homeostasis in the Framingham offspring cohort, J Am Coll Nutr, Dec; 25(6):486-492, 2006 23. Tang, X, Shay, N.F., Zinc has an insulin-like effect on glucose transport mediated by phosphoinositol-3-kinase and Akt in 3T3-L1 fibroblasts and adipocytes, J Nutr, May; 131(5):1414-1420, 2001 24. Blostein-Fujii, A., et al, Short-term zinc supplementation in women with non-insulin-dependent diabetes mellitus: effects on plasma 5'-nucleoti-dase activities, insulin-like growth factor I concentrations, and lipoprotein oxidation rates in vitro, Am J Clin Nutr, 66(3):639-642,1997 25. Anderson, R.A., et al, Potential antioxidant effects of zinc and chromium supplementation in people with type 2 diabetes mellitus, J Am Coll Nutr, 20(3):212-218, 2001 26. O'Connell, Belinda S., Select vitamins and minerals in the management of diabetes, Diabetes Spectrum, 14(3):133-148, 2001 27. Welch, G.N., et al, Homocysteine and atherothrombosis, NEJM, 338:1042-1050, 1998 28. Hoogeveen, E.K., et al, Hyperhomocysteinemia increases risk of death, especially in type 2 diabetes: 5-year follow-up of Hoorn study, Circulation, Apr 4; 101(13):1506-11, 2000 29. Packer, Lester, Oxidative Stress and Antioxidants: The Antioxidant Network, Alpha-Lipoic Acid, and Diabetes, in Antioxidants in Diabetes Management, Lester Packer, Peter Rosen, Hans J. Tritschler, George King and Angelo Azzi Editors, Marcel Dekker, New York, 2000, pp1-15. 30. Cigolini, Massimo, et al, Serum 25-hydroxyvitamin D3 concentrations and prevalence of cardiovascular disease among type 2 diabetic patients, Diabetes Care, Mar; 29(3):722-724, 2006 31. Boucher, B.J. et al, Glucose intolerance and impairment of insulin secretion in relation to vitamin D deficiency in East London Asians, Diabetologia, 38:1239-1245, 1995 32. Isaia, G., et al, High prevalence of hypovitaminosis D in female type 2 diabetic population (Letter), Diabetes Care, 24:1496, 2001 33. Scragg, R., et al, Serum 25-hydroxyvitamin D, diabetes, and ethnicity in the Third National Health and Nutrition Examination Survey, Diabetes Care, 27:2813-2818, 2004 34. Boucher, B.J., Inadequate vitamin D status: does it contribute to the disorders comprising syndrome X?, Br J Nutr, 79:315-327,1998 35. Ford, E.S., et al, Concentrations of serum vitamin D and the metabolic syndrome among U.S. adults, Diabetes Care, 28:1228-1230, 2005 36. Chiu, K.C., et al, Hypovitaminosis D is associated with insulin resistance and beta cell dysfunction, Am J Clin Nutr, 79:820-825, 2004 37. Scragg, R., et al, Myocardial infarction is inversely associated with plasma 25-hydroxyvitamin D3 levels: a community-based study, Int J Epidemiol 19: 559-563, 1990
These statements have not been evaluated by the Food and Drug Administration (FDA). Products are intended to support general well being and are not intended to treat, diagnose, mitigate, prevent, or cure any condition or disease.
