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The Science *

A varied diet of real, fresh food provides the most reliable nutrition for the human body.

Inside the capsule

All our supplement product lines are formulated to be as close to real food as possible: no artificial additives, doses like those you’ll find in foods, nutrients in forms that the body can readily utilize, with a rich variety of other micronutrients and phytonutrients supplied by real freeze-dried fruits and vegetables inside the capsule itself.

What do we mean by “real, fresh food”?

It’s the simple, straightforward definition: plants and animals that are modified only enough to maximize nutrient availability, while also being safe to eat. This means fruits and vegetables that are washed (and steamed when necessary), nuts and grains that are hulled and cleaned, and animal products that are thoroughly cooked. These foods contain a huge variety of nutrients that play different roles in maintaining the life and health of the human body.

Nutrients fit into 3 categories, broadly speaking:

  1. macronutrients (fats, proteins, carbs, and fibers)
  2. micronutrients (vitamins and minerals)
  3. phytonutrients (organic compounds that provide numerous benefits to the body)

It’s almost impossible to supply significant amounts of macronutrients and fibers in a small capsule—especially in a way that is aligned with the properties of real foods. So our goal in designing MAF supplements was to approximate the micronutrient and phytonutrient content of food as close as possible.

Bibliography

  1. Kennedy G, Nantel G, Shetty P. The scourge of” hidden hunger”: global dimensions of micronutrient deficiencies. Food Nutr Agric. 2003(32):8-16.
  2. Tontisirin K, Nantel G, Bhattacharjee L. Food-based strategies to meet the challenges of micronutrient malnutrition in the developing world. Proc Nutr Soc. 2002;61(2):243-50.
Scientific Rationale

The scientific literature supports the idea that food is the best nutrition.

MAF Supplements - Multi Vitamin

MAF Multi

The MAF Multi is our flagship supplement—a vitamin-mineral-phytonutrient complex designed to supply most of the most commonly needed groups of nutrients. It contains a full complement of the B and E vitamins, vitamin C, and a variety of minerals including calcium, magnesium, selenium and zinc. Finally, we added a wide variety of natural nutrients that help the body make its most powerful antioxidant, glutathione.

A wealth of vitamins, minerals, and phytonutrients is essential for maintaining proper bodily function, and promoting healthy development, growth, and recovery. Micronutrient deficiency is usually caused by a diet lacking in a variety of fruits, vegetables, animal products, and fats 1. This is why we encourage a healthy diet of real, fresh food as a primary source of nutrition.

Junk foods—such as those high in added sugars—are void of real nutrition. They correlate with a lower intake of micronutrients, and may lead to micronutrient deficiencies even in individuals whose caloric needs are met 1-3.

The nutrients included in the MAF Multi (and their functions) are:

Vitamin B Complex

B vitamins—plus the nutrient choline—perform some of the most important functions at the cellular level. Without them, the body’s cells would not be able to carry out some of their most basic tasks:

  • Vitamins B1, B2, Niacin, Pantothenic Acid and B6 enable energy metabolism (the production of energy from fuels like fat and sugar). Without them, cells would not be able to produce the energy they need to operate 4.
  • Vitamin B9 (folate) plays a primary role in methylation (a biochemical process that keeps DNA healthy and functioning) 5. Vitamins B2, B6, B12, and choline are necessary for this process to happen correctly 5. Poor methylation has implications in many chronic diseases, including cardiovascular disease and Alzheimer’s disease 4-14.

Go to our B Complex section to read more about the B vitamins and their function.

Vitamin C

Vitamin C is a powerful antioxidant, which protects tissues and cells from free radical damage 15, 16. In particular, it helps mitigate oxidative stress in exercise 17.

Vitamin C also supports many of the body’s functions, including the immune system, genetic expression, tissue health, wound healing and others 16, 18, 19.

Go to our C Complex section to read more about the role vitamin C plays in the body.

Vitamin E Complex

Vitamin E is a fat-soluble vitamin which functions primarily as a lipid antioxidant: it protects fats—including LDL cholesterol—from free radical damage.

Vitamin E is actually a complex of 8 nutrients: 4 tocopherols and 4 tocotrienols. While only one nutrient—alpha tocopherol—is typically lauded for the biochemical functions of vitamin E, the other 7 nutrients have distinct characteristics and functions, which may be more important than those of alpha tocopherol. Furthermore, the levels of all 8 compounds must be balanced for vitamin E to perform all of its functions 20, 21. Here are some of those functions:

  • Vitamin E mitigates atherosclerosis—an important contributor to cardiovascular disease—by stopping LDL cholesterol from oxidizing 22, 23.
  • Delta tocopherol and tocotrienols have been found to induce cancer cell death (apoptosis) 24.
  • Tocotrienols may lower cholesterol levels, and may have anti-tumor effects 25.
  • Tocotrienols reduce angiogenesis (the growth of blood vessels that feed tumors) 25, 26.

