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vitamin d deficiency

  • Which supplements should people take to help promote good health, and at what doses? Vitamins? Minerals? Herbs? Nutraceuticals? Perhaps the best answer is before experimenting with exotic dietary supplement ingredients, it first makes sense to start out with the three dietary supplements that everyone should be taking. This includes a multivitamin, vitamin D and omega- fatty acids.


    There is a good case for the daily use of a multivitamin, as a nutrition insurance policy that helps to fill in the gaps for those nutrients people may not be getting in their diet. Furthermore, in a study1 of 90,771 men and women, the regular use of a multivitamin was found to significantly improve adequate intake of nutrients compared to non-users. Also, research2 found that multivitamin supplements are generally well tolerated, do not increase the risk of mortality, cerebrovascular disease, or heart failure, and their use likely outweighs any risk in the general population (and may be particularly beneficial for older people). So, the bottom line is that multivitamins really do work as a nutrition insurance policy.

    Other multivitamin benefits
    In addition to functioning as a nutrition insurance policy, the daily use of a multivitamin may offer other benefits as well.

    Cardiovascular Disease
    A 12-week, randomized, placebo-controlled study3 of 182 men and women (24 to 79 years) found that a multivitamin was able to lower homocysteine levels and the oxidation of LDLcholesterol—both of which are highly beneficial in reducing the risk for cardiovascular disease. Other multivitamin research4 has also demonstrated effectiveness in lowering homocysteine levels.

    A 6-month, randomized, double-blind, placebo-controlled study5 of 87 men and women (30 to 70 years) found that multivitamin use was associated with lower levels of C-reactive protein, a measurement of inflammation associated with cardiovascular disease and other degenerative diseases. Other multivitamin research6 in women has shown similar results.

    A Swedish, population-based, case-control study7 of 1296 men and women (45 to 70 years) who previously had a heart attack and 1685 healthy men and women as controls, found those using a multivitamin were less likely to have a heart attack. Other multivitamin research8 in Swedish women has shown similar results.

    A large-scale, randomized, double-blind, placebo-controlled study9 was conducted with 14,641 male U.S. physicians initially 50 years or older, including 1312 men with a history of cancer, to determine the long-term effects of multivitamin supplementation on the incidence of various types of cancers. Results showed that during a median follow-up of 11.2 years, men with a history of cancer who took a daily multivitamin had a statistically significant reduction in the incidence of total cancer compared to those taking a placebo.

    A human clinical study10 with 96 healthy men (18 to 46 years) examined the effect of multivitamin supplementation in relation to plasma interleukin-6 (IL-6, a pro-inflammatory chemical produced by the body) and anger, hostility, and severity of depressive symptoms. The results showed that plasma IL-6 was associated with anger, hostility, and severity of depressive symptoms, and that multivitamin use was associated with lower plasma IL-6 levels.

    A review11 of the scientific literature indicated that patients complaining of fatigue, tiredness, and low energy levels may have low levels of vitamins and minerals. Certain risk groups like the elderly and pregnant women were identified, as was the role of B-vitamins in energy metabolism. Results found that supplementation with nutrients including B-vitamins (e.g., a multivitamin) can alleviate deficiencies, but supplements must be taken for an adequate period of time.

    A meta-analysis12 of eight randomized and placebo-controlled studies evaluated the influence of diet supplementation on stress and mood. Results showed that supplementation reduced the levels of perceived stress, mild psychiatric symptoms, anxiety, fatigue, and confusion. Supplements containing high doses of B-vitamins (e.g., multivitamins) may be more effective in improving mood states.

    At the ends of our chromosomes are stretches of DNA called telomeres. These telomeres protect our genetic data, making it possible for cells to divide. Each time a cell divides, telomeres get shorter. When they get too short, the cell can no longer divide and becomes inactive or "senescent" or dies. This process is associated with aging. In a cross-sectional analysis of data from 586 women (35 to 74 years), multivitamin use was assessed, and relative telomere length was measured. The results were that multivitamin use was significantly associated with longer telomeres. Compared with nonusers, the relative telomere length was on average 5.1 percent longer among daily multivitamin users. It is possible, therefore, that multivitamins may help us live longer.


    Vitamin D is the "sunshine vitamin," so coined because exposure to the sun's ultraviolet light will convert a form of cholesterol under the skin into vitamin D. This nutrient is best known for its role in helping to facilitate the absorption of calcium and phosphorus (as well as magnesium), and so helping to promote bone health.13 Over the past decade, however, research on vitamin D has identified numerous other roles it plays in human health and wellness, which includes:

    • Inhibiting the uncontrolled proliferation of cells (as in the case of cancer) and stimulating the differentiation of cells (specialization of cells for specific functions).14
    • Helping prevent cancers of the prostate and colon.15,16
    • Functioning as a potent immune system modulator.17,18
    • Helping prevent autoimmune reactions.19,20,21
    • Helping improve insulin secretion.22,23,24
    • Decreasing the risk of high blood pressure via the reninangiotensin system's regulation of blood pressure.25
    • Reducing osteoporotic fractures.26,27,28
    • Reducing the incidence of falls in older adults.29,30
    • Reducing the risk of developing premenstrual syndrome (PMS).31
    • Reducing the prevalence of depression, especially in the elderly.32
    • Reducing the prevalence of urinary infections and lower urinary tract symptoms (e.g., benign prostatic hyperplasia or BPH).33

    Vitamin D deficiency and insufficiency
    Outright vitamin D deficiency is present in 41.6 percent of the U.S. population,34 while vitamin D insufficiency (i.e., lacking sufficient vitamin D) is present in 77 percent of the world's population.35 If you are deficient in vitamin D you will not be able to absorb enough calcium to satisfy your body's calcium needs.36 It has long been known that severe vitamin D deficiency has serious consequences for bone health, but other research indicates that lesser degrees of vitamin D deficiency are common and increase the risk of osteoporosis and other health problems.37,38

    Vitamin D sufficiency is measured by serum 25-hydroxyvitamin D levels in the body.39 Laboratory reference ranges for serum 25-hydroxyvitamin D levels are based upon average values from healthy populations. However, recent research examining the prevention of secondary hyperparathyroidism and bone loss suggest that the range for healthy 25-hydroxyvitamin D levels should be considerably higher. Based upon the most current research, here are the ranges for serum 25-hydroxyvitamin D values:

    • Less than 20–25 nmol/L: Indicates severe deficiency associated with rickets and osteomalacia.40,41
    • 50–80 nmol/L: Previously suggested as normal range.42
    • 75–125 nmol/L: More recent research suggests that parathyroid hormone43,44 and calcium absorption45 are optimized at this level; this is a healthy range.46

    Based upon the 75–125 nmol/L range, it is estimated that one billion people in the world are currently vitamin D deficient.47 Furthermore, research indicates that supplementation with at least 800–1,000 IU daily are required to achieve serum 25-hydroxyvitamin D levels of at least 80 nmol/L.48,49 Furthermore, there are many groups of individuals who currently are at risk for vitamin D deficiency. These include:

