Vitamin D

Discussion in 'Men's Health Forum' started by Michael Scally MD, Jul 27, 2010.

  1. Michael Scally MD

    Michael Scally MD Doctor of Medicine

    Writing in the New York Times (7/27, D7) "Personal Health" column, Jane E. Brody reports that "a huge part of the population" may be deficient in vitamin D. Notably, "every tissue in the body, including the brain, heart, muscles and immune system, has receptors for vitamin D, meaning that this nutrient is needed at proper levels for these tissues to function well." Current research suggests that "the effects of a vitamin D deficiency include an elevated risk of developing (and dying from) cancers of the colon, breast and prostate; high blood pressure and cardiovascular disease; osteoarthritis; and immune-system abnormalities that can result in infections and autoimmune disorders like multiple sclerosis, type 1 diabetes, and rheumatoid arthritis." [HAN, I expect you to chime in, but try to not go overboard!]

    What Do You Lack? Probably Vitamin D

    July 26, 2010

    Vitamin D promises to be the most talked-about and written-about supplement of the decade. While studies continue to refine optimal blood levels and recommended dietary amounts, the fact remains that a huge part of the population — from robust newborns to the frail elderly, and many others in between — are deficient in this essential nutrient.

    If the findings of existing clinical trials hold up in future research, the potential consequences of this deficiency are likely to go far beyond inadequate bone development and excessive bone loss that can result in falls and fractures. Every tissue in the body, including the brain, heart, muscles and immune system, has receptors for vitamin D, meaning that this nutrient is needed at proper levels for these tissues to function well.

    Studies indicate that the effects of a vitamin D deficiency include an elevated risk of developing (and dying from) cancers of the colon, breast and prostate; high blood pressure and cardiovascular disease; osteoarthritis; and immune-system abnormalities that can result in infections and autoimmune disorders like multiple sclerosis, Type 1 diabetes and rheumatoid arthritis.

    Most people in the modern world have lifestyles that prevent them from acquiring the levels of vitamin D that evolution intended us to have. The sun’s ultraviolet-B rays absorbed through the skin are the body’s main source of this nutrient. Early humans evolved near the equator, where sun exposure is intense year round, and minimally clothed people spent most of the day outdoors.

    “As a species, we do not get as much sun exposure as we used to, and dietary sources of vitamin D are minimal,” Dr. Edward Giovannucci, nutrition researcher at the Harvard School of Public Health, wrote in The Archives of Internal Medicine. Previtamin D forms in sun-exposed skin, and 10 to 15 percent of the previtamin is immediately converted to vitamin D, the form found in supplements. Vitamin D, in turn, is changed in the liver to 25-hydroxyvitamin D, the main circulating form. Finally, the kidneys convert 25-hydroxyvitamin D into the nutrient’s biologically active form, 1,25-dihydroxyvitamin D, also known as vitamin D hormone.

    A person’s vitamin D level is measured in the blood as 25-hydroxyvitamin D, considered the best indicator of sufficiency. A recent study showed that maximum bone density is achieved when the blood serum level of 25-hydroxyvitamin D reaches 40 nanograms per milliliter or more.

    “Throughout most of human evolution,” Dr. Giovannucci wrote, “when the vitamin D system was developing, the ‘natural’ level of 25-hydroxyvitamin D was probably around 50 nanograms per milliliter or higher. In modern societies, few people attain such high levels.”

    A Common Deficiency

    Although more foods today are supplemented with vitamin D, experts say it is rarely possible to consume adequate amounts through foods. The main dietary sources are wild-caught oily fish (salmon, mackerel, bluefish, and canned tuna) and fortified milk and baby formula, cereal and orange juice.

    People in colder regions form their year’s supply of natural vitamin D in summer, when ultraviolet-B rays are most direct. But the less sun exposure, the darker a person’s skin and the more sunscreen used, the less previtamin D is formed and the lower the serum levels of the vitamin. People who are sun-phobic, babies who are exclusively breast-fed, the elderly and those living innursing homes are particularly at risk of a serious vitamin D deficiency.

    Dr. Michael Holick of Boston University, a leading expert on vitamin D and author of “The Vitamin D Solution” (Penguin Press, 2010), said in an interview, “We want everyone to be above 30 nanograms per milliliter, but currently in the United States, Caucasians average 18 to 22 nanograms and African-Americans average 13 to 15 nanograms.” African-American women are 10 times as likely to have levels at or below 15 nanograms as white women, the third National Health and Nutrition Examination Survey found.

    Such low levels could account for the high incidence of several chronic diseases in this country, Dr. Holick maintains. For example, he said, in the Northeast, where sun exposure is reduced and vitamin D levels consequently are lower, cancer rates are higher than in the South. Likewise, rates of high blood pressure, heart disease, and prostate cancer are higher among dark-skinned Americans than among whites.

    The rising incidence of Type 1 diabetes may be due, in part, to the current practice of protecting the young from sun exposure. When newborn infants in Finland were given 2,000 international units a day, Type 1 diabetes fell by 88 percent, Dr. Holick said.