Glutathione

Glutathione is the body’s most powerful antioxidant 27. While most antioxidants, such as vitamins C and E complex cannot be manufactured by the body, glutathione is special in that it can be synthesized internally from various nutrients 27.

The MAF Multi contains broccoli sprouts, which are rich in the compound sulphoraphane—a critical building block of glutathione 28-30.

(Once the broccoli plant matures, sulphoraphane content drops dramatically.)

Glutathione works together with folate, vitamin C, the vitamin E complex, and many other antioxidants to provide a variety of benefits to the body:

  • It helps fight cancer 31.
  • It is a powerful modulator of the immune system, and helps control inflammation by protecting tissue against oxidative stress 32, 33.
  • It helps convert oxidized vitamin C (that was already “spent” in capturing a free radical) back into reusable vitamin C 16.
  • Glutathione, selenium, and vitamin E work together to control the presence of reactive lipids 34, 35.
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Bibliography

  1. Kennedy G, Nantel G, Shetty P. The scourge of” hidden hunger”: global dimensions of micronutrient deficiencies. Food Nutr Agric. 2003(32):8-16.
  2. Louie JCY, Tapsell LC. Association between intake of total vs added sugar on diet quality: a systematic review. Nutr Rev. 2015;73(12):837-57. doi:10.1093/nutrit/nuv044
  3. DiNicolantonio JJ, Berger A. Added sugars drive nutrient and energy deficit in obesity: a new paradigm. Open heart. 2016;3(2):e000469. doi:10.1136/openhrt-2016-000469
  4. The B Vitamins and Choline: Overview and Methods. Institute of Medicine Standing Committee on the Scientific Evaluation of Dietary Reference Intakes., 1998.
  5. Selhub J. Folate, vitamin B12 and vitamin B6 and one carbon metabolism. J Nutr Health Aging. 2001;6(1):39-42.
  6. Blom HJ, Smulders Y. Overview of homocysteine and folate metabolism. With special references to cardiovascular disease and neural tube defects. J Inherit Metab Dis. 2011;34(1):75-81. doi:10.1007/s10545-010-9177-4
  7. Rimm EB, Willett WC, Hu FB, Sampson L, Colditz GA, Manson JE, et al. Folate and vitamin B6 from diet and supplements in relation to risk of coronary heart disease among women. JAMA. 1998;279(5):359-64.
  8. Verhoef P, Stampfer MJ, Buring JF, Gaziano JM, Allen RH, Stabler SP, et al. Homocysteine metabolism and risk of myocardial infarction: relation with vitamins B6, B12, and folate. Am J Epidemiol. 1996;143(9):845-59.
  9. Pancharuniti N, Lewis CA, Sauberlich HE, Perkins LL, Go R, Alvarez J, et al. Plasma homocyst (e) ine, folate, and vitamin B-12 concentrations and risk for early-onset coronary artery disease. Am J Clin Nutr. 1994;59(4):940-8.
  10. Folsom AR, Nieto FJ, McGovern PG, Tsai MY, Malinow MR, Eckfeldt JH, et al. Prospective study of coronary heart disease incidence in relation to fasting total homocysteine, related genetic polymorphisms, and B vitamins. Circulation. 1998;98(3):204-10.
  11. Wang H-X, Wahlin Å, Basun H, Fastbom J, Winblad B, Fratiglioni L. Vitamin B12 and folate in relation to the development of Alzheimer’s disease. Neurology. 2001;56(9):1188-94.
  12. Tiemeier H, Van Tuijl HR, Hofman A, Meijer J, Kiliaan AJ, Breteler MM. Vitamin B12, folate, and homocysteine in depression: the Rotterdam Study. Am J Psychiatry. 2002;159(12):2099-101.
  13. Bottiglieri T. Folate, vitamin B12, and neuropsychiatric disorders. Nutr Rev. 1996;54(12):382-90.
