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  1. All, After bashing on the Huffington Post for their poor coverage of yesterday's fish oil protects against Alzheimer's disease study, I want to be fair. Today they've got a pretty thorough and well-researched article on vitamin D. They advocate three things I can agree with: The best way to get vitamin D is via modest sun exposure and supplements if necessary depending on your latitude/climate/lifestyle The serum vitamin D level to target is 30-50 ng/ml (75-125 nmol/L) You don't want to be too high or too low. The best way to determine how much to supplement is to get a blood test, and then titrate your supplement level to get into the 30-50 ngl/ml range by starting with these dosages: 100 IU (2.5 mcg) per day increases vitamin D blood levels 1 ng/ml (2.5 nmol/L). 500 IU (12.5 mcg) per day increases vitamin D blood levels 5 ng/ml (12.5 nmol/L). 1000 IU (25 mcg) per day increases vitamin D blood levels 10 ng/ml (25 nmol/L). 2000 IU (50 mcg) per day increases vitamin D blood levels 20 ng/ml (50 nmol/L). Thoughts on the article, and the wisdom of the approach to vitamin D it advocates? --Dean
  2. Dean Pomerleau

    Dean's Vegan Supplement Regime

    Several people have recently asked me (via email) about my supplement regime. So I figured I post it here, both to share it with a wider audience, and to get people's feedback & suggestions, if they are so inclined. Several things to note in general about my supplement strategy: I'm a vegan, so several things I take because they are harder to get in a vegan diet (e.g. B12). I eat a very high fiber, unprocessed and mostly raw diet, meaning absorption of vitamins and minerals is likely to be lower than on a typical diet. I've definitely found this for iron. I've become anemic on two occasions in the past when not supplementing with iron. Now, for the last few years, supplement 300% of the RDA of iron per day, my hemoglobin and ferritin levels stay near the bottom of the reference range, and I'm able to donate blood regularly. Based on my 23andMe genetic testing results, and some observations from my eye doctor, I'm at increased risk (5-7x normal risk) of macular degeneration (AMD), so I take Lutein and Zeaxanthin, per the AREDS study that found these two antioxidants in the doses I take to be protective against progression of AMD. Sorry if the formatting isn't very good, and the lines wrap on a small screen. I've included a screen capture below in case its easier for people to read. Supplement Quantity Notes (Brand) --------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------- Vit B12 1 Tab/6 Days 100mcg/6 days = ~800% RDA/day as cyanocobalamin. Nibble 1/6th tab/day. Missing in vegan diet. Solgar Vit D3 1200 IU/Day 1000IU/day (+ D in calcium supp. below). Sundown Calcium 1 Cap/Day 250mg Ca / day, + about 175 IU vit D. Bone health. Source Naturals CCM Calcium Vit K2 1 Cap/2 Days 2.5mg / day. Bone health. Carlson Strontium 1 Cap/2 Days 340mg / day. Bone health. Vitacost Iodine 1 Tab/Day 150mg = 100% RDA / day as kelp tablet. I don't eat iodized salt or processed food. Good 'N Natural Iron 1 Cap/Day 300% RDA / day as Ferrous Sulfate (65mg). Low absorbable sources in vegan diet. Nature Made Zinc 1 Tab/Day 50mg / day Low in vegan diet. NOW Lutein/Zea 1 Cap/Day 25mg Lutein & 5mg Zeaxanthin. AREDS dosages for macular degeneration (AMD) prevention. Trunature DHA/EPA 1 Cap/3 Days Each cap has 320/130mg DHA/EPA. ~1 serving fish/wk, Prevent AMD - I'm at high risk. Ovega-3 Selenium 1 Cap/4 Days 75% of RDA / day. To make up for diet shortfall. Replaced 1/2 brazil nut on 10/23/15. Now Probiotic 1 Tab/2 Days Gut health. 5 billion CFU. 15 strains, slow release. Hyperbiotic Pro-15 Milk Thistle 1 Cap/2 Days 200mg/day. Liver health. Had liver issue (high ALT/AST) for a while in early 2015. LEF Here is the same table as an screen capture image (click to enlarge): --Dean
  3. Dean Pomerleau

    Calcium, Bone Health & Fracture Risk

    Bone health is a concern for CR practitioners, since CR practitioners have been shown to have less bone mass (along with less fat and lean mass) than the general population, both in a one-year randomized control trial [3], and more significantly in a study of a number of us long-term CR practitioners by Luigi Fontana et al. [4]. Fortunately, bone quality does not appear to be compromised in us long-term practitioners [4]. Due to our lower total body mass (hence less force when we fall / crash) but also less fat mass (hence less padding when we fall / crash), it's not clear what the net effect of our thinner but structurally-sound bones is on our risk of fracture. So it was interesting to see that two new meta-analyses in this month's British Medical Journal by the same group of New Zealand researchers addressed the relationship between dietary and supplemental calcium (with or without vitamin D) on bone mineral density (BMD) [1] and fracture risk [2]. After looking at all the available epidemiological and randomized control trials of the effects of calcium intake on BMD and fracture risk, the authors conclude that: Increasing calcium intake from dietary sources or by taking calcium supplements produces small non-progressive increases in BMD, which are unlikely to lead to a clinically significant reduction in risk of fracture. [1] and: Dietary calcium intake is not associated with risk of fracture, and there is no clinical trial evidence that increasing calcium intake from dietary sources prevents fractures. Evidence that calcium supplements prevent fractures is weak and inconsistent. [2] While [2] did find supplemental calcium was associated with a small reduction in total and vertebral fractures, there was no reduction in hip or wrist fractures, and some of the included studies were suspect / low quality. When they included only the four most well-conducted randomized control trials in their analysis (which included 44,500 subjects), supplemental calcium didn't reduce total fractures or fractures at any specific site. Overall, it doesn't appear that either dietary or supplemental calcium (with or without vitamin D) will improve our odds of avoiding fractures. At the same time bisphosphonates and other BMD boosting medications have a checkered track record and sometimes serious side effects [5]. So interventions like exercise [4], maintaining our coordination & balance via activities like yoga and sports, and minimizing risk of traumatic injuries (e.g. by wearing seat belts when driving, helmets when biking, holding handrails when climbing stairs etc.) appear to be the best strategies for keeping our bones safe. --Dean ----------- [1] BMJ 2015; 351 doi: http://dx.doi.org/10.1136/bmj.h4183(Published 29 September 2015) Cite this as: BMJ 2015;351:h4183 Calcium intake and bone mineral density: systematic review and