    The current recommended intake of vitamin D, established by the Institute of Medicine, is 200 I.U. a day from birth to age 50 (including pregnant women); 400 for adults aged 50 to 70; and 600 for those older than 70. While a revision upward of these amounts is in the works, most experts expect it will err on the low side. Dr. Holick, among others, recommends a daily supplement of 1,000 to 2,000 units for all sun-deprived individuals, pregnant and lactating women, and adults older than 50. The American Academy of Pediatrics recommends that breast-fed infants receive a daily supplement of 400 units until they are weaned and consuming a quart or more each day of fortified milk or formula.

    Given appropriate sun exposure in summer, it is possible to meet the body’s yearlong need for vitamin D. But so many factors influence the rate of vitamin D formation in skin that it is difficult to establish a universal public health recommendation. Asked for a general recommendation, Dr. Holick suggests going outside in summer unprotected by sunscreen (except for the face, which should always be protected) wearing minimal clothing from 10 a.m. to 3 p.m. two or three times a week for 5 to 10 minutes.

    Slathering skin with sunscreen with an SPF of 30 will reduce exposure to ultraviolet-B rays by 95 to 98 percent. But if you make enough vitamin D in your skin in summer, it can meet the body’s needs for the rest of the year, Dr. Holick said.

    Can You Get Too Much?

    If acquired naturally through skin, the body’s supply of vitamin D has a built-in cutoff. When enough is made, further exposure to sunlight will destroy any excess. Not so when the source is an ingested supplement, which goes directly to the liver.

    Symptoms of vitamin D toxicity include nausea, vomiting, poor appetite, constipation, weakness and weight loss, as well as dangerous amounts of calcium that can result in kidney stones, confusion and abnormal heart rhythms.

    But both Dr. Giovannucci and Dr. Holick say it is very hard to reach such toxic levels. Healthy adults have taken 10,000 I.U. a day for six months or longer with no adverse effects. People with a serious vitamin D deficiency are often prescribed weekly doses of 50,000 units until the problem is corrected. To minimize the risk of any long-term toxicity, these experts recommend that adults take a daily supplement of 1,000 to 2,000 units.
    Last edited: Jul 27, 2010
    Eman, vivame and twistulikepretzel like this.
  2. virtuosa150

    virtuosa150 Junior Member

    I've been taking 16000iu of bio-d mulsion forte. I've been taking this much for about 6 months. Although I don't have the bloodtest in front of me, my level was to the bottom of the range.

    This seems to be a chronic problem with me. I've got all sorts of other things that at low as well. The're all interrelated most likely.
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  3. Tyler81

    Tyler81 Member

    I had a severely low vitamin D.

    My endo put me on 50,000iu's vitamin D3 to start, in addition to vitamin D2.

    I believe a portion of my fatigue (and perhaps low T) was due to a vitamin D deficiency.
  4. yates row

    yates row Junior Member

    I feel everyone should be asking their dr for 25-OH to be drawn yearly at physical.
  5. we check every 5-6 weeks untill they are at optimal levels og 75-90 this is where the magic happens.
  6. virtuosa150

    virtuosa150 Junior Member

    How are we going to get mine up. It's been around 46 for months now. I upped my dose to 20000iu's, but was told to cut back to 16000.
  7. u may have a disorder in your genes defective in VDR and require more then average person..keep moving it up slowly and monitor.
  8. m_ob

    m_ob Member

    I feel damn good at 81 which is the result, mostly, of me being a lifeguard and spending all day, everyday in the sun, and partially due to my supplementation. Iowa winters suck the vitamin D right outta' me though, lol.. Not looking forward to it.
  9. Besure to get check in novmebe-december. It takes a good 2 months to drop off. I have seen roofers test at 81-90 in summer time then by 2 months back down to 30's. OUCH ...
  10. Michael Scally MD

    Michael Scally MD Doctor of Medicine

    Cashman KD, Hill TR, Lucey AJ, et al. Estimation of the dietary requirement for vitamin D in healthy adults. Am J Clin Nutr 2008;88(6):1535-42. Estimation of the dietary requirement for vitamin D in healthy adults -- Cashman et al. 88 (6): 1535 -- American Journal of Clinical Nutrition

    Background: Knowledge gaps have contributed to considerable variation among international dietary recommendations for vitamin D.

    Objective: We aimed to establish the distribution of dietary vitamin D required to maintain serum 25-hydroxyvitamin D [25(OH)D] concentrations above several proposed cutoffs (ie, 25, 37.5, 50, and 80 nmol/L) during wintertime after adjustment for the effect of summer sunshine exposure and diet.

    Design: A randomized, placebo-controlled, double-blind 22-wk intervention study was conducted in men and women aged 20-40 y (n = 238) by using different supplemental doses (0, 5, 10, and 15 {micro}g/d) of vitamin D3 throughout the winter. Serum 25(OH)D concentrations were measured by using enzyme-linked immunoassay at baseline (October 2006) and endpoint (March 2007).