  14. Zhang CX, Pan MX, Li B, Wang L, Mo XF, Chen YM, et al. Choline and betaine intake is inversely associated with breast cancer risk: A two‐stage case‐control study in China. Cancer Sci. 2013;104(2):250-8. doi:10.1111/cas.12064
  15. Padayatty SJ, Katz A, Wang Y, Eck P, Kwon O, Lee J-H, et al. Vitamin C as an antioxidant: evaluation of its role in disease prevention. J Am Coll Nutr. 2003;22(1):18-35.
  16. Meister A. Glutathione, ascorbate, and cellular protection. Cancer Res. 1994;54(7 Supplement):1969s-75s.
  17. Alessio HM, Goldfarb AH, Cao G. Exercise-induced oxidative stress before and after vitamin C supplementation. Int J Sport Nutr. 1997;7(1):1-9.
  18. Cannon JG, Blumberg JB. Acute phase immune responses in exercise. Handbook of oxidants and antioxidants in exercise. 2000. p. 177-93.
  19. Lee SH, Oe T, Blair IA. Vitamin C-induced decomposition of lipid hydroperoxides to endogenous genotoxins. Science. 2001;292(5524):2083-6.
  20. Huang H-Y, Appel LJ. Supplementation of diets with α-tocopherol reduces serum concentrations of γ-and δ-tocopherol in humans. J Nutr. 2003;133(10):3137-40.
  21. Brigelius-Flohe R, Traber MG. Vitamin E: function and metabolism. FASEB J. 1999;13(10):1145-55.
  22. Dieber-Rotheneder M, Puhl H, Waeg G, Striegl G, Esterbauer H. Effect of oral supplementation with D-alpha-tocopherol on the vitamin E content of human low density lipoproteins and resistance to oxidation. J Lipid Res. 1991;32(8):1325-32.
  23. Zhang P, Xu X, Li X. Cardiovascular diseases: oxidative damage and antioxidant protection. Eur Rev Med Pharmacol Sci. 2014;18(20):3091-6.
  24. Yu W, Simmons‐Menchaca M, Gapor A, Sanders BG, Kline K. Induction of apoptosis in human breast cancer cells by tocopherols and tocotrienols. Nutr Cancer. 1999;33(1):26-32. doi:10.1080/01635589909514744
  25. Theriault A, Chao J-T, Wang Q, Gapor A, Adeli K. Tocotrienol: a review of its therapeutic potential. Clin Biochem. 1999;32(5):309-19.
  26. Miyazawa T, Shibata A, Nakagawa K, Tsuzuki T. Anti-angiogenic function of tocotrienol. Asia Pac J Clin Nutr. 2008;17(S1):253-6.
  27. Lu SC. Glutathione synthesis. Biochim Biophys Acta. 2013;1830(5):3143-53. doi:10.1016/j.bbagen.2012.09.008
  28. Kim B-R, Hu R, Keum Y-S, Hebbar V, Shen G, Nair SS, et al. Effects of glutathione on antioxidant response element-mediated gene expression and apoptosis elicited by sulforaphane. Cancer Res. 2003;63(21):7520-5.
  29. Vasanthi HR, Mukherjee S, Das DK. Potential health benefits of broccoli-a chemico-biological overview. Mini Rev Med Chem. 2009;9(6):749-59. doi:10.2174/138955709788452685
  30. Gasper AV, Al-janobi A, Smith JA, Bacon JR, Fortun P, Atherton C, et al. Glutathione S-transferase M1 polymorphism and metabolism of sulforaphane from standard and high-glucosinolate broccoli. Am J Clin Nutr. 2005;82(6):1283-91.
  31. Traverso N, Ricciarelli R, Nitti M, Marengo B, Furfaro AL, Pronzato MA, et al. Role of glutathione in cancer progression and chemoresistance. Oxid Med Cell Longev. 2013;2013. doi:10.1155/2013/972913
  32. Rahman I, MacNee W. Oxidative stress and regulation of glutathione in lung inflammation. Eur Respir J. 2000;16(3):534-54.
  33. Dröge W, Breitkreutz R. Glutathione and immune function. Proc Nutr Soc. 2000;59(4):595-600.
  34. Rotruck J, Pope A, Ganther H, Swanson A, Hafeman DG, Hoekstra W. Selenium: biochemical role as a component of glutathione peroxidase. Science. 1973;179(4073):588-90.
  35. Hoekstra WG. Biochemical function of selenium and its relation to vitamin E. Federation proceedings; 1975.
MAF Supplements - Vitamin B

