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After re-reading MR's section on calcium in his supplementation for veg(etari)ans, I started to edit, in cronometer, Ca out of spinach and oxalate-rich vegetables. Also, I realized that calcium in tofu may not be there if the coagulant used is not Ca-based. So, my cronometer levels of Ca plummeted down. No kale here in Italy, only some is available and dried. And no fortified foods. What to do beyond pure supplementation? I was pondering, when the very obvious answer materialized in my mind. Very much obvious, but lost in the background mental noise. Water was the answer. I googled the calcium content in commercial mineral waters (those available in supermarkets), and there it is, a list with the top entries. The highest one, of a volcanic origin, contains 390 mg per liter. And that of course is very much available, being in its ionic form. Yesterday I went to the supermarket and made of stock of that water. Since I never drink less than 1.5 liters per day, that's already almost 600 mg of available Ca, about 60% of the RDA. In the summer I very often drink 2 liters and more, which will allow me to be consistently above the RDA, together with the other vegan food. Hope I won't have now to start worrying about too much calcium...
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
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 , and more significantly in a study of a number of us long-term CR practitioners by Luigi Fontana et al. . Fortunately, bone quality does not appear to be compromised in us long-term practitioners . 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)  and fracture risk . 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.  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.  While  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 . So interventions like exercise , 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 -----------  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. -------------  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. -------------  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 ---------------  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. firstname.lastname@example.org 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 ----------------  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. email@example.com 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
brendanhill posted a topic in CR PracticeI was compiling some data about vegan sources of calcium and thought I had formed a reasonable spreadsheet. Then I came across the following page, describing how variable the bioavailability of calcium across various sources really is: http://plenteousveg.com/vegan-sources-calcium/ For example, without factoring in bioavailability we would think that 1 cup of Chinese cabbage would meet ~70% of our calcium requirements. When factoring in bioavailability, it is closer to ~20%. Conversely, a cup of collard greens go from ~27% to ~50%. These are significant differences when trying to formulate a nutritionally complete diet and yet all nutrition databases I have seen online seem to ignore this difference. Is the description of calcium bioavailability in the link above accurate? If so, is there any point using standard online nutrition databases to evaluate calcium sources? Is this degree of variability in bioavailability across various sources the case for many other vitamins eg. B12, iron etc? Regards, -Brendan