    Results: There were clear dose-related increments (P < 0.0001) in serum 25(OH)D with increasing supplemental vitamin D3. The slope of the relation between vitamin D intake and serum 25(OH)D was 1.96 nmol{middle dot}L-1{middle dot}{micro}g-1 intake. The vitamin D intake that maintained serum 25(OH)D concentrations of >25 nmol/L in 97.5% of the sample was 8.7 {micro}g/d. This intake ranged from 7.2 {micro}g/d in those who enjoyed sunshine exposure, 8.8 {micro}g/d in those who sometimes had sun exposure, and 12.3 {micro}g/d in those who avoided sunshine. Vitamin D intakes required to maintain serum 25(OH)D concentrations of >37.5, >50, and >80 nmol/L in 97.5% of the sample were 19.9, 28.0, and 41.1 {micro}g/d, respectively.

    Conclusion: The range of vitamin D intakes required to ensure maintenance of wintertime vitamin D status [as defined by incremental cutoffs of serum 25(OH)D] in the vast majority (>97.5%) of 20-40-y-old adults, considering a variety of sun exposure preferences, is between 7.2 and 41.1 {micro}g/d.
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  11. Michael Scally MD

    Michael Scally MD Doctor of Medicine

    In the past, many health care professionals believed that the major health problems resulting from vitamin D deficiency were rickets in children and osteomalacia in adults, which were greatly reduced by the fortification of foods with vitamin D. Recently, there has been intense interest in the role of vitamin D in a variety of nonskeletal medical conditions. Indeed, vitamin D insufficiency has been associated with increases in cardiovasculardisease, cancer, and infection. Vitamin D supplementation appears to mitigate the incidence and adverse outcomes of these diseases and may reduce all-cause mortality.

    The Institute of Medicine currently recommends vitamin D supplementation of 200 IU/d from birth to 50 years of age, 400 IU/d for adults aged 51 to 70 years, and 600 IU/d for adults 71 years or older. However, these recommendations appear limited by the goals of treatment, which focus primarily on bone health. Until recently, serum 25-hydroxyvitamin D (25[OH]D) levels of 20 ng/mL or more (to convert to nanomoles per liter, multiply by 2.496) appeared adequate based on improved skeletal outcomes, but increasing evidence suggests that 30 ng/mL or even 40 ng/mL may be required for optimum health. Indeed, several authors argue that current recommended doses of vitamin D supplementation are woefully inadequate to meet higher serum 25(OH)D levels on a population level.

    Sunlight exposure is the primary determinant of vitamin D status in humans and, particularly in northern latitudes from November to March, there are insufficient UV-B rays to produce vitamin D. Successful campaigns to control sun exposure through avoidance and sun protection, coupled with decreases in outdoor physical activity, may have increased the prevalence of vitamin D insufficiency. In addition, because many studies of vitamin D have focused on particular subgroups (ie, older adults, women, and racial subgroups), the Third National Health and Nutrition Examination Survey (NHANES III) has served as the primary source of population-based prevalence data for vitamin D status in the United States. Because these data were collected from 1988 to 1994, changes in prevalence of vitamin D insufficiency during the past decade could affect national recommendations about vitamin D status.

    Trends of serum 25(OH)D levels in the US population, particularly for direct comparison with older data, have not been previously reported. In this study, National data demonstrate a marked decrease in serum 25(OH)D levels from the 1988-1994 to the 2001-2004 NHANES data collections. Racial/ethnic differences have persisted and may have important implications for known health disparities. Current recommendations for vitamin D supplementation are inadequate to address the growing epidemic of vitamin D insufficiency.

    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(6):626-32.

    Background Vitamin D insufficiency is associated with suboptimal health. The prevalence of vitamin D insufficiency may be rising, but population-based trends are uncertain. We sought to evaluate US population trends in vitamin D insufficiency.

    Methods We compared serum 25-hydroxyvitamin D (25[OH]D) levels from the Third National Health and Nutrition Examination Survey (NHANES III), collected during 1988 through 1994, with NHANES data collected from 2001 through 2004 (NHANES 2001-2004). Complete data were available for 18 883 participants in NHANES III and 13 369 participants in NHANES 2001-2004.

    Results The mean serum 25(OH)D level was 30 (95% confidence interval [CI], 29-30) ng/mL during NHANES III and decreased to 24 (23-25) ng/mL during NHANES 2001-2004. Accordingly, the prevalence of 25(OH)D levels of less than 10 ng/mL increased from 2% (95% CI, 2%-2%) to 6% (5%-8%), and 25(OH)D levels of 30 ng/mL or more decreased from 45% (43%-47%) to 23% (20%-26%). The prevalence of 25(OH)D levels of less than 10 ng/mL in non-Hispanic blacks rose from 9% during NHANES III to 29% during NHANES 2001-2004, with a corresponding decrease in the prevalence of levels of 30 ng/mL or more from 12% to 3%. Differences by age strata (mean serum 25[OH]D levels ranging from 28-32 ng/mL) and sex (28 ng/mL for women and 32 ng/mL for men) during NHANES III equalized during NHANES 2001-2004 (24 vs 24 ng/mL for age and 24 vs 24 ng/mL for sex).