MAF B Complex

Our B Complex formula contains a full-complement of all the B vitamins, plus choline—a vitamin-like essential nutrient necessary for many of the B vitamins to do their job.

Folate may be the most important vitamin in our B Complex. You may think you know it by a different name: folic acid. However, folic acid is a synthetic, inactive form of the vitamin that cannot produce its advertised effects until the body transforms it into the active folate 1. (Our formulation contains 5-methyltetrahydrofolate (5-MTHF)—the most active form of folate.)

This is also true for all inactive vitamins. For that reason, we made sure that our B Complex includes only the active forms that are immediately usable by the body.

B vitamins perform some of the most important functions at the cellular level. Without them, cells would not be able to carry out some of their most basic tasks, including energy production, as well as protecting DNA health and function. In doing so, B vitamins play a role in the prevention of many chronic diseases including cardiovascular disease, and Alzheimer’s. Here’s a breakdown:

Energy metabolism

Vitamins B1 + B2 + Niacin + Pantethine + B6

These vitamins are required for a complicated sequence of chemical reactions related to energy metabolism (the production of energy from fuels like fat and sugar). Several of these are also important for synthesizing various compounds related to energy utilization, including hormones, amino acids, glucose, and others 2.

Methylation

Folate + vitamins B2 + B6 + B12 + choline.

Don’t underestimate the importance of methylation! Folate (vitamin B9) plays a primary role in this little-known but vital biochemical process which directly affects DNA by controlling which genes become expressed 2, 3. Vitamins B2, B6, B12, and choline are necessary cofactors that enable this process 2, 3.

Due to its impact on DNA, methylation plays a role in many other fundamental functions: creating the building blocks for DNA and RNA, hormones, neurotransmitters, cell membranes, protein synthesis, and others 2, 4. Because methylation is so fundamental, B vitamin deficiency has been implicated in many chronic diseases:

Cardiovascular Disease. Folate, as well as vitamins B6 and B12, are essential for regulating the molecule homocysteine—an important risk factor for cardiovascular disease 3, 5-7. Impairment of methylation due to low levels of folate and B12 was the main cause of high homocysteine 8. Low levels of folate and B6 were associated with an increased risk of heart attack 9.

Alzheimer’s disease and depression. Deficiency of folate and vitamin B12 is known to cause impaired methylation in the central nervous system, which may lead to neurological disease and other psychiatric disorders. Studies have found that risk of developing Alzheimer’s disease and depression are higher when levels of folate and B12 were low 3, 10-12.

Neural tube defects. In pregnant mothers, folate deficiency plays an important role in the development of neural tube defects in the fetus—also due to impaired methylation 8. Folate deficiency in the mother has also been associated with lower neurological and cognitive outcomes in children 15.

Importance of active B vitamins

Inactive folic acid must first be converted into the active folate form—5-methyltetrahydrofolate (5-MTHF)—before it is usable by the body 1. However, it takes 1,300 (thirteen hundred!) times longer to convert folic acid into folate than to convert the natural folate precursors found in spinach and asparagus, and other greens 1. This means it is much easier to fulfill the body’s folate quota from real food or supplements that contain 5-MTHF.

Studies have also found 2 main issues with folic acid intake:

  1. Common dosage levels of folic acid often result in unmetabolized folic acid (UFA) collecting in the bloodstream 16. Studies have found a relationship between UFA and inhibition of immune activity, and masking of vitamin B12 deficiency 13, 17-23.
  2. A common genetic trait impairs the ability to transform folic acid into folate by up to 70% in some people 24. This increases the risk of many illnesses associated with folate deficiency, including the development of neural tube defects in the fetus during pregnancy 25.
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Bibliography