meta-analysis Vicky Tai, William Leung, Andrew Grey, Ian R Reid, Mark J Bolland Abstract Objective To determine whether increasing calcium intake from dietary sources affects bone mineral density (BMD) and, if so, whether the effects are similar to those of calcium supplements. Design Random effects meta-analysis of randomised controlled trials. Data sources Ovid Medline, Embase, Pubmed, and references from relevant systematic reviews. Initial searches were undertaken in July 2013 and updated in September 2014. Eligibility criteria for selecting studies Randomised controlled trials of dietary sources of calcium or calcium supplements (with or without vitamin D) in participants aged over 50 with BMD at the lumbar spine, total hip, femoral neck, total body, or forearm as an outcome. Results We identified 59 eligible randomised controlled trials: 15 studied dietary sources of calcium (n=1533) and 51 studied calcium supplements (n=12 257). Increasing calcium intake from dietary sources increased BMD by 0.6-1.0% at the total hip and total body at one year and by 0.7-1.8% at these sites and the lumbar spine and femoral neck at two years. There was no effect on BMD in the forearm. Calcium supplements increased BMD by 0.7-1.8% at all five skeletal sites at one, two, and over two and a half years, but the size of the increase in BMD at later time points was similar to the increase at one year. Increases in BMD were similar in trials of dietary sources of calcium and calcium supplements (except at the forearm), in trials of calcium monotherapy versus co-administered calcium and vitamin D, in trials with calcium doses of ≥1000 versus <1000 mg/day and ≤500 versus >500 mg/day, and in trials where the baseline dietary calcium intake was <800 versus ≥800 mg/day. Conclusions Increasing calcium intake from dietary sources or by taking calcium supplements produces small non-progressive increases in BMD, which are unlikely to lead to a clinically significant reduction in risk of fracture. ------------- [2] BMJ 2015; 351 doi: http://dx.doi.org/10.1136/bmj.h4580(Published 29 September 2015) Cite this as: BMJ 2015;351:h4580 Calcium intake and risk of fracture: systematic review Mark J Bolland, William Leung, Vicky Tai, Sonja Bastin, Greg D Gamble, Andrew Grey, Ian R Reid Abstract Objective To examine the evidence underpinning recommendations to increase calcium intake through dietary sources or calcium supplements to prevent fractures. Design Systematic review of randomised controlled trials and observational studies of calcium intake with fracture as an endpoint. Results from trials were pooled with random effects meta-analyses. Data sources Ovid Medline, Embase, PubMed, and references from relevant systematic reviews. Initial searches undertaken in July 2013 and updated in September 2014. Eligibility criteria for selecting studies Randomised controlled trials or cohort studies of dietary calcium, milk or dairy intake, or calcium supplements (with or without vitamin D) with fracture as an outcome and participants aged >50. Results There were only two eligible randomised controlled trials of dietary sources of calcium (n=262), but 50 reports from 44 cohort studies of relations between dietary calcium (n=37), milk (n=14), or dairy intake (n=8) and fracture outcomes. For dietary calcium, most studies reported no association between calcium intake and fracture (14/22 for total, 17/21 for hip, 7/8 for vertebral, and 5/7 for forearm fracture). For milk (25/28) and dairy intake (11/13), most studies also reported no associations. In 26 randomised controlled trials, calcium supplements reduced the risk of total fracture (20 studies, n=58 573; relative risk 0.89, 95% confidence interval 0.81 to 0.96) and vertebral fracture (12 studies, n=48 967. 0.86, 0.74 to 1.00) but not hip (13 studies, n=56 648; 0.95, 0.76 to 1.18) or forearm fracture (eight studies, n=51 775; 0.96, 0.85 to 1.09). Funnel plot inspection and Egger’s regression suggested bias toward calcium supplements in the published data. In randomised controlled trials at lowest risk of bias (four studies, n=44 505), there was no effect on risk of fracture at any site. Results were similar for trials of calcium monotherapy and co-administered calcium and vitamin D. Only one trial in frail elderly women in residential care with low dietary calcium intake and vitamin D concentrations showed significant reductions in risk of fracture. Conclusions Dietary calcium intake is not associated with risk of fracture, and there is no clinical trial evidence that increasing calcium intake from dietary sources prevents fractures. Evidence that calcium supplements prevent fractures is weak and inconsistent. ------------- [3] Aging Cell. 2011 Feb;10(1):96-102. doi: 10.1111/j.1474-9726.2010.00643.x. Epub 2010 Nov 15. Reduced bone mineral density is not associated with significantly reduced bone quality in men and women practicing long-term calorie restriction with adequate nutrition. Villareal DT(1), Kotyk JJ, Armamento-Villareal RC, Kenguva V, Seaman P, Shahar A, Wald MJ, Kleerekoper M, Fontana L. Author information: (1)Division of Geriatrics and Nutritional Science, Washington University School of Medicine, 660 S. Euclid Avenue, St. Louis, MO 63110, USA. Calorie restriction (CR) reduces bone quantity but not bone quality in rodents. Nothing is known regarding the long-term effects of CR with adequate intake of vitamin and minerals on bone quantity and quality in middle-aged lean individuals. In this study, we evaluated body composition, bone mineral density (BMD), and serum markers of bone turnover and inflammation in 32 volunteers who had been eating a CR diet (approximately 35% less calories than controls) for an average of 6.8 ± 5.2 years (mean age 52.7 ± 10.3 years) and 32 age- and sex-matched sedentary controls eating Western diets (WD). In a subgroup of 10 CR and 10 WD volunteers, we also measured trabecular bone (TB) microarchitecture of the distal radius using high-resolution magnetic resonance imaging. We found that the CR volunteers had significantly lower body mass index than the WD volunteers (18.9 ± 1.2 vs. 26.5 ± 2.2 kg m(-2) ; P = 0.0001). BMD of the lumbar spine (0.870 ± 0.11 vs. 1.138 ± 0.12 g cm(-2) , P = 0.0001) and hip (0.806 ± 0.12 vs. 1.047 ± 0.12 g cm(-2) , P = 0.0001) was also lower in the CR than in the WD group. Serum C-terminal telopeptide and bone-specific alkaline phosphatase concentration were similar between groups, while serum C-reactive protein (0.19 ± 0.26 vs. 1.46 ± 1.56 mg L(-1) , P = 0.0001) was lower in the CR group. Trabecular bone microarchitecture parameters such as the erosion index (0.916 ± 0.087 vs. 0.877 ± 0.088; P = 0.739) and surface-to-curve ratio (10.3 ± 1.4 vs. 12.1 ± 2.1, P = 0.440) were not significantly different between groups. These findings suggest that markedly reduced BMD