    Conclusions National data demonstrate a marked decrease in serum 25(OH)D levels from the 1988-1994 to the 2001-2004 NHANES data collections. Racial/ethnic differences have persisted and may have important implications for known health disparities. Current recommendations for vitamin D supplementation are inadequate to address the growing epidemic of vitamin D insufficiency.

    Attached Files:

  12. zkt

    zkt Member

  13. BBC3

    BBC3 Member

    You know, I am not sure what type vitamin D they supplement in Milk. But I am not so sure I dont really appreciate it. When younger and training vigorously (19-25yrs) I would put down a gallon of skim milk a day. The only problem eventually at the age of 27 was that it started to aggrivate my hip arthritis, which may even just be I-band strain (not sure). I never was sure why, but on a diet around age 27 and about a gallon a day, the pain was excruciating, and I put 2 and 2 together and quit. I kinda assumed it was due to the hormones or chemicals in production... Whatever, I am sure a gal/day was excessive...

    Since now having young kids nearly 40 and its back in the house, I really find myself almost craving it. I have tried to deny it, but a glass a day is hitting the spot. SO IS IT THE VIT D that I am after??? All these years in between I used water in my Metabolol II shakes instead. But now I am using milk again, and 2%, and REALLY FEEL BETTER. Mentally primarily I think.... I Have not read the article. Just food for thought....
  14. zkt

    zkt Member

    Vitamin D: an evolutionary perspective

    [ame=""]YouTube - Vitamin D and Prevention of Chronic Diseases[/ame]
  15. HeadDoc

    HeadDoc Psychologist

    Vitamin D, adiposity, arterial stiffness

    Endocrine Society JCEM

    This version published online on July 21, 2010
    Journal of Clinical Endocrinology & Metabolism , doi:10.1210/jc.2010-0606

    Submitted on March 15, 2010
    Accepted on June 14, 2010
    A 16-Week Randomized Clinical Trial of 2000 International Units Daily Vitamin D3 Supplementation in Black Youth: 25-Hydroxyvitamin D, Adiposity, and Arterial Stiffness
    Yanbin Dong*, Inger S. Stallmann-Jorgensen, Norman K. Pollock, Ryan A. Harris, Daniel Keeton, Ying Huang, Ke Li, Reda Bassali, De-huang Guo, Jeffrey Thomas, Gary L. Pierce, Jennifer White, Michael F. Holick, and Haidong Zhu

    Georgia Prevention Institute, Department of Pediatrics (Y.D., I.S.S.-J., N.K.P., R.A.H., D.K., Y.H., K.L., D.G., J.T., G.L.P., H.Z.); General Pediatrics, Department of Pediatrics (R.B.), and Endocrinology, Department of Medicine (J.W.), Medical College of Georgia, Augusta, Georgia 30912; and Endocrinology, Department of Medicine (M.F.H.), Boston University Medical Center, School of Medicine, Boston, Massachusetts 02118

    * To whom correspondence should be addressed. E-mail:

    Context: Vitamin D insufficiency/deficiency is commonly observed in black youth.

    Objective: The aim was to determine 25-hydroxyvitamin D [25(OH)D] in response to 2000 IU vitamin D supplementation over time; to evaluate the relation between 25(OH)D concentrations and total body fat mass by dual-energy x-ray absorptiometry; and to determine whether vitamin D supplementation improves arterial stiffness measured by pulse wave velocity (PWV).

    Design: We conducted a randomized, blinded, controlled clinical trial.

    Setting and Participants: Forty-nine normotensive black boys and girls, aged 16.3 ± 1.4 yr, were randomly assigned to either the control group (400 IU/d; n = 24) or the experimental group (2000 IU/d; n = 25).

    Results: Plasma 25(OH)D values at baseline and at 4, 8, and 16 wk were 34.0 ± 10.6, 44.9 ± 9.4, 51.2 ± 11.1, and 59.8 ± 18.2 nmol/liter, respectively, for the control group; and 33.1 ± 8.7, 55.0 ± 11.8, 70.9 ± 22.0, and 85.7 ± 30.1 nmol/liter, respectively, for the experimental group. The experimental group vs. the control group reached significantly higher 25(OH)D concentrations at 8 and 16 wk, respectively. Partial correlation analyses indicated that total body fat mass at baseline was significantly and inversely associated with 25(OH)D concentrations in response to the 2000-IU supplement across time. Furthermore, carotid-femoral PWV increased from baseline (5.38 ± 0.53 m/sec) to posttest (5.71 ± 0.75 m/sec) in the control group (P = 0.016), whereas in the experimental group carotid-femoral PWV decreased from baseline (5.41 ± 0.73 m/sec) to posttest (5.33 ± 0.79 m/sec) (P = 0.031).