  1. Bailey SW, Ayling JE. The extremely slow and variable activity of dihydrofolate reductase in human liver and its implications for high folic acid intake. Proc Natl Acad Sci U S A. 2009;106(36):15424-9. doi:10.1073/pnas.0902072106
  2. The B Vitamins and Choline: Overview and Methods. Institute of Medicine Standing Committee on the Scientific Evaluation of Dietary Reference Intakes., 1998.
  3. Selhub J. Folate, vitamin B12 and vitamin B6 and one carbon metabolism. J Nutr Health Aging. 2001;6(1):39-42.
  4. Obeid R. The metabolic burden of methyl donor deficiency with focus on the betaine homocysteine methyltransferase pathway. Nutrients. 2013;5(9):3481-95. doi:10.3390/nu5093481
  5. Rimm EB, Willett WC, Hu FB, Sampson L, Colditz GA, Manson JE, et al. Folate and vitamin B6 from diet and supplements in relation to risk of coronary heart disease among women. JAMA. 1998;279(5):359-64.
  6. Pancharuniti N, Lewis CA, Sauberlich HE, Perkins LL, Go R, Alvarez J, et al. Plasma homocyst (e) ine, folate, and vitamin B-12 concentrations and risk for early-onset coronary artery disease. Am J Clin Nutr. 1994;59(4):940-8.
  7. Folsom AR, Nieto FJ, McGovern PG, Tsai MY, Malinow MR, Eckfeldt JH, et al. Prospective study of coronary heart disease incidence in relation to fasting total homocysteine, related genetic polymorphisms, and B vitamins. Circulation. 1998;98(3):204-10.
  8. Blom HJ, Smulders Y. Overview of homocysteine and folate metabolism. With special references to cardiovascular disease and neural tube defects. J Inherit Metab Dis. 2011;34(1):75-81. doi:10.1007/s10545-010-9177-4
  9. Verhoef P, Stampfer MJ, Buring JF, Gaziano JM, Allen RH, Stabler SP, et al. Homocysteine metabolism and risk of myocardial infarction: relation with vitamins B6, B12, and folate. Am J Epidemiol. 1996;143(9):845-59.
  10. Wang H-X, Wahlin Å, Basun H, Fastbom J, Winblad B, Fratiglioni L. Vitamin B12 and folate in relation to the development of Alzheimer’s disease. Neurology. 2001;56(9):1188-94.
  11. Tiemeier H, Van Tuijl HR, Hofman A, Meijer J, Kiliaan AJ, Breteler MM. Vitamin B12, folate, and homocysteine in depression: the Rotterdam Study. Am J Psychiatry. 2002;159(12):2099-101.
  12. Bottiglieri T. Folate, vitamin B12, and neuropsychiatric disorders. Nutr Rev. 1996;54(12):382-90.
  13. Blount BC, Mack MM, Wehr CM, MacGregor JT, Hiatt RA, Wang G, et al. Folate deficiency causes uracil misincorporation into human DNA and chromosome breakage: implications for cancer and neuronal damage. Proc Natl Acad Sci. 1997;94(7):3290-5.
  14. Zhang CX, Pan MX, Li B, Wang L, Mo XF, Chen YM, et al. Choline and betaine intake is inversely associated with breast cancer risk: A two‐stage case‐control study in China. Cancer Sci. 2013;104(2):250-8. doi:10.1111/cas.12064
  15. Valera-Gran D, Navarrete-Muñoz EM, de la Hera MG, Fernández-Somoano A, Tardón A, Ibarluzea J, et al. Effect of maternal high dosages of folic acid supplements on neurocognitive development in children at 4–5 y of age: the prospective birth cohort Infancia y Medio Ambiente (INMA) study. Am J Clin Nutr. 2017;106(3):878-87. doi:10.3945/ajcn.117.152769
  16. Kelly P, McPartlin J, Goggins M, Weir DG, Scott JM. Unmetabolized folic acid in serum: acute studies in subjects consuming fortified food and supplements. Am J Clin Nutr. 1997;65(6):1790-95.
  17. Paniz C, Bertinato JF, Lucena MR, De Carli E, da Silva Amorim PM, Gomes GW, et al. A daily dose of 5 mg folic acid for 90 days Is associated with increased serum unmetabolized folic acid and reduced natural killer cell cytotoxicity in healthy Brazilian adults. J Nutr. 2017;147(9):1677-85. doi:10.3945/jn.117.247445
  18. Troen AM, Mitchell B, Sorensen B, Wener MH, Johnston A, Wood B, et al. Unmetabolized folic acid in plasma is associated with reduced natural killer cell cytotoxicity among postmenopausal women. J Nutr. 2006;136(1):189-94.
  19. Cole BF, Baron JA, Sandler RS, Haile RW, Ahnen DJ, Bresalier RS, et al. Folic acid for the prevention of colorectal adenomas: a randomized clinical trial. Jama. 2007;297(21):2351-9.
  20. Figueiredo JC, Grau MV, Haile RW, Sandler RS, Summers RW, Bresalier RS, et al. Folic acid and risk of prostate cancer: results from a randomized clinical trial. J Natl Cancer Inst. 2009;101(6):432-35. doi:10.1093/jnci/djp019
  21. Morris MS, Jacques PF, Rosenberg IH, Selhub J. Folate and vitamin B-12 status in relation to anemia, macrocytosis, and cognitive impairment in older Americans in the age of folic acid fortification. Am J Clin Nutr. 2007;85(1):193-200.
  22. Reynolds E. Benefits and risks of folic acid to the nervous system. J Neurol Neurosurg Psychiatry. 2002;72(5):567-71.
  23. Dickinson C. Does folic acid harm people with vitamin B12 deficiency? QJM. 1995;88(5):357-64.
  24. Stern LL, Mason JB, Selhub J, Choi S-W. Genomic DNA hypomethylation, a characteristic of most cancers, is present in peripheral leukocytes of individuals who are homozygous for the C677T polymorphism in the methylenetetrahydrofolate reductase gene. Cancer Epidemiol Biomarkers Prev. 2000;9(8):849-53.
  25. Ueland PM, Hustad S, Schneede J, Refsum H, Vollset SE. Biological and clinical implications of the MTHFR C677T polymorphism. Trends Pharmacol Sci. 2001;22(4):195-201. doi:10.1016/S0165-6147(00)01675-8
MAF Supplements - Vitamin C

MAF C Complex

Our MAF C Complex is made from freeze-dried organic foods rich in vitamin C. It contains a dose of 200 mg—about as much as you’ll find in a daily fare of high-vitamin C foods. We limit the dosages for two reasons:

  1. Excessive doses of many nutrients (including vitamin C) have been found to produce negative health consequences 1-4.
  2. 100mg/day of vitamin C was found to optimally reduce chronic disease risk in healthy nonsmoking adults 5.