is not associated with significantly reduced bone quality in middle-aged men and women practicing long-term calorie restriction with adequate nutrition. PMCID: PMC3607368 PMID: 20969721 --------------- [4] Arch Intern Med. 2006 Dec 11-25;166(22):2502-10. Bone mineral density response to caloric restriction-induced weight loss or exercise-induced weight loss: a randomized controlled trial. Villareal DT(1), Fontana L, Weiss EP, Racette SB, Steger-May K, Schechtman KB, Klein S, Holloszy JO. Author information: (1)Division of Geriatrics and Nutritional Sciences, Department of Medicine, Washington University School of Medicine, St Louis, MO 63110, USA. dvillare@wustl.edu Erratum in Arch Intern Med. 2007 Mar 12;167(5):452. BACKGROUND: Bone loss often accompanies weight loss induced by caloric restriction (CR), but whether bone loss accompanies similar weight loss induced by exercise (EX) is unknown. We tested the hypothesis that EX-induced weight loss is associated with less bone loss compared with CR-induced weight loss. METHODS: Forty-eight adults (30 women; 18 men; mean +/- SD age, 57 +/- 3 years; and mean +/- SD body mass index, 27 +/- 2 kg/m2) were randomized to 1 of 3 groups for 1 year: CR group (n = 19), regular EX group (n = 19), or a healthy lifestyle (HL) control group (n = 10). Primary outcome measure was change in hip and spine bone mineral density (BMD). Secondary outcomes were bone markers and hormones. RESULTS: Body weight decreased similarly in the CR and EX groups (10.7% +/- 6.3% [-8.2 +/- 4.8 kg] vs 8.4% +/- 6.3% [-6.7 +/- 5.6 kg]; P = .21), whereas weight did not change in the HL group (-1.2% +/- 2.5% [-0.9 +/- 2.0 kg]). Compared with the HL group, the CR group had decreases in BMD at the total hip (-2.2% +/- 3.1% vs 1.2% +/- 2.1%; P = .02) and intertrochanter (-2.1% +/- 3.4% vs 1.7 +/- 2.8%; P = .03). The CR group had a decrease in spine BMD (-2.2% +/- 3.3%; P = .009). Despite weight loss, the EX group did not demonstrate a decrease in BMD at any site. Body weight changes correlated with BMD changes in the CR (R = 0.61; P = .007) but not in the EX group. Bone turnover increased in both CR and EX groups. CONCLUSIONS: CR-induced weight loss, but not EX-induced weight loss, is associated with reductions in BMD at clinically important sites of fracture. These data suggest that EX should be an important component of a weight loss program to offset adverse effects of CR on bone. PMID: 17159017 ---------------- [5] Acta Medica (Hradec Kralove). 2012;55(3):111-5. Bisphosphonate-related osteonecrosis of the jaws. A severe side effect of bisphosphonate therapy. Janovská Z(1). Author information: (1)Department of Dentistry, Charles University in Prague, Faculty of Medicine and University Hospital, Hradec Králové, Czech Republic. janovani@centrum.cz Bisphosphonates (BP) are potent inhibitors of bone resorption used mainly in the treatment of metastatic bone disease and osteoporosis. By inhibiting bone resorption, they prevent complications as pathological fracture, pain, tumor-induced hypercalcemia. Even though patient's benefit of BP therapy is huge, various side effects may develop. Bisphosphonate-related osteonecrosis of the jaws (BRONJ) is among the most serious ones. Oncologic patients receiving high doses of BP intravenously are at high risk of BRONJ development. BPs impair bone turnover leading to compromised bone healing which may result in the exposure of necrotic bone in the oral cavity frequently following tooth extraction or trauma of the oral mucosa. Frank bone exposure may be complicated by secondary infection leading to osteomyelitis development with various symptoms and radiological findings. In the management of BRONJ, conservative therapy aiming to reduce the symptoms plays the main role. In patients with extensive bone involvement resective surgery may lead to complete recovery, provided that the procedure is correctly indicated. Since the treatment of BRONJ is difficult, prevention is the main goal. Therefore in high risk patients dental preventive measures should be taken prior to bisphosphonate administration. This requires adequate communication between the prescribing physician, the patient and the dentist. PMID: 23297518
  4. Here is a new study [1] (popular press article) that caught my attention. After following nearly 30,000 Swedish women for 20 years, the researchers found those with the highest intentional sun exposure lived 0.6 - 2.1 years longer on average. While the rate of skin cancer in the high exposure group was higher, they died less from CVD and non-cancer / non-CVD causes during the study, which more than made up for the extra few deaths from skin cancer. The authors suggest it may be the health benefits of higher vitamin D or melatonin that is responsible for the reduced mortality in sun-lovers. I'm not going to go into great depth on this one, because I think the study is pretty flawed. First, Sweden is a very northerly country with an average latitude of 62°. That is equivalently far north as Anchorage Alaska. So people are probably more likely to be vitamin D deficient living that far north, and even a high amount of sun exposure at such northerly latitudes is unlikely to have the same effects (either good or bad) as sun exposure at more southerly points on the globe where most of the world live. But I think the biggest problem is the vast difference in other demographic and behavioral characteristics between those who got a lot of sun exposure and those who didn't. At study entry, compared to those who avoided the sun, those that got a lot of sun were: younger, less obese/overweight, more physically active, wealthier, less likely to suffer from a comorbidity, better educated, smoked more, and drank more alcohol. Of course they tried to statistically factor these differences out. But with so many differences between sun-avoiders and sun-worshippers, it's really difficult to determine cause and effect. In other words, is sun exposure really causing increased longevity, or simply a markers for a healthier lifestyle, or better health in general? The authors acknowledge this serious shortcoming in the discussion section: We acknowledge several major limitations of this study. First, it is not possible to differentiate between active sun exposure habits and a healthy lifestyle, and secondly, the results are of an observational nature; therefore, a causal link cannot be proven. So the takeaway is their might be benefits to sun exposure - at least for people living in northern climates. But I'd definitely continue to use sunscreen, particularly if you live more south than Sweden. --Dean --------- [1] J Intern Med. 2016 Mar 16. doi: 10.1111/joim.12496. [Epub ahead of print] Avoidance of sun exposure as a risk factor for major causes of death: a competing risk analysis of the Melanoma in Southern Sweden