    Conclusion: Daily 2000 IU vitamin D supplementation may be effective in optimizing vitamin D status and counteracting the progression of aortic stiffness in black youth. Plasma 25(OH)D concentrations in response to the 2000 IU/d supplementation are negatively modulated by adiposity.
  16. Testiclats

    Testiclats Junior Member

    Re: Vitamin D: an evolutionary perspective

    This is a fascinating video, I loved it!

    I have to wonder how many of my health problems could either be due in part to, or exacerbated by vitamin D deficiency.

    My testosterone is low, but my Dr. didn't test my vitamin D level. I wonder if there could be a connection there. I'm indoors ALL THE TIME. Even on weekends. I really get pretty close to no sun exposure.

    Anyway, if you haven't watched that video, watch it! It's so interesting, makes me want to go to medical school :popcorn:
  17. Michael Scally MD

    Michael Scally MD Doctor of Medicine

    There is increasing awareness of the biological actions of vitamin D. The diversity of effects is remarkable but has not yet been fully placed in an evolutionary context. However, this process has begun with indications that lighter skin color evolved to optimize vitamin D production. Vitamin D deficiency, with resulting rickets-induced pelvic contraction, which is potentially lethal for the maternal–fetal unit, likely has exerted major selective pressures. One billion people worldwide have vitamin D deficiency or insufficiency due to reduced sun exposure or inadequate intake for various reasons. Vitamin D intake has been associated with reduced risk for several diseases, in particular multiple sclerosis (MS), but also rheumatoid arthritis (RA), and type 1 diabetes (T1D).

    The molecular basis by which vitamin D exerts effects on such diseases remains incompletely understood, notably in relation to underlying genetic risk although recent studies have provided limited insights. Much vitamin D signaling occurs through binding by calcitriol, the active form of vitamin D, to its cognate nuclear vitamin D receptor (VDR). A heterodimer, formed with retinoid Xreceptor (RXR), then binds specific genomic sequences (vitamin D response elements, or VDREs) acting to influence gene transcription. A detailed understanding of the biological actions of vitamin D would elucidate relationships between vitamin D and numerous diseases. Recent advances in next-generation DNA sequencing now allow protein– DNA binding interactions to be identified using chromatin immunoprecipitation with massively parallel sequencing (ChIP-seq) with much greater depth, accuracy, and dynamic range than is possible using array-based hybridization approaches. Motivated by the biological and clinical significance of vitamin D–mediated gene regulation, this study presents a comprehensive ChIP-seq genomic map of VDR-DNA binding and gene regulation in lymphoblastoid cell lines (LCLs) and show how this provides insights into genetic susceptibility to disease.

    Ramagopalan SV, Heger A, Berlanga AJ, et al. A ChIP-seq defined genome-wide map of vitamin D receptor binding: Associations with disease and evolution. Genome Research.

    Initially thought to play a restricted role in calcium homeostasis, the pleiotropic actions of vitamin D in biology and their clinical significance are only now becoming apparent. However, the mode of action of vitamin D, through its cognate nuclear vitamin D receptor (VDR), and its contribution to diverse disorders, remain poorly understood. We determined VDR binding throughout the human genome using chromatin immunoprecipitation followed by massively parallel DNA sequencing (ChIP-seq). After calcitriol stimulation, we identified 2776 genomic positions occupied by the VDR and 229 genes with significant changes in expression in response to vitamin D. VDR binding sites were significantly enriched near autoimmune and cancer associated genes identified from genome-wide association (GWA) studies. Notable genes with VDR binding included IRF8, associated with MS, and PTPN2 associated with Crohn's disease and T1D. Furthermore, a number of single nucleotide polymorphism associations from GWA were located directly within VDR binding intervals, for example, rs13385731 associated with SLE and rs947474 associated with T1D. We also observed significant enrichment of VDR intervals within regions of positive selection among individuals of Asian and European descent. ChIP-seq determination of transcription factor binding, in combination with GWA data, provides a powerful approach to further understanding the molecular bases of complex diseases.
  18. Michael Scally MD

    Michael Scally MD Doctor of Medicine

    Holick MF. The D-lemma: To Screen or Not to Screen for 25-Hydroxyvitamin D Concentrations. Clin Chem 2010;56(5):729-31. The D-lemma: To Screen or Not to Screen for 25-Hydroxyvitamin D Concentrations -- Holick 56 (5): 729 -- Clinical Chemistry

    Until recently, there has been little interest in the medical and pediatric communities regarding the vitamin D status of their patients. It had been assumed that everyone was vitamin D sufficient and that only those patients with fat-malabsorption syndromes were at risk(1). African Americans were at risk because of their sunscreening skin pigment, but little attention was placed on their vitamin D status because African Americans were at less risk of fracture than Caucasians. The introduction of drugs to treat osteoporosis made physicians aware that vitamin D deficiency was a contributing factor for osteoporosis.