All the known health benefits and uses of vitamin C stem from its function as an antioxidant. It prevents organic compounds from becoming free radicals: reactive compounds that damage tissue through a process known as oxidative stress 6. Oxidative stress is implicated in a wide range of chronic diseases 6. The functions of vitamin C include:

Full-body support. The antioxidant function of vitamin C helps it support almost all aspects of body function: the immune system, genetic expression, tissue health, wound healing and many others 5, 7.

Exercise benefits. Oxidative stress is an important negative side-effect of high-intensity exercise 8. Vitamin C has been shown to reduce markers of oxidative stress after exercise 9. It has also been shown to reduce the incidence of post-exercise respiratory infections by supporting the immune system 10.

Vitamin C from food

Vitamin C in plant foods and meats is accompanied by an enormous variety of phytonutrients 11. These phytonutrients may enhance many of the effects of vitamin C, including antioxidation 12-15. They are also thought to increase its bioavailability 16.

Negatives of high-dose vitamin C

When it comes to vitamin C and other nutrients, more is not always better 4. Exposure to quantities of a nutrient far outside of the norm can have unexpected and even paradoxical effects 4. In large quantities, vitamin C can switch from being an antioxidant to having pro-oxidant effects 4. It can also interfere in exercise adaptation, and can contribute to vitamin B12 deficiency 1-3.

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Bibliography

  1. Gomez-Cabrera M-C, Domenech E, Romagnoli M, Arduini A, Borras C, Pallardo FV, et al. Oral administration of vitamin C decreases muscle mitochondrial biogenesis and hampers training-induced adaptations in endurance performance. Am J Clin Nutr. 2008;87(1):142-49.
  2. Mix JA. Do megadoses of vitamin C compromise folic acid’s role in the metabolism of plasma homocysteine? Nutr Res. 1999;19(2):161-65.
  3. Tiemeier H, Van Tuijl HR, Hofman A, Meijer J, Kiliaan AJ, Breteler MM. Vitamin B12, folate, and homocysteine in depression: the Rotterdam Study. Am J Psychiatry. 2002;159(12):2099-101.
  4. Snodgrass SR. Vitamin neurotoxicity. Mol Neurobiol. 1992;6(1):41-73.
  5. Padayatty SJ, Katz A, Wang Y, Eck P, Kwon O, Lee J-H, et al. Vitamin C as an antioxidant: evaluation of its role in disease prevention. J Am Coll Nutr. 2003;22(1):18-35.
  6. Meister A. Glutathione, ascorbate, and cellular protection. Cancer Res. 1994;54(7 Supplement):1969s-75s.
  7. Carr AC, Frei B. Toward a new recommended dietary allowance for vitamin C based on antioxidant and health effects in humans. Am J Clin Nutr. 1999;69(6):1086-107.
  8. Radak Z, Chung HY, Koltai E, Taylor AW, Goto S. Exercise, oxidative stress and hormesis. Ageing Res Rev. 2008;7(1):34-42.
  9. Alessio HM, Goldfarb AH, Cao G. Exercise-induced oxidative stress before and after vitamin C supplementation. Int J Sport Nutr. 1997;7(1):1-9.
  10. Cannon JG, Blumberg JB. Acute phase immune responses in exercise. Handbook of oxidants and antioxidants in exercise. 2000. p. 177-93.
  11. Glade MJ. Food, nutrition, and the prevention of cancer: A global perspective. american institute for cancer Research/World cancer research fund, american institute for cancer research, 1997. Nutrition. 1999;15:523-6.
  12. Lugasi A, Hóvári J, Sági KV, Bíró L. The role of antioxidant phytonutrients in the prevention of diseases. Acta Biologica Szegediensis. 2003;47(1-4):119-25.
  13. Liu RH. Potential synergy of phytochemicals in cancer prevention: mechanism of action. The Journal of nutrition. 2004;134(12):3479S-85S.
  14. Lee SH, Oe T, Blair IA. Vitamin C-induced decomposition of lipid hydroperoxides to endogenous genotoxins. Science. 2001;292(5524):2083-6.
  15. Halliwell B. Can oxidative DNA damage be used as a biomarker of cancer risk in humans? Problems, resolutions and preliminary results from nutritional supplementation studies. Free Radic Res. 1998;29(6):469-86.
  16. Vinson JA, Bose P. Comparative bioavailability to humans of ascorbic acid alone or in a citrus extract. Am J Clin Nutr. 1988;48(3):601-4.
MAF Supplements - Vitamin D+K

MAF D+K

The core of our MAF D+K supplement is vitamin D3, the most metabolically active of the D vitamins. Our formula also includes vitamin K1 and K2, magnesium, and zinc—cofactors necessary for vitamin D to perform its many functions.

Vitamin K is essential to vitamin D function: Vitamin D activity stimulates production of proteins that must be modified by vitamin K to work properly 1. Too much dietary vitamin D can reduce the activity of vitamin K 1.