    • Exclusively breast-fed infants: Especially if they do not receive vitamin D supplementation and if they have dark skin and/or receive little sun exposure.50
    • Dark skin: People with dark-colored skin synthesize less vitamin D from sunlight than those with light-colored skin.51 In a U.S. study, 42 percent of African American women were vitamin D deficient compared to four percent of white women.52
    • The Elderly: When exposed to sunlight have reduced capacity to synthesize vitamin D.53
    • Those using sunscreen: Applying sunscreen with an SPF factor of eight reduces production of vitamin D by 95 percent.54
    • Those with fat malabsorption syndromes: The absorption of dietary vitamin D is reduced in Cystic fibrosis and cholestatic liver disease.55
    • Those with inflammatory bowel disease: An increased risk of vitamin D deficiency occurs in those with inflammatory bowel disease like Crohn's disease.56
    • Obese individuals: Obesity increases the risk of vitamin D deficiency.57

    Vitamin D2 and D3
    There are two forms of vitamin D available as a dietary supplement: cholecalciferol (vitamin D3) and ergocalciferol (vitamin D2). Cholecalciferol is the form made in the human body, and it is more active than ergocalciferol. In fact, Vitamin D2 potency is less than one third that of vitamin D3.58

    Commercially, ergocalciferol is derived from yeast, and so is considered vegetarian, while cholecalciferol is commonly derived from lanolin (from sheep) or fish oil—although a vegetarian D3 derived from lichen is available.

    Ideal dosing for vitamin D
    The Linus Pauling Institute recommends that generally healthy adults take 2,000 IU of supplemental vitamin D daily.59 The Vitamin D Council states that if well adults and adolescents regularly avoid sunlight exposure, then it is necessary to supplement with at least 5,000 IU of vitamin D daily.60 The Council for Responsible Nutrition recommends 2,000 IU daily for adults.61 Taking a conservative position, at least 2,000 IU of vitamin makes sense for adults.

    Chemically, a fatty acid is an organic acid that has an acid group at one end of its molecule, and a methyl group at the other end.62 Fatty acids are typically categorized in the omega groups 3, 6 and 9 according to the location of their first double bond (there's also an omega 7 group, but these are less important to human health).63 The body uses fatty acids for the formation of healthy cell membranes, the proper development and functioning of the brain and nervous system, and for the production of hormone-like substances called eicosanoids (thromboxanes, leukotrienes, and prostaglandins). These chemicals regulate numerous body functions including blood pressure, blood viscosity, vasoconstriction, immune and inflammatory responses.64

    Deficiency of omega-3 fatty acids
    While omega-3, 6 and 9 fatty acids are all important for different reasons, it is the omega-3 fatty acids (O3FA) that are currently particularly critical—and specifically the O3FA known as eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA). The reason for this current importance is that Western diets are deficient in O3FA, and have excessive amounts of omega-6 fatty acids. While human beings evolved on a diet with approximately a 1:1 ratio of omega-6 to omega-3 fatty acids (EFA), the current Western diet provides about a 16:1 ratio.65 As a matter of fact, a recent Harvard School of Public Health study indicates that Omega-3 deficiency causes 96,000 U.S. deaths per year.66 Other research has clearly shown that excessive amounts of omega-6 fatty acids and a very high omega-6 to omega-3 ratio, as is found in today's Western diets, promote many diseases, including cardiovascular disease, cancer, and inflammatory and autoimmune diseases, whereas increased levels of omega-3 (a low omega-6 to omega-3 ratio) exert protective effects.67

    Benefits of omega-3 fatty acids

    O3FA offer a broad range of benefits in human health. These benefits are listed below categorically:

    Cardiovascular Health
    In several studies O3FA have been shown to help lower triglyceride levels.68 In fact, the FDA has even approved an O3FA product for this purpose.69 Individually, EPA and DHA also have triglyceride-lowering properties. Consuming 1 gram/day of fish oils from fish (about 3 ounces of fatty fish such as salmon) or fish oil supplements has a cardioprotective effect.70

    Evidence suggests increased consumption of O3FA from fish or fish-oil supplements, but not of alpha-linolenic acid, reduces the rates of all-cause mortality, cardiac and sudden death, and possibly stroke.71 Higher consumption of fish and O3FA has been associated with a lower risk of coronary heart disease.72,73 Clinical research shows that DHA supplementation helps increase HDL cholesterol levels (the "good cholesterol").74,75 Supplementation with fish oil produces modest, but significant reductions in systolic and diastolic blood pressure in patients with mild hypertension.76,77,78

    O3FA have been shown to help relieve inflammation caused by a variety of factors.79,80


    Research81 has demonstrated that fish oil supplementation is effective in the treatment of rheumatoid arthritis.

    Clinical research shows that taking supplements with 500 mg EPA, three times daily, modestly but significantly reduces the frequency of hot flashes compared to placebo in menopausal women.82

    Research has shown children with attention deficit/hyperactive disorder (ADHD) may have low plasma levels of EPA and DHA.83,84 Clinical research suggests that supplementation with DHA might improve aggression and social relationships in ADHD children.85

    Macular degeneration
    Increased dietary consumption of DHA is associated with reducing the risk of macular degeneration.86

    Alzheimer's Disease
    Participants who consumed fish once per week or more had 60 percent less risk of Alzheimer's disease compared with those who rarely or never ate fish, and this was attributed to the DHA content of the fish.87

    The sources of omega-3 fatty acids

    To begin with, the overwhelming majority of research on the health benefits of supplementation with O3FA has been conducted using fish oil products. Consequently, a strong argument can be made that fish oil supplements are the preferred source of O3FA. Amongst these, the primary fish used commercially as the source from which O3FA are derived include mackerel, herring, tuna, halibut, salmon and cod liver.88 Although some fish are touted as superior over others as sources for supplemental fish oil, it is the opinion of this author that they all provide acceptable sources of omega-3s. Still, there are other sources of O3FA besides fish oil. This includes squid, krill, flax seed oil and algae oil.

    Squid-derived O3FA are derived from by-products of squid that are usually discarded when squid are commercially fished, and provides a much higher concentration of DHA (up to 50 percent) than do fish oil. However, there is a lack of human clinical data on squid-source O3FA, although they likely will have similar effects as fish oil.

    Krill oil derived from the shrimp-like crustacean know as krill contain significant amounts of the EPA and DHA omega-3 fatty acids, as well as phospholipids (e.g., phosphatidylcholine),89 vitamin A, vitamin E and astaxanthin, a powerful carotenoid antioxidant.90,91 Human clinical research92 has shown that krill oil has greater absorption than fish oil—although krill provides significantly less EPA/DHA per gram than fish oil.

    Flaxseed oil contains about 52–55 percent omega-3s, but as alpha-linolenic acid (ALA), not EPA/DHA.93 This is significant since ALA has to be converted to EPA and DHA before it will provide the much-touted health benefits attributed to O3FA. This is problematic since studies indicate that in men approximately eight percent of ALA is converted to EPA and 0–4 percent is converted to DHA.94 In women, approximately 21 percent of dietary ALA is converted to EPA and nine percent is converted to DHA.95 This is not to say that flaxseed oil has no value. It does, but just not as significant a value as fish oil.

    Algae oil
    Certain algae extracts provide a vegetarian source of O3FA—but in this case the O3FA are EPA and DHA, not ALA. Consequently, for vegetarians, algae oil is a viable substitute for fish oil. That being said, human clinical research on algae oil sources of O3FA is limited, and the cost is far more than fish oil.