    Vitamin D made in the skin or ingested from the diet is converted in the liver to 25-hydroxyvitamin D [25(OH)D]1 (1)(2), the major circulating form of vitamin D used for evaluating the vitamin D status of patients. 25(OH)D is hydroxylated in the kidneys to form the biologically active metabolite 1,25-dihydroxyvitamin D [1,25(OH)2D](1)(2). Because most children and adults were assumed to be vitamin D sufficient when reference intervals for 25(OH)D were determined, values ranged from 10 µg/L (ng/mL) to 55 µg/L. Studies of adults that evaluated parathyroid hormone (PTH) with 25(OH)D revealed, however, that PTH concentrations began to plateau at 30–40 µg/L(3). Healthy adults receiving vitamin D and calcium supplementation who had blood 25(OH)D concentrations between 11 µg/L and 19 µg/L demonstrated substantial decreases in their PTH concentrations, whereas adults with a 25(OH)D concentration between 20 µg/L and 25 µg/L had no significant change in PTH, suggesting that vitamin D deficiency should be defined as a 25(OH)D concentration <20 µg/L(4). Postmenopausal women whose 25(OH)D concentrationincreased from approximately 20 µg/L to approximately 32 µg/L had a 65% increase in intestinal calcium absorption(5). Thus, vitamin D deficiency was defined as a 25(OH)D concentration of <20 µg/L, but for maximizing the vitamin D effect on calcium metabolism, the recommendation was that a 25(OH)D concentration >30 µg/L was needed. The gap was bridged by defining vitamin D insufficiency as a 25(OH)D concentration of 21–29 µg/L(1)(5).

    In the 1980s came the first suggestion that a person’s vitamin D status may be related to risk of developing and dying from colorectal cancer(6). This seminal observation was quickly followed over the next 2 decades by a plethora of epidemiologic studies relating vitamin D deficiency with an increased risk for many deadly cancers(1)(7)(8). These association studies were supported by a randomized controlled trial with postmenopausal women who received 1100 IU of vitamin D3 plus 1500 mg of calcium per day for 4 years had a >60% reduction in the development of all cancers(9). A multitude of retrospective studies that evaluated the long-term impact of ingesting vitamin D either during the first year of life or through adult life began to reveal intriguing associations between a higher intake of vitamin D or higher serum 25(OH)D concentrations and decreased risks for autoimmune diseases (including type I diabetes, multiple sclerosis, rheumatoid arthritis, and Crohn disease), hypertension, heart disease, and stroke, as well as upper respiratory tract infections, wheezing disorders, asthma, and falling(1)(10).The lay press’s enthusiastic reporting of the potential health benefits of vitamin D has been the catalyst for patients requesting their physician to order a 25(OH)D test. The physician, reluctant to order a relatively expensive blood test, often finally relents and is shocked to find that the patient was right and was vitamin D deficient. This experience leads the physician to order 25(OH)D for all patients and then to discover that essentially all of the patients were vitamin D deficient or insufficient. Such experiences have led to the 25(OH)D assay being one of the most-ordered, if not the most-ordered, esoteric assay in the US. These anecdotal observations by physicians and pediatricians confirm what is well documented in the literature, which is that children and adults in the US are at high risk for vitamin D deficiency and insufficiency. Data from the Third National Health and Nutrition Examination Survey (NHANES III) not only has revealed that the prevalence of vitamin D deficiency and insufficiency is >50% among children and young, middle-aged, and older adults but also has made startling associations with increased risks for hypertension, type II diabetes, colorectal and breast cancers, myocardial infarction, strokes, peripheral vascular disease, and wheezing disorders(1)(10)(11)(12)(13). Retrospective and prospective studies have even linked vitamin D deficiency with an increased risk for preeclampsia and cesarean section(1).

    With the knowledge that most children and adults are vitamin D deficient or insufficient, and that this deficiency places them at high risk for chronic diseases, should everyone be tested for their blood 25(OH)D concentration, as we do for blood lipids, given that vitamin D status may play a more important role in health than almost any other biochemical marker? The skeptics have argued that most of the studies that have related vitamin D status with the risk of chronic disease have been epidemiologic association studies and that randomized controlled clinicaltrials are needed to prove the health benefits of vitamin D.

    The vitamin D deficiency/insufficiency epidemic is caused by the fact that few foods naturally contain or are fortified with vitamin D(1)(12). For adults, 100 IU of vitamin D increases the blood 25(OH)D concentration by approximately 1 µg/L(14)(15). In the winter, the mean 25(OH)D concentration is approximately 18–22 µg/L in Caucasian adults and approximately 15–18 µg/L in African American adults(1)(14)(15). Thus, to raise blood concentrations into a sufficient range requires between 1500 and 2000 IU of vitamin D supplementation per day. Studies of children have suggested that 400 IU of vitamin D per day is inadequate to raise blood concentrations into the sufficient range. Young girls 10–17 years of age who received the equivalent of 2000 IU vitamin D per day for 1 year raised their blood concentrations into the sufficient range(16).