Because of this, it is essential to balance intakes of both vitamins, and prevent excessive intake of dietary vitamin D 1. (While you cannot get excess Vitamin D from the sun, although excess sun exposure can be harmful for other reasons) 2.

The synergy between vitamins D, K, and their cofactors magnesium and zinc, help maintain bone health and reduce the risk of many chronic diseases, including cardiovascular disease and insulin resistance 3, 4. Vitamin D also has functions outside of its partnership with vitamin K, helping regulate and sustain mood and energy levels 5-9.

Bone health. Vitamin D regulates how calcium moves in and out of bone 1. Most studies find that supplementing with a combination of vitamin D and K increases various markers of bone health and reduces the risk of fracture 16, 17. Magnesium is also directly responsible for transporting calcium into bone tissue, while zinc helps increase bone quality 17, 18.

Cardiovascular Disease. Studies show that the combined effect of vitamins D and K can slow the progression of important indicators of cardiovascular disease, including high blood pressure, arterial thickening from atherosclerosis, and arterial calcification 3, 19.

Insulin resistance and the metabolism. Supplementation with vitamin D and K was found to reduce insulin resistance by improving the function of insulin receptors 4. Some studies also found that it helped reduce markers of oxidative stress and inflammation, related to the development of cardiovascular disease 4, 19, 20.

Athletic performance, recovery, and development. Vitamin D plays a key role in muscle function and recovery from training. It can increase the size of the fast twitch muscle fibers, and can improve athletic performance 21-23.

Mitochondrial function. Mitochondria are organelles that produce the vast majority of a cell’s energy. Vitamin K2 helps maintain normal mitochondrial function by improving the efficiency of ATP production—the cell’s main energy source 24.

Don’t forget sunlight!

Supplementing with vitamin D3 doesn’t absolve you of the need for sunlight. Vitamin D from sunlight has very different effects than dietary vitamin D (from food or supplements) 2.

When the skin receives sunlight, it produces vitamin D, which goes on to activate a mechanism known as VDR (Vitamin D Receptor) 13. This receptor activates and deactivates thousands of genes, making vitamin D play a role in various other important functions unrelated to bone health 13.

Another difference is that dietary vitamin D can produce toxicity when taken in excess 1, 2. But vitamin D from sun regulates itself: when the VDR is fully activated any excess vitamin D is immediately broken down, ensuring that levels remain healthy 2.

Here are some of the functions of vitamin D from sunlight:

Immune support and regulation. Vitamin D influences many genes that relate to the body’s immune system, some of which impact the immune response itself, and others which control the production of various antimicrobial molecules 13, 25.

Brain function: mood, cognition, and depression. Vitamin D has been shown to have important neuroprotective effects 5. Some studies show that Vitamin D can be used to enhance mood and cognitive function 6. Similarly, deficiency in the vitamin is correlated with poor mood and cognitive function, as well as seasonal affective disorder (SAD) and depression 7-9.