cohort. Lindqvist PG(1), Epstein E(2), Nielsen K(3), Landin-Olsson M(4), Ingvar C(5), Olsson H(6). Free Full text: http://onlinelibrary.wiley.com/doi/10.1111/joim.12496/epdf OBJECTIVE: Women with active sunlight exposure habits experience a lower mortality rate than women who avoid sun exposure; however, they are at an increased risk of skin cancer. We aimed to explore the differences in main causes of death according to sun exposure. METHODS: We assessed the differences in sun exposure as a risk factor for all-cause mortality in a competing risk scenario for 29 518 Swedish women in a prospective 20-year follow-up of the Melanoma in Southern Sweden (MISS) cohort. Women were recruited from 1990 to 1992 (aged 25-64 years at the start of the study). We obtained detailed information at baseline on sun exposure habits and potential confounders. The data were analysed using modern survival statistics. RESULTS: Women with active sun exposure habits were mainly at a lower risk of cardiovascular disease (CVD) and noncancer/non-CVD death as compared to those who avoided sun exposure. As a result of their increased survival, the relative contribution of cancer death increased in these women. Nonsmokers who avoided sun exposure had a life expectancy similar to smokers in the highest sun exposure group, indicating that avoidance of sun exposure is a risk factor for death of a similar magnitude as smoking. Compared to the highest sun exposure group, life expectancy of avoiders of sun exposure was reduced by 0.6-2.1 years. CONCLUSION: The longer life expectancy amongst women with active sun exposure habits was related to a decrease in CVD and noncancer/non-CVD mortality, causing the relative contribution of death due to cancer to increase. PMID: 26992108
  5. All, On the CR email list Al recently posted a series of studies, included below [1-3], showing that higher levels of serum vitamin D were associated with increased risk of prostate cancer. But the most recent such study Al posted [4], found the opposite - increased vitamin D level was associated with a decreased risk of prostate cancer. What the authors of [4] suggest in the discussion (included below) is that there may be a U-shaped curve between serum vitamin D and prostate cancer risk, with the 'sweet spot' being in the neighborhood of 20-30 ng/ml (or equiv. 50-75 nmol/l) range. The bottom line suggested by [4] appears to be that we want to have sufficient Vitamin D, but not too much, in order to avoid prostate cancer. Of course, men get a lot of their vitamin D from D-fortified dairy products, which may be driving some of this apparent positive association between vitamin D level and prostate cancer, since this recent meta-analysis [5] found: High intakes of dairy products, milk, low-fat milk, cheese, and total, dietary, and dairy calcium, but not supplemental or nondairy calcium, may increase total prostate cancer risk. So it is possible that higher levels of vitamin D are a marker for higher intake of dairy products in the general population, which may be driving the development of prostate cancer. --Dean -------------- [1] Plasma 25-hydroxyvitamin D and prostate cancer risk: the multiethnic cohort. Park SY, Cooney RV, Wilkens LR, Murphy SP, Henderson BE, Kolonel LN. Eur J Cancer. 2010 Mar;46(5):932-6. doi: 10.1016/j.ejca.2009.12.030. Epub 2010 Feb 8. PMID: 20064705 Free PMC Article http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2834847/ file:///C:/Documents%20and%20Settings/user/My%20Documents/Downloads/nihms169878%20(1).pdf Abstract The purpose of this study was to examine the relationship of plasma 25-hydroxyvitamin D (25(OH)D) concentrations to prostate cancer within a large multiethnic cohort in Hawaii and California using a nested case-control design. The study included 329 incident prostate cancer cases of African American, Native Hawaiian, Japanese, Latino, and White ancestry, and 656 controls matched on age, race/ethnicity, date/time of blood collection, and fasting status. Conditional logistic regression was used to estimate odds ratios (OR) and 95% confidence intervals (95% CI). No association with prostate cancer risk was found in an analysis based on quartiles of 25(OH)D. When clinically defined cutpoints were used, there was no increased risk for the lowest 25(OH)D concentration (OR for <20 vs. 30–<50 ng/ml = 1.10, 95% CI = 0.68-1.78), while there was a suggestive increased risk for higher concentrations (OR for =50 ng/ml = 1.52, 95% CI = 0.92-2.51). The findings from this prospective study of men in the Multiethnic Cohort do not support the hypothesis that vitamin D lowers the risk of prostate cancer. Further follow-up is warranted to determine whether the findings are consistent across ethnic groups. Keywords: 25-hydroxyvitamin D, multiethnic cohort, nested case-control study, plasma, prostate neoplasms --------- [2] Circulating levels of 25-hydroxyvitamin D and prostate cancer prognosis. Holt SK, Kolb S, Fu R, Horst R, Feng Z, Stanford JL. Cancer Epidemiol. 2013 Oct;37(5):666-70. doi: 10.1016/j.canep.2013.07.005. Epub 2013 Aug 20. PMID: 23972671 PMC Article http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3864767/ http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3864767/pdf/nihms517958.pdf Abstract OBJECTIVES: Ecological, in vitro, and in vivo studies demonstrate a link between vitamin D and prostate tumor growth and aggressiveness. The goal of this study was to investigate whether plasma concentration of vitamin D is associated with survivorship and disease progression in men diagnosed with prostate cancer. MATERIALS AND METHODS: We conducted a population-based cohort study of 1476 prostate cancer patients to assess disease recurrence/progression and prostate cancer-specific mortality (PCSM) risks associated with serum levels of 25(OH) vitamin D [25(OH)D]. RESULTS: There were 325 recurrence/progression and 95 PCSM events during an average of 10.8 years of follow-up. Serum levels of 25(OH)D were not associated with risk of recurrence/progression or mortality. Clinically deficient vitamin D levels were associated with an increased risk of death from other causes. CONCLUSIONS: We did not find evidence that serum vitamin D levels measured after diagnosis affect prostate cancer prognosis. Lower levels of vitamin D were associated with risk of non-prostate cancer mortality. KEYWORDS: 1,25(OH)(2)D; 1,25-dihydroxyvitamin D(3); 25(OH) vitamin D; 25(OH)D; ADT; BMI; Cohort studies; Epidemiologic studies; FFQ; HR; Humans; Male; Mortality; PCSM; PCa; PH; PSA; Prognosis; Prostatic neoplasms; Vitamin D/blood*; androgen deprivation therapy; body mass index; food frequency questionnaire; hazard ratio; proportional hazards; prostate cancer; prostate cancer-specific mortality; prostate specific antigen ---------- [3] In older men, lower plasma 25-hydroxyvitamin