    With the recognition of widespread vitamin D deficiency/insufficiency in children and adults, there is no need to measure everybody’s blood 25(OH)D. It would be much more cost-effective to implement a vitamin D supplementation program for all children and adults until there is higher fortification of vitamin D in more foods. What also needs to be appreciated is that sensible sun exposure in the spring, summer, and fall is also a good source for vitamin D(1). The highest risk for vitamin D deficiency/insufficiency occurs in the winter, when little if any vitamin D can be produced in the skin if an individual lives at a latitude above Atlanta, Georgia (approximately 33° north latitude)(1). People ofcolor, especially African Americans, are at very high risk, owing to their avoidance of sun exposure and their decreased production of vitamin D due to their skin pigmentation(1)(15). Obesity, which is also epidemic in children and adults, increases the risk of deficiency/insufficiency, partly because of the sequestration of the fat-soluble vitamin in body fat(1)(11)(12). All of these high-risk groups, along with all children and adults, can maintain adequate serum 25(OH)D concentrations through vitamin D supplementation, ingestion of foods fortified with vitamin D, and sensible sun exposure(1).

    There are, however, patients who should be screened for vitamin D deficiency/insufficiency and monitored for their 25(OH)D concentrationwhile being treated with vitamin D. Patients with inflammatory bowel disease, cystic fibrosis, and liver and kidney diseases; gastric-bypass patients; patients taking antiseizure medications, glucocorticoids, or AIDS medications are at high risk for vitamin D deficiency/insufficiency that will negatively affect their musculoskeletal health(1)(10). Patients with primary hyperparathyroidism are often vitamin D deficient and benefit from vitamin D repletion(1). Patients with chronic granulomatous disorders not only are at high risk for vitamin D deficiency because of the extrarenal production of 1,25(OH)2D but also need to have their 25(OH)D concentration monitored so they do not experience the skeletal manifestations of vitamin D deficiency, which include osteomalacia, osteopenia, and osteoporosis. The blood concentrations of suchpatients also need to be monitored more frequently, because if the 25(OH)D concentration exceeds 30 µg/L, such patients are at increased risk for hypercalciuria and hypercalcemia(1)(17).

    It has been suggested that everyone should raise their blood 25(OH)D concentration to >40 µg/L or even 60 µg/L to obtain the maximum health benefits of vitamin D. These recommendations are based on the epidemiologic association data suggesting that children and adults who have the highest blood 25(OH)D concentrations are at the lowest risk for developing hypertension, increased blood sugar, and metabolic syndrome, among other chronic diseases(1)(10)(11). A few intervention studies have suggested that increasing vitamin D intake will have a more positive health outcome, including reducing the risk for cancer(9); however, until randomized controlled trials provide unequivocal evidence that higher blood 25(OH)D concentrations of 40 µg/L or greater are needed for maximum health, it would be premature at this time to monitor everyone’s serum 25(OH)D concentration so that it is >40 µg/L.

    Physicians often order both the 25(OH)D and 1,25(OH)2D tests when evaluating the vitamin D status of their patients or mistakenly order only the 1,25(OH)2D assay. Although the 1,25(OH)2D assay is of value for the differential diagnosis of hypercalcemic syndromes associated with chronic granulomatous disorders and inborn and acquired disorders of 25(OH)D metabolism, this assay is of no value in determining a patient’s vitamin D status and should not be ordered for this purpose(1). 1,25(OH)2D concentrations are usually within reference intervals or increased in vitamin D–deficient/insufficient patients(1).

    Although the medical community has been greatly concerned about vitamin D intoxication, it is one of the rarest reported medical conditions and is usually not observed until >10 000 IU of vitamin D are ingested per day for >5 months(1)(14). Blood 25(OH)D concentrations are usually >200 µg/L before manifestations of vitamin D intoxication, including hypercalcemia, hyperphosphatemia, and soft tissue calcification, are observed(1). There is no downside to increasing everyone’s vitamin D intake by increasing the consumption of foods that naturally contain or are fortified with vitamin D. Dietary sources are not adequate, however, to sustain vitamin D sufficiency in children and adults, and thus taking a vitamin D supplement and taking advantage of the beneficial effect of sun exposure will help guarantee vitamin D sufficiency for maximizing bone health and possibly for other health benefits. I recommend 400–1000 IU/day for infants, 1000–1500 IU/day for children 1–10 years of age, and 1500–2000 IU/day for teenagers and adults.