    1. Murphy SP, White KK, Park SY, Sharma S. Multivitamin-multimineral supplements' effect on total nutrient intake. Am J Clin Nutr. 2007 Jan;85 (1):280S–4S.
    2. Ward E. Addressing nutritional gaps with multivitamin and mineral supplements. Nutr J.2014 Jul 15;13(1):72. 43 Earnest CP, Wood KA, Church TS.
    3. Complex Multivitamin Supplementation Improves Homocysteine and Resistance to LDL-C Oxidation. J Am Coll Nutr. 2003;22(5):400–7.
    4. den Heijer M, Brouwer IA, Bos GM, et al. Vitamin supplementation reduces blood homocysteine levels: a controlled trial in patients with venous thrombosis and healthy volunteers. Arterioscler Thromb Vasc Biol. 1998 Mar;18(3):356–61.
    5. Church TS, Earnest CP, Wood KA. James B. Kampert. Reduction of C-Reactive Protein Levels Through Use of a Multivitamin. Am J Med. 2003;115:702–7.
    6. Wang C, Li Y, Zhu K, Dong YM, Sun CH. Effects of supplementation with multivitamin and mineral on blood pressure and C-reactive protein in obese Chinese women with increased cardiovascular disease risk. Asia Pac J Clin Nutr. 2009;18(1):121–30.
    7. Holmquist C, Larsson S, Wolk A, de Faire U. Multivitamin Supplements Are Inversely Associated with Risk of Myocardial Infarction in Men and Women— Stockholm Heart. Epidemiology Program (SHEEP). J Nutr.2003;133: 2650–4.
    8. Rautiainen S, Akesson A, Levitan EB, Morgenstern R, Mittleman MA, Wolk A. Multivitamin use and the risk of myocardial infarction: a population-based cohort of Swedish women. Am J Clin Nutr. 2010 Nov;92(5):1251–6.
    9. Gaziano JM, Sesso HD, Christen WG, Bubes V, Smith JP, MacFadyen J, Schvartz M, Manson JE, Glynn RJ, Buring JE. Multivitamins in the prevention of cancer in men: the Physicians' Health Study II randomized controlled trial. JAMA. 2012 Nov 14;308(18):1871–80.
    10. Suarez EC. Plasma interleukin-6 is associated with psychological coronary risk factors: moderation by use of multivitamin supplements. Brain Behav Immun. 2003 Aug;17(4):296–303.
    11. Huskisson E, Maggini S, Ruf M. The role of vitamins and minerals in energy metabolism and well-being. J Int Med Res. 2007 May–Jun;35(3):277–89.
    12. Long SJ, Benton D. Effects of vitamin and mineral supplementation on stress, mild psychiatric symptoms, and mood in nonclinical samples: a metaanalysis. Psychosom Med. 2013 Feb;75(2):144–53.
    13. Holick MF. Vitamin D: importance in the prevention of cancers, type 1 diabetes, heart disease, and osteoporosis. Am J Clin Nutr. 2004;79(3):362–71.
    14. Ibid.
    15. Lin R, White JH. The pleiotropic actions of vitamin D. Bioessays. 2004; 26(1):21–8.
    16. Gorham ED, Garland CF, Garland FC, et al. Vitamin D and prevention of colorectal cancer. J Steroid Biochem Mol Biol. 2005;97(1-2):179–94.
    17. Griffin MD, Xing N, Kumar R. Vitamin D and its analogs as regulators of immune activation and antigen presentation. Annu Rev Nutr. 2003;23:117–45.
    18. Hayes CE, Nashold FE, Spach KM, Pedersen LB. The immunological functions of the vitamin D endocrine system. Cell Mol Biol. 2003;49(2):277–300.
    19. Ibid.
    20. Munger KL, Zhang SM, O'Reilly E, et al. Vitamin D intake and incidence of multiple sclerosis. Neurology 2004;62:60–5.
    21. Merlino LA, Curtis J, Mikuls TR, et al. Vitamin D intake is inversely associated with rheumatoid arthritis. Arthritis Rheum 2004;50:72–7.
    22. Zeitz U, Weber K, Soegiarto DW, Wolf E, Balling R, Erben RG. Impaired insulin secretory capacity in mice lacking a functional vitamin D receptor. FASEB J. 2003;17(3):509–11.
    23. Borissova AM, Tankova T, Kirilov G, Dakovska L, Kovacheva R. The effect of vitamin D3 on insulin secretion and peripheral insulin sensitivity in type 2 diabetic patients. Int J Clin Pract. 2003;57(4):258–61.
    24. Inomata S, Kadowaki S, Yamatani T, Fukase M, Fujita T. Effect of 1 alpha (OH)-vitamin D3 on insulin secretion in diabetes mellitus. Bone Miner. 1986;1(3):187–192.
    25. Li YC, Kong J, Wei M, Chen ZF, Liu SQ, Cao LP. 1,25-Dihydroxyvitamin D(3) is a negative endocrine regulator of the renin-angiotensin system. J Clin Invest. 2002;110(2):229–38.
    26. Feskanich D, Willett WC, Colditz GA. Calcium, vitamin D, milk consumption, and hip fractures: a prospective study among postmenopausal women. Am J Clin Nutr. 2003;77(2):504–511.
    27. Bischoff-Ferrari HA, Willett WC, Wong JB, Giovannucci E, Dietrich T, Dawson-Hughes B. Fracture prevention with vitamin D supplementation: a meta-analysis of randomized controlled trials. JAMA. 2005;293(18):2257–64.
    28. Bischoff-Ferrari HA, Giovannucci E, Willett WC, Dietrich T, Dawson-Hughes B. Estimation of optimal serum concentrations of 25-hydroxyvitamin D for multiple health outcomes. Am J Clin Nutr. 2006;84(1):18–28.
    29. Bischoff-Ferrari HA, Dawson-Hughes B, Willett WC, et al. Effect of Vitamin D on falls: a meta-analysis. JAMA 2004;291:1999–2006.
    30. Bischoff HA, Stahelin HB, Dick W, et al. Effects of vitamin D and calcium supplementation on falls: a randomized controlled trial. J Bone Miner Res 2003;18:343–51.
    31. Bertone-Johnson ER, Hankinson SE, Bendich A, et al. Calcium and vitamin D intake and risk of incident premenstrual syndrome. Arch Intern Med 2005;165:1246–52.
    32. Hoogendijk WJG, Lips P, Dik MG, Deeg DJH, Beekman ATF, Penninx BWJH. Depression Is Associated With Decreased 25-Hydroxyvitamin D and Increased Parathyroid Hormone Levels in Older Adults. Archives of General Psychiatry 2008; 65(5):495.
    33. Vaughan CP, Johnson TM 2nd, Goode PS, Redden DT, Burgio KL, Markland AD. Vitamin D and lower urinary tract symptoms among US men: results from the 2005–2006 National Health and Nutrition Examination Survey. Urology. 2011 Dec;78(6):1292–7.
    34. Forrest KY, Stuhldreher WL. Prevalence and correlates of vitamin D deficiency in US adults. Nutr Res. 2011;31(1):48–54.
    35. Ginde AA, Liu MC, Camargo CA Jr. Demographic differences and trends of vitamin D insufficiency in the US population, 1988-2004. Arch Intern Med. 2009;169:626–32.
    36. Holick MF. Vitamin D: A millenium perspective. J Cell Biochem. 2003;88(2):296–307.
    37. Heaney RP. Long-latency deficiency disease: insights from calcium and vitamin D. Am J Clin Nutr. 2003;78(5):912–9.
    38. Zittermann A. Vitamin D in preventive medicine: are we ignoring the evidence? Br J Nutr. 2003;89(5):552–72.
    39. Wharton B, Bishop N. Rickets. Lancet. 2003;362(9393):1389–1400. 40 Heaney RP. Long-latency deficiency disease: insights from calcium and vitamin D. Am J Clin Nutr. 2003;78(5):912–919.
    40. Ibid. 79
    41. Malabanan A, Veronikis IE, Holick MF. Redefining vitamin D insufficiency. Lancet. 1998;351(9105):805–6.
    42. Chapuy MC, Preziosi P, Maamer M, et al. Prevalence of vitamin D insufficiency in an adult normal population. Osteoporos Int. 1997;7(5):439–43.
    43. Thomas MK, Lloyd-Jones DM, Thadhani RI, et al. Hypovitaminosis D in medical inpatients. N Engl J Med. 1998;338(12):777–83.
    44. Heaney RP, Dowell MS, Hale CA, Bendich A. Calcium absorption varies within the reference range for serum 25-hydroxyvitamin D. J Am Coll Nutr. 2003;22(2):142–6.
    45. Holick MF. Vitamin D deficiency: what a pain it is. Mayo Clin Proc. 2003;78(12):1457–9.
    46. Holick MF. Vitamin D deficiency. N Engl J Med. 2007;357(3):266–281.
    47. Vieth R. Vitamin D supplementation, 25-hydroxyvitamin D concentrations, and safety. Am J Clin Nutr. 1999;69(5):842–56.
    48. Tangpricha V, Koutkia P, Rieke SM, Chen TC, Perez AA, Holick MF. Fortification of orange juice with vitamin D: a novel approach for enhancing vitamin D nutritional health. Am J Clin Nutr. 2003;77(6):1478–83.
    49. Wagner CL, Greer FR, and the Section on Breastfeeding and Committee on Nutrition. Prevention of rickets and vitamin D deficiency in infants, children, and adolescents. American Academy of Pediatrics. 2008;122(5):1142–52.
    50. Ibid. 53
    51. Nesby-O'Dell S, Scanlon KS, Cogswell ME, et al. Hypovitaminosis D prevalence and determinants among African American and white women of reproductive age: third National Health and Nutrition Examination Survey, 1988-1994. Am J Clin Nutr. 2002;76(1):187–92.