D is associated with reduced incidence of prostate, but not colorectal or lung cancer. Wong YY, Hyde Z, McCaul KA, Yeap BB, Golledge J, Hankey GJ, Flicker L. PLoS One. 2014 Jun 20;9(6):e99954. doi: 10.1371/journal.pone.0099954. eCollection 2014. Erratum in: PLoS One. 2014;9(9):e109511. PMID: 24949795 Free PMC Article http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4065010/ http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4065010/pdf/pone.0099954.pdf Abstract CONTEXT AND OBJECTIVE: Prostate, colorectal and lung cancers are common in men. In this study, we aimed to determine whether vitamin D status is associated with the incidence of these cancers in older men. DESIGN: Prospective cohort study. SETTING AND PARTICIPANTS: 4208 older men aged 70-88 years in Perth, Western Australia. MAIN OUTCOME MEASURES: Plasma 25-hydroxyvitamin D [25(OH)D] concentration was measured by immunoassay. New diagnoses of prostate, colorectal and lung cancers were determined via electronic record linkage. RESULTS: During a mean follow-up of 6.7±1.8 years, there were 315, 117 and 101 new diagnoses of prostate, colorectal and lung cancer. In multivariate competing risks proportional hazards models, every 10 nmol/l decrease in 25(OH)D concentration was associated with a 4% reduction in prostate cancer incidence (sub-hazard ratio [sHR] 0.96, 95% confidence interval [CI] 0.92-1.00). Every halving of 25(OH)D concentration was associated with a 21% reduction in incident prostate cancer in multivariate analysis (SHR 0.79, 95% CI 0.63-0.99). Following exclusion of prostate cancer cases diagnosed within 3 years of blood sampling, low 25(OH)D <50 nmol/l was associated with lower incident prostate cancer, and higher 25(OH)D >75 nmol/l was associated with higher incidence, when compared to the reference range 50-75 nmol/l, respectively (p = 0.027). Significant associations were also observed when 25(OH)D was modeled as a quantitative variable. No associations were observed between plasma 25(OH)D concentration with incidence of colorectal or lung cancer. CONCLUSION: Lower levels of vitamin D may reduce prostate cancer risk in older men. By contrast, levels of vitamin D did not predict incidence of colorectal or lung cancers. Further studies are needed to determine whether a causal relationship exists between vitamin D and prostate cancer in ageing men. ---------- [4] A prospective study of plasma 25-hydroxyvitamin D concentration and prostate cancer risk. Deschasaux M, Souberbielle JC, Latino-Martel P, Sutton A, Charnaux N, Druesne-Pecollo N, Galan P, Hercberg S, Le Clerc S, Kesse-Guyot E, Ezzedine K, Touvier M. Br J Nutr. 2016 Jan;115(2):305-14. doi: 10.1017/S0007114515004353. Epub 2015 Nov 16. PMID: 26568368 Abstract Mechanistic hypotheses suggest that vitamin D and the closely related parathyroid hormone (PTH) may be involved in prostate carcinogenesis. However, epidemiological evidence is lacking for PTH and inconsistent for vitamin D. Our objectives were to prospectively investigate the association between vitamin D status, vitamin D-related gene polymorphisms, PTH and prostate cancer risk. A total of 129 cases diagnosed within the Supplémentation en Vitamines et Minéraux Antioxydants cohort were included in a nested case-control study and matched to 167 controls (13 years of follow-up). 25-Hydroxyvitamin D (25(OH)D) and PTH concentrations were assessed from baseline plasma samples. Conditional logistic regression models were computed. Higher 25(OH)D concentration was associated with decreased risk of prostate cancer (ORQ4 v. Q1 0·30; 95 % CI 0·12, 0·77; P trend=0·007). PTH concentration was not associated with prostate cancer risk (P trend=0·4) neither did the studied vitamin D-related gene polymorphisms. In this prospective study, prostate cancer risk was inversely associated with 25(OH)D concentration but not with PTH concentration. These results bring a new contribution to the understanding of the relationship between vitamin D and prostate cancer, which deserves further investigation. KEYWORDS: 1; 25(OH)2D 1; 25(OH)D 25-hydroxyvitamin D; 25-Hydroxyvitamin D; 25-dihydroxyvitamin D; 25-dihydroxyvitamin D3 24-hydroxylase; CYP24A1 1; CaSR Ca-sensing receptor; GC vitamin D-binding globulin; MAF minor allele frequency; Nested case–control studies; PTH parathyroid hormone; Parathyroid hormone; Prostate cancer risk; RXR retinoid X receptor; SNP; SU.VI.MAX Supplémentation en Vitamines et Minéraux Antioxydants; VDR vitamin D receptor; gc-globulin or group-specific component Vitamin D is a prohormone synthesised in the skin from UVB exposure and absorbed from scarce dietary sources. It is first converted to 25-hydroxyvitamin D (25(OH)D) – its main circulating form – and then to 1,25-dihydroxyvitamin D (1,25(OH)2D) – its biologically active form. As 25(OH)D-to-1,25(OH)2D conversion and 1,25(OH)2D signalling can take place directly in prostate tissues(1), vitamin D is thought to play a role in the prevention of prostate cancer through pro-differentiation, pro-apoptosis, anti-proliferative and growth control activities, as suggested by experimental studies(2–4). However, so far, epidemiological evidence regarding the relationship between 25(OH)D concentration and prostate cancer risk has been inconsistent. On the basis of a dose–response meta-analysis that involved fifteen prospective studies, the World Cancer Research Fund/American Institute for Cancer Research (WCRF/AICR)(5), as part of the Continuous Update Project 2014 on prostate cancer, stated that the level of proof for the association between 25(OH)D concentration and prostate cancer risk was still ‘limited-no conclusion’. Most of the studies included in this meta-analysis observed null results. Besides, vitamin D is primarily involved in Ca homoeostasis: 1,25(OH)2D increases Ca concentration through enhanced intestinal Ca absorption, reabsorption of Ca from kidneys and bone resorption. Renal 25(OH)D-to-1,25(OH)2D conversion is induced by parathyroid hormone (PTH) secretion in response to low Ca concentration. 