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Bibliography

  1. van Ballegooijen AJ, Pilz S, Tomaschitz A, Grübler MR, Verheyen N. The synergistic interplay between vitamins D and K for bone and cardiovascular health: A narrative review. Intl J Endocrinol. 2017;2017. doi:10.1155/2017/7454376
  2. Holick MF. Photobiology, metabolism, mechanism of action, and clinical applications. Primer on the Metabolic Bone Diseases an Disorders of Bone Mineral Metabolism. 1996.
  3. van Ballegooijen AJ, Cepelis A, Visser M, Brouwer IA, van Schoor NM, Beulens JW. Joint association of low vitamin D and vitamin K status with blood pressure and hypertension: novelty and significance. Hypertension. 2017;69(6):1165-72. doi:10.1161/HYPERTENSIONAHA.116.08869
  4. Karamali M, Ashrafi M, Razavi M, Jamilian M, Kashanian M, Akbari M, et al. The effects of calcium, vitamins D and K co-supplementation on markers of insulin metabolism and lipid profiles in vitamin D-deficient women with polycystic ovary syndrome. Exp Clin Endocrinol Diabetes. 2017. doi:10.1055/s-0043-104530
  5. Garcion E, Wion-Barbot N, Montero-Menei CN, Berger F, Wion D. New clues about vitamin D functions in the nervous system. Trends Endocrinol Metab. 2002;13(3):100-5.
  6. Lansdowne AT, Provost SC. Vitamin D3 enhances mood in healthy subjects during winter. Psychopharmacology. 1998;135(4):319-23.
  7. Wilkins CH, Sheline YI, Roe CM, Birge SJ, Morris JC. Vitamin D deficiency is associated with low mood and worse cognitive performance in older adults. Am J Geriatr Psychiatry. 2006;14(12):1032-40.
  8. Berk M, Sanders KM, Pasco JA, Jacka FN, Williams LJ, Hayles AL, et al. Vitamin D deficiency may play a role in depression. Med Hypotheses. 2007;69(6):1316-9.
  9. Anglin RE, Samaan Z, Walter SD, McDonald SD. Vitamin D deficiency and depression in adults: systematic review and meta-analysis. Br J Psychiatry. 2013;202(2):100-7. doi:10.1192/bjp.bp.111.106666
  10. Garland C, Garland F, Shaw E, Comstock G, Helsing K, Gorham E. Serum 25-hydroxyvitamin D and colon cancer: eight-year prospective study. Lancet. 1989;334(8673):1176-8.
  11. Bertone-Johnson ER, Chen WY, Holick MF, Hollis BW, Colditz GA, Willett WC, et al. Plasma 25-hydroxyvitamin D and 1, 25-dihydroxyvitamin D and risk of breast cancer. Cancer Epidemiol Biomarkers Prev. 2005;14(8):1991-7.
  12. Ahonen MH, Tenkanen L, Teppo L, Hakama M, Tuohimaa P. Prostate cancer risk and prediagnostic serum 25-hydroxyvitamin D levels (Finland). Cancer Causes Control. 2000;11(9):847-52.
  13. Marshall TG. Vitamin D discovery outpaces FDA decision making. Bioessays. 2008;30(2):173-82. doi:10.1002/bies.20708
  14. Deeb KK, Trump DL, Johnson CS. Vitamin D signalling pathways in cancer: potential for anticancer therapeutics. Nat Rev Cancer. 2007;7(9):684-700.
  15. Berwick M, Armstrong BK, Ben-Porat L, Fine J, Kricker A, Eberle C, et al. Sun exposure and mortality from melanoma. J Natl Cancer Inst. 2005;97(3):195-99.
  16. Je SH, Joo N-S, Choi B-h, Kim K-M, Kim B-T, Park S-B, et al. Vitamin K supplement along with vitamin D and calcium reduced serum concentration of undercarboxylated osteocalcin while increasing bone mineral density in Korean postmenopausal women over sixty-years-old. Korean Med Sci. 2011;26(8):1093-98. doi:10.3346/jkms.2011.26.8.1093
  17. Iwamoto J, Takeda T, Ichimura S. Effect of combined administration of vitamin D3 and vitamin K2 on bone mineral density of the lumbar spine in postmenopausal women with osteoporosis. J Orthop Sci 2000;5(6):546-51.
  18. Amizuka N, Li M, Maeda T. The interplay of magnesium and vitamin K2 on bone mineralization. Clin Calcium. 2005;15(7):57-61.
  19. Mozos I, Stoian D, Luca CT. Crosstalk between Vitamins A, B12, D, K, C, and E Status and Arterial Stiffness. Dis Markers. 2017;2017(8784971). doi:10.1155/2017/8784971
  20. Yoshida M, Jacques PF, Meigs JB, Saltzman E, Shea MK, Gundberg C, et al. Effect of vitamin K supplementation on insulin resistance in older men and women. Diabetes Care. 2008;31(11):2092-6. doi:10.2337/dc08-1204
  21. Owens DJ. The role of vitamin D in skeletal muscle function and regeneration: Liverpool John Moores University; 2015.
  22. Owens DJ, Sharples AP, Polydorou I, Alwan N, Donovan T, Tang J, et al. A systems-based investigation into vitamin D and skeletal muscle repair, regeneration, and hypertrophy. Am J Physiol – Endocrinol and Metabol. 2015;309(12):E1019-E31. doi:10.1152/ajpendo.00375.2015
  23. Cannell JJ, Hollis BW, Sorenson MB, Taft TN, Anderson JJ. Athletic performance and vitamin D. Med Sci Sports Exerc. 2009;41(5):1102-10. doi:10.1249/MSS.0b013e3181930c2b
  24. Vos M, Esposito G, Edirisinghe JN, Vilain S, Haddad DM, Slabbaert JR, et al. Vitamin K2 is a mitochondrial electron carrier that rescues pink1 deficiency. Science. 2012;336(6086):1306-10. doi:10.1126/science.1218632
  25. Wang T-T, Nestel FP, Bourdeau V, Nagai Y, Wang Q, Liao J, et al. Cutting edge: 1, 25-dihydroxyvitamin D3 is a direct inducer of antimicrobial peptide gene expression. J Immunol. 2004;173(5):2909-12.

Dr. Phil Maffetone

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The MAF supplement lines were formulated by Dr. Phil Maffetone based on over 40 years of clinical experience and scientific research in the fields of health, fitness, and human development. Dr. Maffetone is a well-respected author and innovator. Over the course of his career he has published over 20, formulated several lines of healthy dietary supplements, and developed many other products.

Dr. Phil Maffetone
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