    52. Harris SS, Soteriades E, Coolidge JA, Mudgal S, Dawson-Hughes B. Vitamin D insufficiency and hyperparathyroidism in a low income, multiracial, elderly population. J Clin Endocrinol Metab. 2000;85(11):4125–30.
    53. Ibid. 53
    54. Food and Nutrition Board, Institute of Medicine. Vitamin D. Dietary Reference Intakes: Calcium, Phosphorus, Magnesium, Vitamin D, and Fluoride. Washington D.C.: National Academies Press; 1999:250–87.
    55. Jahnsen J, Falch JA, Mowinckel P, Aadland E. Vitamin D status, parathyroid hormone and bone mineral density in patients with inflammatory bowel disease. Scand J Gastroenterol. 2002;37(2):192–9.
    56. Arunabh S, Pollack S, Yeh J, Aloia JF. Body fat content and 25-hydroxyvitamin D levels in healthy women. J Clin Endocrinol Metab. 2003;88(1):157–161.
    57. Armas LA, Hollis BW, Heaney RP. Vitamin D2 is much less effective than vitamin D3 in humans. J Clin Endocrinol Metab. 2004;89(11):5387–91.
    58. Higdon J, Drake VJ, DeLuca HF.Vitamin D. The Linus Pauling Institute Micronutrient Information Center 2000–2010; Last updated 11/30/10. Retrieved December 6, 2010 from
    59. Understanding Vitamin D Cholecalciferol. The Vitamin D Council, n.d., Retrieved December 6, 2010 from
    60. CRN Reacts to Institute of Medicine DRI Recommendations for Vitamin D. November 30, 2010. Retrieved December 6, 2010 from
    61. Whitney EN, Cataldo CB, Rolfes SR. Understanding Normal and Clinical Nutrition, 5th ed. Belmont, CA:West/Wadsworth; 1998:141–75.
    62. Jones PJH, Papamandjaris AA. "Chapter 10 - Lipids: Cellular Metabolism" IN Present Knowledge in Nutrition, 8th ed. Bowman BA, Russell RM (eds). Washington, DC: ILSI Press; 2001:104–14
    63. Davis B. Essential Fatty Acids in Vegetarian Nutrition. Andrews University Nutrition Department. Accessed August 18, 2005 from
    64. Simopoulos AP. The importance of the ratio of omega-6/omega-3 essential fatty acids. Biomed Pharmacother. 2002;56(8):365–79.
    65. Danaei G, Ding EL, Mozaffarian D, et al. The Preventable Causes of Death in the United States: Comparative Risk Assessment of Dietary, Lifestyle, and Metabolic Risk Factors. PLoS Med. 2009 Apr 28;6(4):e1000058.
    66. Ibid. 105
    67. Harris WS. n-3 fatty acids and serum lipoproteins: human studies. Am J Clin Nutr. 1997;65(5 Suppl):1645S–54S.
    68. Lovaza: Omega-3 Acid Ethyl Esters. Retrieved August 6, 2009 from
    69. Kris-Etherton PM, Harris WS, Appel LJ. Fish consumption, fish oil, omega-3 fatty acids, and cardiovascular disease. Circulation. 2002;106(21):2747–57.
    70. Wang C, Harris WS, Chung M, et al. n-3 Fatty acids from fish or fish-oil supplements, but not alpha-linolenic acid, benefit cardiovascular disease outcomes in primary- and secondary-prevention studies: a systematic review. Am J Clin Nutr. 2006;84(1):5–17.
    71. Hu FB, Bronner L, Willett WC, et al. Fish and omega-3 fatty acid intake and risk of coronary heart disease in women. JAMA. 2002;287(14):1815–21.
    72. Jarvinen R, Knekt P, Rissanen H, Reunanen A. Intake of fish and long-chain n-3 fatty acids and the risk of coronary heart mortality in men and women. Br J Nutr. 2006;95(4):824–9.
    73. Agren JJ, Hanninen O, Julkunen A, et al. Fish diet, fish oil and docosahexaenoic acid rich oil lower fasting and postprandial plasma lipid levels. Eur J Clin Nutr 1996;50:765–71.
    74. Mori TA, Burke V, Puddey IB, et al. Purified eicosapentaenoic and docosahexaenoic acids have differential effects on serum lipids and lipoproteins, LDL particle size, glucose, and insulin in mildly hyperlipidemic men. Am J Clin Nutr 2000;71:1085–94.
    75. Prisco D, Paniccia R, Bandinelli B, et al. Effect of medium-term supplementation with a moderate dose of n-3 polyunsaturated fatty acids on blood pressure in mild hypertensive patients. Thromb Res 1998;1:105–12.
    76. Toft I, Bonaa KH, Ingebretsen OC, et al. Effects of n-3 polyunsaturated fatty acids on glucose homeostasis and blood pressure in essential hypertension. A randomized, controlled trial. Ann Intern Med 1995;123:911–8.
    77. Yosefy C, Viskoper JR, Laszt A, et al. The effect of fish oil on hypertension, plasma lipids and hemostasis in hypertensive, obese, dyslipidemic patients with and without diabetes mellitus. Prostaglandins Leukot Essent Fatty Acids 1999;61:83–7.
    78. Wall R, Ross RP, Fitzgerald GF, Stanton C. Fatty acids from fish: the anti-inflammatory potential of long-chain omega-3 fatty acids. Nutr Rev. 2010;68(5):280–9.
    79. Calder PC. n-3 polyunsaturated fatty acids, inflammation, and inflammatory diseases. Am J Clin Nutr. 2006;83:1505S–19S.
    80. Fortin PR, Lew RA, Liang MH, et al. Validation of a meta-analysis: the effects of fish oil in rheumatoid arthritis. J Clin Epidemiol. 1995;48(11):1379–90.
    81. Lucas M, Asselin G, Merette C, et al. Effects of ethyl-eicosapentaenoic acid omega-3 fatty acid supplementation on hot flashes and quality of life among middle-aged women: a double-blind, placebo-controlled, randomized clinical trial. Menopause. 2009;16:357–66.
    82. Stevens LJ, Zentall SS, Deck JL, et al. Essential fatty acid metabolism in boys with attention-deficit hyperactivity disorder. Am J Clin Nutr. 1995;62:761–8.
    83. Voigt RG, Llorente AM, Jensen CL, et al. A randomized, double-blind, placebo-controlled trial of docosahexaenoic acid supplementation in children with attention-deficit/hyperactivity disorder. J Pediatr. 2001;139:189–6.
    84. Hamazaki T, Hirayama S. The effect of docosahexaenoic acid-containing food administration on symptoms of attention-deficit/hyperactivity disorder-a placebo-controlled double-blind study. Eur J Clin Nutr. 2004;58:838.
    85. Cho E, Hung S, Willet W, et al. Prospective study of dietary fat and the risk of age-related macular degeneration. Am J Clin Nutr. 2001;73:209–18.
    86. Morris MC, Evans DA, Bienias JL, et al. Consumption of fish and n-3 fatty acids and risk of incident Alzheimer disease. Arch Neurol. 2003;60:940–6.
    87. MedlinePlus. Fish Oil. U.S. National Library of Medicine. Last reviewed–12/10/2011.
    88. Bottino NR. Lipid composition of two species of Antarctic krill: Euphausia superba and E. crystallorophias. Comp Biochem Physiol B 1975;50:479–84.
    89. Ibid.
    90. Dunlap WC, Fujisawa A, Yamamoto Y, et al. Notothenioid fish, krill and phytoplankton from Antarctica contain a vitamin E constituent (alphatocomonoenol) functionally associated with cold-water adaptation. Comp Biochem Physiol B Biochem Mol Biol 2002;133:299–305.
    91. Ulven SM, Kirkhus B, Lamglait A, Basu S, Elind E, Haider T, Berge K, Vik H, Pedersen JI. Metabolic effects of krill oil are essentially similar to those of fish oil but at lower dose of EPA and DHA, in healthy volunteers. Lipids 2011;46(1):37–46.
    92. Vereshagin AG and Novitskaya GV. The triglyceride composition of linseed oil. Journal of the American Oil Chemists' Society 1965;42:970–4.
    93. Burdge GC, Jones AE, Wootton SA. Eicosapentaenoic and docosapentaenoic acids are the principal products of alpha-linolenic acid metabolism in young men. Br J Nutr. 2002;88(4):355–64.
    94. Burdge GC, Wootton SA. Conversion of alpha-linolenic acid to eicosapentaenoic, docosapentaenoic and docosahexaenoic acids in young women. Br J Nutr. 2002;88(4):411–20.
  • Obesity has gone prime time. We Find evidence of its presence where ever we look: in every neighborhood, every mall, every school and every workplace. Hardly a day goes by without the news reporting on some aspect of the looming obesity crisis. However, the epidemic is not confined to just the wealthy developed world. Even desperately poor countries such as Nigeria and Uganda are wrestling with the dilemma of obesity. China, which was once one of the world’s leanest countries, is not immune. In fact, it has one of the fastest-growing obesity rates in the world and one quarter of its urban youth is presently overweight. It is projected that by 2015, 200 million Chinese will be not just obese, but morbidly obese. The looming obesity epidemic is sending chills through the global community. Worldwide, more than 1.3 billion people are overweight, whereas only 800 million are underweight—and these statistics are diverging rapidly.