1,25(OH)2D exerts in turn a negative feedback on PTH secretion(6–8). Vitamin D and PTH are thus closely related. To our knowledge, only one prospective study has investigated the association between PTH concentration and prostate cancer risk, with null result(9). Several genes involved in vitamin D metabolism, in particular signalling (vitamin D receptor (VDR) and retinoid X receptor (RXR)), transportation (vitamin D-binding protein, also known as gc-globulin or group-specific component (GC)) and degradation (1,25-dihydroxyvitamin D3 24-hydroxylase (CYP24A1)), or in Ca homoeostasis (Ca-sensing receptor (CaSR)) could also play a role in prostate cancer aetiology(2). Recent meta-analyses found null associations between VDR BsmI, FokI and Cdx2 polymorphisms and prostate cancer risk(10–12). The epidemiological literature dealing with polymorphisms of other genes (GC, CYP24A1, RXR and CaSR) in relation to prostate cancer risk is scarce(13–16). Thus, our objective was to prospectively investigate the associations between prostate cancer risk and vitamin D status (25(OH)D concentration), plasma PTH concentration and polymorphisms of genes involved in vitamin D metabolism. Methods Subjects The Supplémentation en Vitamines et Minéraux Antioxydants (SU.VI.MAX) study was initially designed as a double-blind placebo-controlled trial (Trial Registration clinicaltrials.gov Identifier: NCT00272428) with purpose to assess the influence of a daily supplementation with nutritional doses of antioxidants (single capsule of a combination of ascorbic acid (120 mg), vitamin E (30 mg), ß-carotene (6 mg), Se (100 µg) and Zn (20 mg) or placebo) on the incidence of CVD and cancers(17). A total of 13 017 participants were enrolled in 1994–1995 for an 8-year-intervention trial and followed up for health events until September 2007. Participants were advised against taking any self-prescribed supplements (vitamin D and others) during the trial. ... Results A total of 129 prostate cancer cases diagnosed within the SU.VI.MAX cohort were included in this study. Mean age at diagnosis was 63·0 years and mean baseline-to-diagnosis time was 8·3 years. Of the cases, 49·2 % had a Gleason’s score =/>7. A total of 167 controls were randomly selected and matched to the cases. Table 1 summarises the characteristics of prostate cancer cases and controls. Compared with controls, prostate cancer cases were more likely to have a lower vitamin D status at baseline and to be better educated. Severe vitamin D deficiency (<10 ng/ml) was observed for 14·0 % of cases and 13·8 % of controls, and vitamin D insufficiency (<20 ng/ml) was observed for 62·8 % of cases and 54·5 % of controls, with no statistically significant difference between cases and controls. A seasonal fluctuation of vitamin D status was observed in controls with decreasing vitamin D status from October to March (shortening days) and increasing vitamin D status in April–May (extending days). All studied SNP respected the Hardy–Weinberg’s equilibrium (P>0·05). The repartition of subjects across the different genotypes was in accordance with that observed in European reference populations (CSHL-HapMap-CEU and 1000GENOMES-phase_1_EUR) for all SNP (P>0·05). 25(OH)D concentration was inversely associated with prostate cancer risk (ORper 1 ng/ml 0·96; 95 % CI 0·93, 1·00; Ptrend=0·04; ORQ4 v. Q1 0·30; 95 % CI 0·12, 0·77; Ptrend=0·007; OR<20 v. =/>20 ng/ml 0·44; 95 % CI 0·23, 0·85; P=0·01, Table 2; ORper 30 nmol/l 0·64; 95 % CI 0·42, 0·97; Ptrend=0·04, data not tabulated). Using the quartile coding this inverse association was observed in particular for cases with a Gleason’s score <7 (sixty-nine cases/ninety controls, ORQ4 v. Q1 0·03; 95 % CI 0·003, 0·40; Ptrend=0·02; data not tabulated), whereas it was not significant for cases with a Gleason’s score =/>7 (sixty cases/seventy-seven controls, ORQ4 v. Q1 0·96; 95 % CI 0·23, 4·05; Ptrend=0·5; data not tabulated). However, using the continuous 25(OH)D variable or the 20 ng/ml cut-off, these associations were not significant in both Gleason’s subgroups. Exclusion of cases diagnosed during the first 5 years of follow-up provided similar results (109 cases/140 controls, ORper 1 ng/ml 0·96; 95 % CI 0·93, 1·00; Ptrend=0·04; ORQ4 v. Q1 0·33; 95 % CI 0·12, 0·86; Ptrend=0·01; OR<20 v. =/>20 ng/ml 0·45; 95 % CI 0·23, 0·89; P=0·02; data not tabulated). No interaction was observed between 25(OH)D concentration and the intervention group of the SU.VI.MAX trial (Pinteraction>0·1 for all codings). Associations between 25-hydroxyvitamin D (25(OH)D) and parathyroid hormone (PTH) plasma concentrations, and prostate cancer risk, from conditional logistic regression, Supplémentation en Vitamines et Minéraux Antioxydants (SU.VI.MAX) cohort, France (1994–2007) (Odds ratios and 95 % confidence intervals) Table 2 Associations between 25-hydroxyvitamin D (25(OH)D) and parathyroid hormone (PTH) plasma concentrations, and prostate cancer risk, from conditional logistic regression, Supplémentation en Vitamines et Minéraux Antioxydants (SU.VI.MAX) cohort, France (1994–2007) (Odds ratios and 95 % confidence intervals) % confidence intervals) -------------------------------------------------- - === - ===Quartiles*===Insufficiency - === Per 1 unit increment===Q1 Q2 Q3 Q4 <20 ng/ml =/>20 ng/ml - === OR 95 % CI Ptrend===OR OR 95 % CI OR 95 % CI OR 95 % CI Ptrend OR OR 95 % CI P -------------------------------------------------- 25(OH)D (ng/ml) Cases/controls 129/167 42/32 31/43 25/49 31/43 81/91 48/76 Model 1† 0·96 0·93, 1·00 0·04 1·00 0·44 0·19, 1·04 0·18 0·07, 0·49 0·30 0·12, 0·77 0·007 1·00 0·44 0·23, 0·85 0·01 Cases/controls 96/123 27/20 23/35 20/35 26/33 57/66 39/57 Model 2† 0·95 0·91, 1·00 0·06 1·00 0·35 0·12, 1·07 0·13 0·04, 0·49 0·25 0·08, 0·81 0·02 1·00 0·43 0·19, 1·00 0·05 Cases/controls 96/123 27/20 23/35 20/35 26/33 57/66 39/57 Model 3† 0·96 0·91, 1·01 0·08 1·00 0·33 0·11, 1·03 0·12 0·03, 0·46 0·28 0·08, 0·95 0·03 1·00 0·43 0·18, 1·01 0·05 -------------------------------------------------- PTH (pg/ml) Cases/controls 129/167 31/43 34/40 34/40 30/44 Model 1† 0·97 0·94, 1·01 0·1 1·00 0·90 0·40, 2·05 0·95 0·40, 2·27 0·66 0·28, 1·55 0·4 Cases/controls 96/123 20/35 30/26 27/30 19/32 Model 2† 0·96 0·91, 1·01 0·09 1·00 1·72 0·60, 4·90 1·95 0·62, 6·18 0·77 0·25, 2·36 0·6 Cases/controls 96/123 20/35 30/26 27/30 19/32 Model 3† 0·96 0·91, 1·01 0·1 1·00 1·63 0·56, 4·77 2·25 0·67, 7·59 0·81 0·25, 2·62 0·8 -------------------------------------------------- Q, quartiles. * Model 1: cut-offs for quartiles of 25(OH)D plasma concentration (ng/ml) and PTH plasma concentration (pg/ml) were, respectively, 12·9/18·2/24·7 and 20·9/26·0/30·6. Models 2 and 3 are restricted to men who provided at least three valid 24 h-dietary records (ninety-six cases/123 controls): cut-offs for quartiles of 25(OH)D plasma concentration (ng/ml) and PTH plasma concentration (pg/ml) were, respectively, 13·7/18·5/25·2 and 20·9/25·9/30·2. † Model 1 was adjusted for age at baseline (continuous, matching factor), intervention group of the initial SU.VI.MAX trial (antioxidants/placebo, matching factor), month of blood draw (October–November/December–January/February–March/April–May), educational level (primary/secondary/superior), physical activity (irregular/<1 h/d walking equivalent/=/>1 h/d walking equivalent), alcohol intake (g/d, continuous), smoking status (never/former/current), height (cm, continuous), BMI (kg/m², continuous, matching factor), family history of prostate cancer (yes/no) and baseline serum prostate-specific antigen concentration (<3/=/>3 ng/l). Model 2 corresponds to model 1 further adjusted for energy intake (without