    Adams JS, Hewison M. Update in Vitamin D. J Clin Endocrinol Metab 2010;95(2):471-8. JCEM -- Sign In Page

    The past decade, particularly the last 18 months, witnessed a vigorous increase in interest in vitamin D from both the lay and biomedical worlds. Much of the growing interest in vitamin D is powered by new data being extracted from the National Health and Nutrition Examination Survey (NHANES). The newest statistics demonstrate that more than 90% of the pigmented populace of the United States (Blacks, Hispanics, and Asians) now suffer from vitamin D insufficiency (25-hydroxyvitamin D <30 ng/ml), with nearly three fourths of the white population in this country also being vitamin D insufficient. This represents a near doubling of the prevalence of vitamin D insufficiency seen just 10 yr ago in the same population. This review attempts to provide some explanation for: 1) the rapid decline in vitamin D status in the United States; 2) the adverse impact of vitamin D insufficiency on skeletal, infectious/inflammatory, and metabolic health in humans; and 3) the therapeutic rationale and reliable means for vigorous supplementation of our diets with vitamin D.
  19. cvictorg

    cvictorg Member

    eMJA: Annual intramuscular injection of a megadose of cholecalciferol for treatment of vitamin D deficiency: efficacy and safety data

    Annual intramuscular injection of a megadose of cholecalciferol for treatment of vitamin D deficiency: efficacy and safety data

    Participants: Five men and 45 women (mean age 66.3 years) with vitamin D deficiency who were given a single therapeutic intramuscular injection of 600 000 IU (15 mg) cholecalciferol (vitamin D3).

    Conclusions: Once-yearly intramuscular cholecalciferol injection (600 000 IU) is effective therapy for vitamin D deficiency. While this therapy appears to be safe, the potential for developing hypercalciuria needs to be examined in a large randomised controlled trial.

    In our study, a single annual intramuscular injection of 600 000 IU cholecalciferol was administered to 50 vitamin D-deficient participants. The therapy was effective, with normalisation of serum 25OHD levels and maintenance of a level well above 50 nmol/L at 12 months. This result was achieved with very little change in serum calcium levels and no deterioration in renal function, although there was a progressive increase in urine calcium excretion indices. The latter usually suggests an obligatory calcium loss, and may have been affected by oral calcium intakes. These findings raise the possibility of hypercalciuria. Future randomised controlled trials which include 24-hour urine calcium excretion measurements will be essential for validating the safety of megadose intramuscular cholecalciferol therapy.

    We suggest that a once-yearly intramuscular cholecalciferol injection (600 000 IU) should be further investigated as a therapeutic option for treating vitamin D deficiency. This treatment is currently unavailable in Australia, and there is no ideal preparation of megadose vitamin D2 or D3 to fill this therapeutic gap. However, at a cost of $5–$10 per injection annually compared with $35 for a monthly course of 5 Ostelin capsules daily (suggested dosages to treat vitamin D deficiency),4 it is remarkably cost-effective. The simple dosing regimen also allows convenient outpatient management and may improve patient compliance.


    We identified 36 discrete prescribing regimens. The 3 most common regimens were ergocalciferol 50,000 IU once weekly for 4 weeks followed by 50,000 IU once monthly for 5 months (n = 48); ergocalciferol 50,000 IU once monthly for 6 months (n = 80); and ergocalciferol 50,000 IU 3 times weekly for 6 weeks (n = 27). Each of these 3 treatments significantly increased serum 25-OHD (P<.01), but vitamin D sufficiency was achieved in only 38%, 42%, and 82% of study subjects, respectively. Regimens with >600,000 IU of ergocalciferol given for a mean of 60 ± 40 days achieved sufficiency in 64% of cases, without vitamin D toxicity

    In this study, regimens that contained at least 600,000 IU of ergocalciferol appeared to be the most effective in achieving vitamin D sufficiency. Guidelines for the treatment of vitamin D insufficiency in healthy adults should be developed.
  20. Martin777

    Martin777 Junior Member

    Based on what I read on this forum, various articles, anecgotal evidence on other sites and one study saying there appears to be a link between testosterone levels and vitamin d levels, I self medicated with Vit D high doses and drove myself from 13 ng/ml to ....... 116 ng/ml within 3 months...

    I aimed for high levels of the scale, advocated by many , including Han, but apparently I took a little too much of it.

    Anyway, I had two testosterone measurements of around 295 ng/dl, one in summer 2009 and the other in July this year.

    3 months later, despite taking these high Vit D3 doses and reaching that unusually high level, my T increased only to 359 ng/dl, and it might be also contributed to taking Zinc supplements as well some positive changes in my personal life. (weight stayed the same, still significantly overweight)

    Based on only me, I'd say, vitamin D is quite needed but it appears to be overhyped when it comes to hormones and testosterone.

    Perhaps the link between high levels of Vit D and high testosterone is not direct, it just happens that healthier people have both of these things high, and unhealthy people have both of them low.

    BTW do I have to worry about hypercalcemia now? should I check my serum calcium levels?

    wiki says

    Levels of 25-hydroxy-vitamin D that are consistently above 200 ng/mL (500 nmol/L) are thought to be potentially toxic, although data from humans is sparse. In animal studies levels up to 400 ng/mL (1,000 nmol/L) were not associated with toxicity.[5] Vitamin D toxicity usually results from taking supplements in excess. Hypercalcemia is typically the cause of symptoms, and levels of 25-hydroxy-vitamin D above 150 ng/mL (375 nmol/L) are usually found, although in some cases 25-hydroxy-vitamin D levels may appear to be normal. It is recommended to periodically measure serum calcium in individuals receiving large doses of vitamin D.[38]