    The problem of expanding waistlines is more than merely a vanity concern. There are serious health consequences from sporting that beer belly. Being overweight can radically change the course of a person’s life. Fat is toxic and potentially lethal. Just carrying as few as an extra 4.5 kilos (10 pounds), over your ideal weight is considered a serious risk factor for heart disease, diabetes, high blood pressure, dementia and Alzheimer’s disease, liver disease, hormonal imbalances depression and cancer. In fact, at least 30 different diseases are related to being overweight. So, what’s going on here? If people were to follow the advice offered by medical professional, public health officials and the experts from the weight loss industry, the problem should be easily solved. Their call to action basically involves turning your back on all those sugary, high carbohydrate, processed, junk foods and switch to a low calorie diet fortified by plenty of exercise. They say it all boils down to a very simple equation: take in fewer calories and burn more.

    Sounds logical. The only problem is that this decades old approach is a dismal failure. For the vast majority of people, it doesn’t work. In fact, long-term success for attaining permanent weight loss is only achieved by a mere 2–5 percent of those very determined and lucky dieters.

    A definition of insanity is doing the same thing over and over again and expecting a different outcome. It certainly appears that the traditional approach to winning the battle of the bulge does indeed, seem insane.

    If there are answers and successful strategies to stem the tide of this serious health epidemic, they will need to be sought elsewhere.

    It’s time to discover some of the missing pieces of the weight loss puzzle.

    Secrets of the Brain-Belly Connection
    Do you value your brainpower? Certainly the one faculty that everyone wants to hold onto throughout a life’s lifetime is a fully functioning, intact brain. Unfortunately belly fat can deliver a serious blow to your aspirations.

    Overwhelming evidence now reveals that your expanding waistline will put a serious crimp on your brain size as well as brainpower.

    Researchers set out to discover if being overweight posed a danger to the brain. They scanned the brains of 94 people over the age of 70. They were looking to see the differences in the brains of people who were of normal weight (BMI under 25), overweight (BMI 25–30), and obese (BMI over 30). (BMI stands for body mass index, an approximation of body fat based on height and weight.)

    Their results were quit shocking. Overweight people have 4 percent less brain tissue than people of normal weight. And, for obese people, the findings were even worse. They had 8 percent less brain tissue than people of normal weight.

    The study not only showed that carrying extra weight degenerated the brain but it also accelerated its aging. Researcher Paul Thompson shared his observation, “The brains of overweight people looked eight years older than the brains of those who were lean, and 16 years older in obese people. Type 2 diabetes, which is common in the overweight, is known to accelerate the aging of the brain and the onset of dementia. But the relationship between brain size and weight still stood when the researchers accounted for this, suggesting it is the fat itself that is causing the problem. It is thought that high levels of fat raise the odds of the arteries clogging up, cutting the flow of blood and oxygen to the brain. This could cause brain cells to die and the organ to shrink.” The high demands put on these brain areas may make them more sensitive to changes in oxygen levels.