alcohol) (continuous, kJ/d (kcal/d)), dietary intakes of Ca intake (continuous, mg/d) and dairy products (continuous, g/d), plasma Se (continuous, µmol/l) and Alpha-tocopherol (continuous, µmol/l) concentrations. Model 3 corresponds to model 2 with further mutual adjustment for 25(OH)D and PTH plasma concentrations (continuous). Plasma PTH concentration was not associated with prostate cancer risk (ORQ4 v. Q1 0·66; 95 % CI 0·28, 1·55; Ptrend=0·4) (Table 2). This result was similar (124 cases/157 controls) after removing participants with possibly abnormal PTH values that may suggest potential hyperparathyroidism (i.e. PTH=/>50·8 pg/ml if 25(OH)D<20 ng/ml, PTH=/>45·5 pg/ml if 20 ng/ml</=25(OH)D<30 ng/ml and PTH=/>45·3 pg/ml if 25(OH)D=/>30 ng/ml, as previously recommended(22)). Dietary Ca intake was not associated with prostate cancer risk (ninety-six cases/123 controls, ORQ4 v. Q1 0·83; 95 % CI 0·20, 3·43; Ptrend=0·5, data not tabulated), nor did dietary intake of vitamin D (ninety-six cases/123 controls, ORQ4 v. Q1 1·05; 95 % CI 0·40, 2·81; Ptrend=0·7, data not tabulated). All results were similar when models were further adjusted for dietary variables (although some of the results were only borderline significant due to loss of statistical power: ninety-six cases/123 controls), dietary Ca and mutual adjustments for 25(OH)D and PTH. Two-way interactions between 25(OH)D, PTH and dietary Ca intake were not statistically significant (all P>0·1, data not shown). No association was observed between the ten studied vitamin D-related SNP and prostate cancer risk in the codominant (Table 3), dominant and recessive models (data not tabulated). No interaction was observed between the SNP and 25(OH)D concentration (all P>0·1, data not shown). As no association was detected between the ten SNP and prostate cancer with a P value threshold of 0·05, no association was detected after adjustment for multiple testing (Bonferroni correction) (data not shown). Associations between SNP of genes involved in vitamin D metabolism and prostate cancer risk, from conditional logistic regression, Supplémentation en Vitamines et Minéraux Antioxydants (SU.VI.MAX) cohort, France (1994–2007) (Odds ratios and 95 % confidence intervals) Discussion In this prospective study, plasma 25(OH)D concentration was inversely associated with prostate cancer risk. No association was detected for plasma PTH concentration or the studied SNP. We observed an inverse association between 25(OH)D concentration and prostate cancer risk. Recently, a high v. low meta-analysis by Xu et al.(27) (summary ORhigh v. low 1·17; 95 % CI 1·05, 1·30) and a dose–response meta-analysis by the WCRF(5) (summary RRper 30 nmol/l 1·04; 95 % CI 1·00, 1·07) suggested an increased risk. However, in a previous study by Tuohimaa et al.(28), both high and low 25(OH)D concentrations were associated with increased prostate cancer risk: increased risk was observed for 25(OH)D concentration =/>32 or <15·6 ng/ml compared with 16–23·6 ng/ml. This U-shaped association is supported by the evidence of non-linearity observed in the WCRF dose–response meta-analysis(5). In our study, the range of 25(OH)D concentrations observed (95th percentile=36·3 ng/ml) may be positioned in the left part of this U-shaped curve, which may explain why a decreased prostate cancer risk was observed for 25(OH)D=/>20 ng/ml (insufficiency) or =/>18·2 ng/ml (median) compared with 25(OH)D<20 or <12·9 ng/ml (quartile 1 (Q1)), respectively. Consistently, a recent study by Kristal et al.(29) observed a decreased prostate cancer risk associated with 25(OH)D concentrations between 23·3 and 29·2 ng/ml (3rd quintile) compared with 25(OH)D<17·7 ng/ml (1st quintile). In contrast, some studies observing an increased risk may involve 25(OH)D concentrations situated in the right part of the U-shaped curve. For example, Brandstedt et al.(9) observed an increased risk for 25(OH)D concentrations=/>34 ng/ml compared with 25(OH)D concentrations</=27·2 ng/ml, and Meyer et al.(30) observed an increased risk for 25(OH)D concentrations=/>28 ng/ml compared with 25(OH)D concentrations between 20 and 28 ng/ml. Studies observing non-significant results may involve middle-range concentrations (such as the study by Skaaby et al.(31)). However, this point remains unclear as some studies that involved high 25(OH)D concentrations observed non-significant results(32,33), and some other studies observed a significant direct association between prostate cancer risk and 25(OH)D concentrations, even at relatively low levels(34). Thus, further studies are needed that take into account the distribution of 25(OH)D concentrations in the studied population and its position in the potential U-shaped curve. In addition, it has been suggested that large seasonal fluctuations of vitamin D status may also contribute to explain the positive association between 25(OH)D concentration and prostate cancer risk in some studies(35), adding to the complexity of this relationship. In the SU.VI.MAX cohort (Touvier et al.(21) and Table 1), seasonal fluctuation of vitamin D status was moderate with the lowest 25(OH)D concentrations observed in late winter/early spring (shorter days), consistently with the existing literature in France(36) and in other countries such as the USA(37–39). The potentially protective role of vitamin D in prostate carcinogenesis observed in our study is supported by mechanistic hypotheses. Indeed, prostate cells can express the 25(OH)D-to-1,25(OH)2D conversion enzyme and the vitamin D receptor(1) and vitamin D is thought to be involved in several cell regulation pathways: pro-differentiation, pro-apoptosis, anti-proliferation and cell growth(2–4). In our study, when 25(OH)D was coded into quartiles, a decreased prostate cancer risk was observed for Gleason’s score <7 but not for Gleason’s score =/>7. However, when using the other codings (continuous and 20 ng/ml cut-off), the association was non-significant in both cancer subgroups. As statistical power was limited in stratified analyses, these results should be considered with caution and further explored in large prospective studies. Thus far, the results regarding potential differences according to prostate cancer stage/grade are unclear, as shown in the WCRF meta-analysis(5), where no difference was observed between advanced/high-grade or non-advanced/low-grade prostate cancers (non-significant results in both groups), or in a recent study by Kristal et al.(29), where a decreased prostate cancer risk was observed whatever the Gleason’s score. The lack of association between the ten studied SNP and prostate cancer risk in our study does not seem to support the protective role of vitamin D in prostate carcinogenesis suggested by our results on plasma 25(OH)D concentration. However, in this study, statistical power was limited in the analyses of SNP, especially for the homozygote mutant genotypes. This could explain the null associations observed. Consistent with our findings, several meta-analyses(10–12) and one recent prospective study(13) found null associations between VDR BsmI, FokI and Cdx2 polymorphisms and prostate cancer risk. Another study (not included in these meta-analyses) observed an increased prostate cancer associated with VDR BsmI GG genotype among men in the first tertile of plasma 25(OH)D concentration. The epidemiological literature dealing with the other studied polymorphisms is scarce. One study(13) observed an increased prostate cancer risk associated with GC rs4588 T allele or GC rs7041 A allele. In SU.VI.MAX(21), these alleles were associated with a lower vitamin D status. Another study(15) observed a decreased lethal prostate cancer risk associated with CaSR rs1801725 among men with low plasma 25(OH)D concentration. To our knowledge, no study has investigated the other selected SNP (CYP24A1 rs4809958, RXR rs7861779 and rs12004589 and CaSR rs4678174) in relation to prostate cancer risk. Besides, other vitamin D-related SNP than the ones included in the present study may also be associated with prostate cancer risk, as observed by Mondul et al.(14), and deserve further investigation. Plasma PTH concentration was not associated with the risk of prostate cancer. To our knowledge, our study was only the second to investigate this relationship, the first one having observed null results(9). In a previous study performed in the SU.VI.MAX cohort(22), we observed an inverse correlation between 25(OH)D and PTH concentrations, with a threshold value for PTH when 25(OH)D was approximately 30 ng/ml. Thus, it could be expected that PTH concentration would decrease as 25(OH)D concentration increases. Mechanistic data are unclear regarding a potential involvement of PTH in prostate carcinogenesis. Although some data have suggested a potential pro-carcinogenic role of PTH(40–42) (potential mitogenic activity in preneoplastic lesions), others support a potential protective role. Indeed, high PTH concentration may decrease growth hormone secretion, thereby decreasing circulating insulin-like growth factor-1 (IGF-1) concentration(43,44); IGF-1 being considered as a potential risk factor for prostate cancer(45,46). Thus, further investigation is needed on the association between PTH concentration and prostate cancer risk. Strengths of our study pertained to its prospective design, long follow-up, simultaneous assessment of 25(OH)D and PTH plasma concentrations, vitamin D-related gene polymorphisms and dietary intakes, and the consideration of numerous confounding factors. However, limitations should be acknowledged. First, blood Ca concentration was not available in our study. Ca concentration would have provided more information regarding the association between 25(OH)D, PTH, Ca and prostate cancer risk. Dietary Ca intake was available, but intakes within normal range are poorly correlated with blood Ca concentration(47), which is under homoeostatic control. Second, only one plasma 25(OH)D and PTH measurement was available at baseline. Repeated measures could have been of interest to study their evolution across time. Third, although the number of cases was appropriate for the analyses described here, it has limited our ability to perform separate analyses in specific subgroups, in particular regarding genetic polymorphisms or prostate cancer grade. Finally, the observed inverse association between vitamin D status and prostate cancer could be partly explained by reverse causality, considering the long lasting development of this cancer. However, results were similar when excluding cases diagnosed within the first 5 years of follow-up, thus arguing against reverse causality. In this prospective study, the association between vitamin D and prostate cancer risk was addressed through 25(OH)D concentration, polymorphisms of vitamin D-related genes and PTH concentration. Prostate cancer risk was inversely associated with 25(OH)D concentration but not with PTH concentration. These results, supported by mechanistic data, bring a new contribution to the understanding of the relationship between vitamin D and prostate cancer risk and deserve further exploration. ------ [5] Am J Clin Nutr. 2015 Jan;101(1):87-117. doi: 10.3945/ajcn.113.067157. Epub 2014 Nov 19. Dairy products, calcium, and prostate cancer risk: a systematic review and meta-analysis of cohort studies. Aune D(1), Navarro Rosenblatt DA(1), Chan DS(1), Vieira AR(1), Vieira R(1), Greenwood DC(1), Vatten LJ(1), Norat T(1). Author information: (1)From the Department of Public Health and General Practice, Faculty of Medicine, Norwegian University of Science and Technology, Trondheim, Norway (DA and LJV); the Department of Epidemiology and Public Health, Imperial College, London, United, Kingdom (DA, DANR, DSMC, ARV, RV, and TN); and the Biostatistics Unit, Centre for Epidemiology and Biostatistics, University of Leeds, Leeds, United Kingdom (DCG). BACKGROUND: Dairy product and calcium intakes have been associated with increased prostate cancer risk, but whether specific dairy products or calcium sources are associated with risk is unclear. OBJECTIVE: In the Continuous Update Project, we conducted a meta-analysis of prospective studies on intakes of dairy products and calcium and prostate cancer risk. DESIGN: PubMed and several other databases were searched up to April 2013. Summary RRs were estimated by using a random-effects model. RESULTS: Thirty-two studies were included. Intakes of total dairy products [summary RR: 1.07 (95% CI: 1.02, 1.12; n = 15) per 400 g/d], total milk [summary RR: 1.03 (95% CI: 1.00, 1.07; n = 14) per 200 g/d], low-fat milk [summary RR: 1.06 (95% CI: 1.01, 1.11; n = 6) per 200 g/d], cheese [summary RR: 1.09 (95% CI: 1.02, 1.18; n = 11) per 50 g/d], and dietary calcium [summary RR: 1.05 (95% CI: 1.02, 1.09; n = 15) per 400 mg/d] were associated with increased total prostate cancer risk. Total calcium and dairy calcium intakes, but not nondairy calcium or supplemental calcium intakes, were also positively associated with total prostate cancer risk. Supplemental calcium was associated with increased risk of fatal prostate cancer. CONCLUSIONS: High intakes of dairy products, milk, low-fat milk, cheese, and total, dietary, and dairy calcium, but not supplemental or nondairy calcium, may increase total prostate cancer risk. The diverging results for types of dairy products and sources of calcium suggest that other components of dairy rather than fat and calcium may increase prostate cancer risk. Any additional studies should report detailed results for subtypes of prostate cancer. © 2015 American Society for Nutrition. PMID: 25527754
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