    Another study used magnetic resonance imaging to compare the brains of 44 obese individuals with those of 19 lean people of similar age and background. The obese individuals had more water in the amygdale—a part of the brain involved in eating behavior. It also showed smaller orbitofrontal cortices in obese individuals, important for impulse control and also involved in eating behavior. These findings strengthen the “slippery slope” theory of obesity. The neural changes that occur when you are overweight, affects the parts of your brain that influence and control so many behaviors necessary to make healthy choices.

    Further studies indicate that those with the most belly fat (visceral fat mass) suffer the greatest mental declines over time—and that central or abdominal obesity, in particular, accounts for more than a three-fold increase in dementia risk.

    What’s even more worrying is that increased belly fat is linked to decreases in total brain volume, independent of BMI. This can cause changes in another area of the brain, called the hippocampus, which is responsible for long-term memory, spatial memory and navigation. Finally, excess belly fat also appears to contribute to lesions in the brain’s white matter, especially in diabetic patients—linking it not just to memory loss, but also to increased risk of stroke.

    Obesity is also causes changes to the immune system, which are fanning the flames of inflammation throughout the body. This increased inflammation can impact the brain and lead to a vicious cycle of gaining more and more weight: obesity leads to inflammation, which damages certain parts of the brain, which in turn leads to more uncontrolled eating and more obesity.

    There are many areas of the brain that are affected by being overweight.

    • Frontal and temporal lobes—critical for planning, memory and impulse control
    • Anterior cingulate gyrus—responsible for attention and executive functions
    • Hippocampus—important for long-term memory, spatial memory and navigation
    • Basal ganglia—essential for proper movement and coordination

    Here is the catch-22. Those extra kilos impair brain function and compromise the particular areas of brain that impact a person’s ability to have a keen memory, control impulses and follow through on any kind of planning. It, therefore, becomes more difficult to successfully commit to any kind of program, especially a weight loss program. Since the impulse control part of the brain is affected, controlling those urges to help yourself to another donut or a second helping of mashed potatoes is a Herculean effort and generally doomed to fail.

    Vitamin D —A Key to a Healthy Metabolism
    There is one really important nutritional player when it comes to our health. This superstar nutrient is the sunshine hormone, vitamin D. (Vitamin D is really a steroid hormone rather than an actual vitamin.)

    Vitamin D truly deserves the title of superstar. Each year, vitamin D research discovers additional health benefits conferred by this sunshine vitamin. Vitamin D receptors are found throughout the body including the brain. Optimal levels are absolutely necessary to insure healthy bones, healthy arteries, a robust immune system, balanced moods, optimal cognitive function, protection from hypertension, allergies, multiple sclerosis, Alzheimer’s disease, autoimmune conditions, and fertility and PMS. Most significantly, vitamin D has been proven to be protective against 13 different kinds of cancer.

    Optimal Levels of Vitamin D Are Critical for Health Here are some basic facts you need to know about vitamin D. It is a fat-soluble steroid hormone that is both made by the body and from our diet. In order for the body to produce vitamin D (cholecalciferol), the skin must be exposed to ultraviolet light, primarily from the sun. Vitamin D is further metabolized in the liver and kidneys to create the fully active form of vitamin D. Thus variations in sun exposure due to latitude, season, time of day, sunscreen use, skin pigmentation, and age will determine how much vitamin D the body makes.

    Although it is known that vitamin D play a vital role for the well-being of infants, children, adults and the elderly, we presently have a global pandemic of chronically low vitamin D levels. It’s estimated that 85 percent of the American public are deficient, and as much as 95 percent of all its senior citizens. Vitamin D deficiencies are also widespread throughout the UK, with 86 percent of the population deficient in the winter and 57 percent in the summer.

    Even though Australia’s is described as “sun burnt” country and is one of the sunniest countries in the world, a surprising number of its citizens are severely lacking in vitamin D. A recent report stated that as many as 1 in 3 Australians may have low vitamin D levels.

    For all those on a weight loss quest, vitamin D is one of those missing pieces you have been searching for. There is overwhelming evidence that confirms the importance of keeping your vitamin D levels up to get your extra kilos down. Not only does it help achieve weight loss, it also improves other risk factors such as insulin resistance, metabolic syndrome and blood sugar imbalances. If you are feeling hungry all the time no matter how much you eat, you might want to have your vitamin D levels checked. What drives insatiable hunger is the relationship between low vitamin D levels and a hormone called leptin. Leptin is a messenger molecule made in fat cells that communicates to the hypothalamus, letting it know how much fat is stored in the body. It is the hormone that communicates that you are full.

    Low vitamin D levels interfere with the effectiveness of leptin. Researchers at Aberdeen University, Scotland found that obese people produced 10 per cent less vitamin D than people of average weight. The study discovered that low levels of the vitamin in blood interfered with the function of leptin, which tells the brain when the stomach is full. The study also found that excess body fat absorbs vitamin D, stopping it from entering the bloodstream. Dr Helen MacDonald, of Aberdeen University’s department of medicine and therapeutics, said: “Obese people had less vitamin D and the link between obesity and vitamin D deficiency was statistically significant.” Overweight people, shirking the sun or not taking adequate vitamin D supplementation thwart their dieting efforts in another way. Low vitamin D levels have been shown to increases fat storage. A 2009 Canadian study found that weight and body fat were significantly lower in women with normal vitamin D levels than women with insufficient levels.

    It seems that fat people may be less able to convert vitamin D into its hormonally active form. A Norway study found that the more participants weighed, the lower their vitamin D levels tended to be. The researcher, Zoya Lagunova, MD, believes that obesity is associated with lower vitamin D levels since vitamin D is a fat-soluble vitamin. “Much of the vitamin D produced in the skin or ingested is distributed in fat tissue, so obese people may take in as much vitamin D from the sun, food, or supplements as people who are not obese, but their [blood] levels will tend to be lower. Obese people may need more vitamin D to end up with the same levels as a person whose weight is normal.”

    How much less vitamin does an overweight person make? As it turns out, increased fatty cells can decrease the ability to make vitamin D by a factor of 4. That means that if you are carry extra weight, you may make only one quarter the amount of vitamin D compared to a leaner person. Vitamin D is also an important factor in diabetes. Low levels of vitamin D has been linked to an increased risk of developing type 2 diabetes. After following more than 5,000 people for five years, an Australian research team found that those with lower than average vitamin D levels had a 57 percent increased risk of developing diabetes, compared to those within the recommended range.

    Low levels of vitamin D are also known to nearly double the risk of cardiovascular disease if you already have diabetes. Diabetics, who are deficient in vitamin D and cannot process cholesterol normally, tend to have it build up in their blood vessels, hence increasing the risk of heart attack and stroke.

    Vitamin D also helps keep blood sugar levels under control. In type 2 diabetes the body can’t use insulin it produces efficiently to control blood sugar levels. Vitamin D plays a role by increasing the release of insulin. In one study, researchers evaluated the vitamin D levels and the chance of developing unbalanced blood sugar metabolism. In this study, subjects were evaluated for serum vitamin D levels and followed for 7 years to determine the effects on blood sugar metabolism. The study showed that the subjects with the highest vitamin D levels had a 40 percent increase in supporting optimal future blood sugar balance.

    If you want to lose weight and keep it off, it is critical to check your vitamin D levels. The higher your vitamin D levels the higher your leptin levels and the more your blood sugar will remain balanced. Vitamin D helps your body respond to the correct metabolic messages. High vitamin D levels increase your ability to lose weight and losing weight will increase your vitamin D levels. All of which will reduce your risk of metabolic syndrome, insulin resistance, diabetes, and cardiovascular disease, not to mention most chronic illnesses.

    While it is important for most people to take vitamin D supplementation, especially the overweight, children and elderly, it is critically important to check your vitamin D levels. Taking a vitamin D supplement may not get you into optimal range, which is where you want to be. Its optimal blood vitamin D levels that count. The proper blood test is called 25-hydroxyvitamin D (25-OH), which is included in the basic blood workup. In Australia optimal levels should be 150–200 nmol/L. In the U.S., optimal levels should be between 70–100 ng/mL. Do not settle for less than optimal levels if your goal is the best health possible.

  • As COVID-19 ravages the countryside, we have garnered a new understanding of how this disease preys on a weakened immune system. The Centers for Disease Control and Prevention is now tracking the top three conditions linked to the virus: diabetes mellitus, chronic lung disease and cardiovascular disease.1 Each is linked to vitamin D deficiency.

    Former CDC Chief, Dr. Tom Friedan was recently quoted on Fox News affirming, “Vitamin D supplementation reduces the risk of respiratory infection2, regulates cytokine production3 and can limit the risk of other viruses4 such as influenza. A respiratory infection can result in cytokine storms5—a vicious cycle in which our inflammatory cells damage organs throughout the body— which increase mortality for those with COVID-19.” Dr. JoAnn Manson, Professor of Medicine, Harvard Medical School6 states in a video presentation on Medscape, “There is emerging and growing evidence that vitamin D status may be relevant to the risk of developing COVID-19 infection and to the severity of the disease,” adding, “Vitamin D has an immune modulating effect and can lower inflammation.”

    Sadly, we are also seeing evidence of health care disparity among African Americans who, in an analysis conducted by the Washington Post7, are contracting and dying of the disease at a higher rate. The Post analysis shows that counties that are majority-black have three times the rate of infections and almost six times the rate of deaths as counties where white residents are in the majority. In Michigan, African Americans, who represent 14 percent of the population, account for more than 33 percent of cases and 40 percent of deaths. Similar statistics are mirrored in Chicago where 70 percent of COVID-19 related deaths were black, a rate six times higher than that of white residents. It is bears noting that vitamin D deficiency is more prevalent among African Americans than other Americans and, in North America, most young, healthy blacks do not achieve what scientists consider an optimal blood serum level, defined as 30 ng/ml by the Institutes of Medicine at any time of year.8

    The CDC has acknowledged that the data suggests health disparities, including underlying health conditions, access to health care, and living and work conditions, make the African American population particularly vulnerable9. According to their analysis of COVID-19 deaths for New York, where race and ethnicity data were available, the death rate among Black/African American persons was 92.3 deaths per 100,000 population, and 74.3 for Hispanic/Latino persons; figures substantially higher than that of white (45.2) or Asian (34.5) persons. Which takes us back to vitamin D.

    There is a sound body of research on the health and immune system benefits of vitamin D and a flurry of new reports, some of which have not yet been peer reviewed, from scientists and health care providers around the world who are working to connect the dots between vitamin D deficiency and the underlying conditions associated with increased severity or complications of COVID-19. The most recent is a report on the mean levels of vitamin D for 20 European countries. The study concluded low levels of vitamin D were strongly linked to morbidity and mortality associated with COVID-19 in yet another highly vulnerable group, the elderly population.10

    Achieving an effective vitamin D level is essential for your overall health and it is a critical component for building your immune system. An estimated 89 percent of U.S. adults overall, and 91 percent of U.S. children and teens, aren’t getting recommended levels of vitamin D.11 What is the recommended level? Forty-eight high-profile vitamin D researchers from around the globe agree that 40–60 ng/ml is the ideal range for vitamin D. If you’ve had your level tested recently it’s likely your test result ranged from 10-30 ng/ml. If you do take vitamin D on a regular basis, you may be higher. Efective supplementation, however, requires you know your serum level.

    The primary source of vitamin D is the sun, and we live in a society that no longer tolerates extended time in the sun without applying sunscreen. Stay-at-home orders have complicated getting enough sun and frankly, unlike many nutrients, you can't eat your way to a healthy vitamin D level. Fortunately, vitamin D supplementation is an inexpensive, effective and simple way to resolve deficiencies if taken in the right amounts. Knowing your levels requires testing, and that can be done from the comfort of your own home.

    Put the power of prevention in your own hands12.
    GrassrootsHealth, offers a simple blood spot test you can have delivered to your home. With your results, you can use the vitamin D calculator to see how much vitamin D you need to take to get achieve that optimal level of 40-60 ng/ml. According to published research, vitamin D levels of 50 ng/ml appear to protect against viral respiratory infection.12 Everyone has just enough time before the winter flu and cold season to monitor and increase your vitamin D level to bolster your immune system.

    There is no reason to hesitate. Supplementation is safe. The latest Institute of Medicine report indicates 10,000 IU/day is considered the NOAEL (no observed adverse effect level) and 4,000 IU/day is safe for adults who are age 19 and older. The appropriate intake for you depends on your age, race, lifestyle and latitude of residence. Know your vitamin D level so you can live your future life well.



  • There is a vitamin revolution brewing, and it is important to the health of young and old alike as researchers respond to what has been called the “vitamin D deficiency epidemic.” More than a dozen scientists at leading universities both in the United States and abroad have minced no words about it: many of us need more vitamin D. (See “Cod liver oil, vitamin A toxicity, frequent respiratory infections, and the vitamin D deficiency epidemic.”)1 The issue of deficiency may be especially true of children, yet it is also applicable to adults. Quite surprisingly as far as vitamin D is concerned, the suggested intakes in recent decades have fallen rather wide of the mark. Not only are the recommendations of 400 IU/day as an adequate intake (100 percent of U.S. Daily Value) and 2,000 IU/day as an upper limit too low, but also recommendations may have been more realistic 70 years ago. As detailed below, in a tale of two vitamins, A and D, scientists initially bet on the wrong one.

    Vitamin D Versus Viral Respiratory Infections
    All the way back in 1926, it was theorized that a disorder in vitamin metabolism linked to a lack of sun exposure is responsible for the rise in infections experienced during the winter months.2 Experiments in the 1930s provided considerable support for this hypothesis. Using a cod liver oil much higher in vitamin D content than is typical today, one large trial involving 185 adults for four months discovered that supplementation reduced the rate of infections with colds by 50 percent.3 Another study tracking 1,561 adults found the rate of respiratory infections fell by 30 percent.4 Recent work comparing 410 teenage athletes who received vitamin-D producing radiation against 446 athletes who did not over a period of three years demonstrated the same range of benefits as was seen with cod liver oil supplementation in the 1930s: 50 percent fewer respiratory infections and 300 percent fewer lost days due to absences.5

    How does vitamin D provide protection against infections? This has been the subject of considerable work and the answer seems to be vitamin D produced in the skin in response to sunlight provides the body with the vitamin in its hormonal form known as 1,25(OH)2D, actually a type of steroid hormone. Indeed, the skin has the capacity to synthesize the biologically active vitamin D metabolite 1,25(OH)(2)D3.6 The active form of vitamin D serves both to reduce the excessive production of inflammatory factors and, yet, to increase the power of other immune elements, such as the “oxidative burst” of the macrophages, the immune system’s first line of defense. The effects of the vitamin on the immune system are particularly striking in an area that touches directly on defenses against colds and respiratory infections/flu. The lining of the respiratory tract is full of neutrophils, monocytes and natural killer cells, all of which contain anti-microbial peptides that are empowered by vitamin D.7

    These benefits are known for sun exposure. Great news for the summer months, but can the use of vitamin D supplements help to provide the same protection? Luckily, the answer is “yes.” In a randomized placebo-controlled intervention trial lasting three years, it was discovered African American women receiving vitamin D exhibited only one third the likelihood of reporting cold or flu symptoms as did controls. The amount of vitamin D needed to abolish completely the tendency towards more colds and flu in the winter months was only 800 IU/day. Increasing the intake of supplemental vitamin D to 2,000 IU/day almost entirely eliminated reports of upper respiratory tract infections.8

    Vitamin D and Vitamin A: A Conflicted Relationship
    Recent studies using cod liver oil have not produced as robust a response in preventing infections as those found in the 1930s. Why not? The answer appears to be tied to the tendency over the last few decades to overrate the importance of vitamin A and to underrate the importance of vitamin D. Cod liver oil-based studies in recent years have used supplements typically providing 3,500 to 5,000 IU vitamin A as preformed retinol and only in the neighborhood of 700 IU vitamin D. The problem in this is vitamin A and vitamin D competes against one another because they make use of common cofactors. Vitamin A acts as an antagonist to vitamin D and its active metabolite.

    That there might be an untoward interaction between vitamin A and vitamin D has been suspected for quite some time. Research at several laboratories has confirmed this suspicion. In an animal study, it was found there is an in vivo antagonism of vitamin D action on intestine and bone by retinyl acetate.9 Exactly how vitamin A antagonizes vitamin D is not entirely clear, but the fact is being ever more soundly established.10 Moreover, in human beings the amount of vitamin A needed to interfere with aspects of vitamin D metabolism is not high. For instance, one serving of liver as a vitamin A source interferes with vitamin D’s effects on the intestinal response to calcium.11 Many Americans are marginal or outright deficient in vitamin D. In such cases, the amount of vitamin A supplied by multi-vitamins and other sources is sufficient to tip matters over the edge into significant manifestations, such as reduced bone health.12 Although vitamin A deficiency is a serious issue in parts of the developing world, predominantly due to a lack of adequate fat in diet impeding absorption of this fat-soluble vitamin, once vitamin A requirements are met, there is a significant negative interaction with vitamin D.

    Cardiovascular Health and the Sunshine Vitamin
    The role of vitamin D in cardiovascular health is one of the currently “hot” topics in research circles, and for good reason. Vitamin D levels have been linked to a number of aspects of heart and circulatory health. Take blood pressure, for instance. It generally is assumed that blood pressure, primarily systolic blood pressure (the upper figure), increases naturally with age. This is the reason the elevation over time is named “age-associated increase in systolic blood pressure.” Interestingly, maintaining “optimal” vitamin D status reduces or attenuates the elevation in blood pressure that is expected with age.13 Another circulatory condition, lower-extremity peripheral arterial disease, similarly is related to vitamin D status. Nearly one third of the higher prevalence of this condition in adult blacks compared to whites is explainable by vitamin D levels being lower in blacks.14

    Another way of thinking about vitamin D and cardiovascular health is to consider the lively discussions ongoing in research circles regarding the relationship of statins and vitamin D. Cardiovascular disease has a large inflammatory component and some scientists have argued that statins act, in large part, by serving as vitamin D analogs. Moreover, another aspect of cardiovascular disease concerns vascular calcification and statins recently have begun to be touted for bone health as well as reducing calcification of the arteries.

    As is true of many substances, vitamin D is biphasic in some of its actions. Too much is a bad thing, but too little can lead to some of the same results as too much. Above it was mentioned that the vitamin plays a role in reducing inflammation. This is significant to heart health because arterial inflammation is an important step in the process leading to calcification. Hence, it is of note that in an animal model, low levels of the vitamin D hormone calcitriol are associated with massive vascular and soft tissue calcifications.15 That’s right: low levels of vitamin D-related compounds may lead to vascular and soft tissue calcification. Findings are interesting enough that researchers have begun to discuss vitamin D in the prevention and treatment of coronary heart disease.16

    So what about statins and vitamin D? Much evidence available for over a decade suggests that statin drugs are cardio-protective via anti-inflammatory effects on the artery wall and not through any impact on cholesterol levels. Hence it is of note that treatment with statins, at least over the short and medium term, increases serum vitamin D by an unknown mechanism.17 At the same time, vitamin D deficiency, which is quite common in those with cardiovascular problems, appears to play a role in the myalgia associated with statin use.18

    In other words, at least some of the benefits attributed to statin drugs, whether cardiovascular or bone-related, appear to be linked to improved vitamin D status. Likewise, at least one of the side effects of statin usage is linked to vitamin D deficiency.

    Guarding Cognitive Health
    Poor mood often is associated with advancing years. Recent data suggests that poor vitamin D status may be common in the elderly and low levels of vitamin D are associated with poor mood. There are a number of trials that have suggested a role for supplementary vitamin D in the treatment of depression.19 The impact of vitamin D status, however, appears to go far beyond merely improving mood. A large trial involving 1,766 adults over the age of 65 identified vitamin D levels as related to cognitive function and dementia. The relationship is strong enough that the researchers suggested supplementation with vitamin D as a possible way to reduce the risk of developing dementia.20

    How Much is Enough?
    As usual, the devil is in the details. How much vitamin D is enough? Quite obviously, there likely is a range and not any one figure involved. People are different, get different amounts of sun exposure, have different diets, different stresses, and so forth. One recent study argues that the amount of vitamin D intake needed to attain the desired serum 25-hydroxyvitamin D concentration may run between 3,800 and 5,000 IU per day, amounts in excess of the currently officially endorsed upper limit of intake.21 These amounts are based on the researchers’ estimate of the intake of vitamin D3 needed to raise serum 25(OH)D to equal to or greater than 75 nmol/L and is in line with long-time recommendations of many experts of 3,000 to 5,000 IU/day.22 Other researchers using a different model of sun exposure and intake from food while restricting themselves to the requirements of Caucasians only still determined that a reasonable level of intake to prevent seasonal fluctuations may be as much as approximately 1,600 IU/day.23 Again, this is a far cry from the presently recommended 400 IU/day. Moreover, some individuals have low vitamin D status even with abundant sun exposure.24 All of this suggests the recommendation for vitamin D intake may soon be revised strongly upwards and that the currently suggested upper limit of intake of 2,000 IU/day may, instead, become closer to baseline.

    For references send a SASE envelope to totalhealth magazine.