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Found 12 results

  1. The strategies are pretty standard but still pretty interesting for anyone who’s looked into ‘biohacking’. The guy is a CEO of a company that does half a billion dollars a year in revenue so he definitely has to be high performing. Funny enough he follows a ketogenic diet, fasts frequently and uses ssri’s for mood improvement. Here’s his whole protocol: https://hackernoon.com/im-32-and-spent-200k-on-biohacking-became-calmer-thinner-extroverted-healthier-happier-2a2e846ae113
  2. [Admin Note: This is a new thread to consolidate the important discussion of Vitamin B12 levels, deficiency and supplementation started by Cloud in this thread originally by Zeta on his Extreme blood values. The topic of B12 deficiency, particularly for CR Practitioners who don't generally consume a lot of meat, deserves its own thread. -Dean] Hello, can I ask a question? What happens if the body can't absorb the iron from diet? I am asking about the relationship between serum iron and ferritin. In March I had serum iron at 134 mcg/dL, ferritin at 71.30 mcg/dL (and B12 very low 79 mcg/dL) , now at the latest analysis serum iron is 209 mcg/dL and ferritin is 96.60 mcg/dL and because I am supplementing B12 is 156. I am wondering what mean this so high serum iron. Could it come from food containing iron that I can not absorb? In the last months the only foods, containing much iron I introduced as new, was pistachios and dark chocolate. I also, as some of you, drink about 1 L/day of green tea, that should limit a lot iron absorption. I still have to show this data to my doctor. Thanks!
  3. - Some media articles interviewing an author of the new study and also referencing previous studies showing links between B12 and B6 supplementation and cancer: https://www.sciencedaily.com/releases/2017/08/170822175515.htm https://www.theatlantic.com/health/archive/2017/08/b12-energy/537654/
  4. I am seeing more of this sorta "supplement" - it claims to be actual food that has been processed into a drinkable powder - does this count as a supplement? I ask because of the posts regarding the use of vitamins and other supplementation recommending "real food" instead. I love eating real food for my nutrients but sometimes this kind of thing appeals to me for occasional convenience - does anyone have any info on this kind of thing? I love getting the imprimatur of my CR pals before trying anything! Thanks Neil Nutrient-Dense, Raw, Organic, Superfood Complex (4768 mg): Organic Spirulina, Organic Apple, Organic Sea Kelp, Organic Kale, Organic Spinach, Organic Chlorella, Organic Aloe Vera Leaf, Organic Broccoli Sprout, Organic Dulse Antioxidant Complex (2938 mg): Organic Amla, Organic Acerola, Organic Pineapple, Organic Reishi Mushroom, Organic Ginger Root, Organic Turmeric, Organic Monk Fruit Extract, Organic Carrot, Organic Raspberry, Organic Blueberry Digestive Enzyme Complex (43 mg): Amylase, Protease, Cellulase, Lactase, Lipase Other ingredients: Organic Apple Flavor, Organic Berry Flavor, Organic Lemon Lime flavor, Organic Peppermint Flavor
  5. 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
  6. 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
  7. 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
  8. Al Pater posted study [1] to the CR email list (thanks Al), that was a meta-analysis of studies of the relationship between vitamin intake and stomach (gastric) cancer risk. It found that several vitamins, including Vitamin A, C and E, in modest doses, could indeed reduce the risk of stomach cancer by about 25%. But high doses of those same vitamins resulted in an increased risk of almost the same magnitude. They also observed that modest doses of these vitamins were only beneficial for gastric cancer when they came from food (plants or animals) - vitamin supplements showed no such benefits. The authors speculate that the reason could be differences in bioavailability of vitamins from foods vs. pills: The current study also draws attention to the fact that vitamins from food (plant or animal) contribute more to reductions in GC risk than synthetic vitamin supplements. Some investigators have noted that the bioavailability of vitamins differs depending on whether the vitamin comes from food or is synthetic, which could explain the results. For example, Carr reported differences in bioavailability between synthetic and kiwifruit-derived vitamin C in a randomized crossover pharmacokinetic study [ref]. But it seems at least as plausible to me that the benefits come not just from these specific vitamins (heck, in the case of vitamin E alone there is really a whole family of vitamins rather than just a single vitamin E), but from the many beneficial phytochemicals in foods, for which these three vitamins are merely markers. --Dean --------- [1] Vitamin intake reduce the risk of gastric cancer: meta-analysis and systematic review of randomized and observational studies. Kong P, Cai Q, Geng Q, Wang J, Lan Y, Zhan Y, Xu D. PLoS One. 2014 Dec 30;9(12):e116060. doi: 10.1371/journal.pone.0116060. eCollection 2014. Review. PMID: 25549091 Free PMC Article http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4280145/ http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4280145/pdf/pone.0116060.pdf Abstract AIM: The association between vitamin intake and gastric cancer (GC) has been widely debated due to the relatively weak evidence. In this study, a meta-analysis of prospective and well designed observational studies were performed to explore this association. METHODS: MEDLINE, Cochrane Library, and Sciencedirect were searched for studies of vitamin consumption and gastric cancer. This produced 47 relevant studies covering 1,221,392 human subjects. Random effects models were used to estimate summary relative risk (RR). Dose-response, subgroup, sensitivity, meta-regression, and publication bias analyses were conducted. RESULTS: The RR of gastric cancer in the group with the highest vitamin intake was compared to that of the lowest intake group. Total vitamin intake was 0.78 (95% CI, 0.71-0.83). In 9 studies that individuals were given doses at least 4 times above the tolerable upper intake (UL) vitamins, the RR was 1.20 (95% CI, 0.99-1.44). However, in 17 studies that individuals received doses below the UL, the RR was 0.76 (95% CI, 0.68-0.86). Dose-response analysis was conducted on different increments in different types of vitamins (vitamin A: 1.5 mg/day, vitamin C: 100 mg/day, vitamin E: 10 mg/day) intake with a significant reduction in the risk of gastric cancer, respectively, 29% in vitamin A, 26% in vitamin C, and 24% in vitamin E. CONCLUSION: This meta-analysis clearly demonstrated that low doses of vitamins can significantly reduce the risk of GC, especially vitamin A, vitamin C, vitamin E. Table 2. Subgroup analyses of vitamins intake and gastric cancer Risk. Heterogeneity test ------------------------------------ Group NO. of reports RR (95%) Chi^2 P(I^2) ------------------------------------\ Vitamin source plant 15 0.79(0.69,0.89) 36.96 0.002 65 animal 11 0.78(0.68,0.89) 25.93 0.0003 61 drug supplement 16 0.95(0.80,1.13) 33.09 0.58 55
  9. Zeta

    Vitacost: good or bad?

    Michael, thanks for making us aware of this. (I get "Page cannot be crawled or displayed due to robots.txt" at the archive.org link by the way) I've been a member of ConsumerLab for around 5 years, and, without exception, all Vitacost products I've seen tested (which are only those I take or am considering taking) have passed ConsumerLab's testing. I wonder whether Vitacost has cleaned up their act. I've seen similarly misleading labels on other R-LA products. If you read the full label you know what you're getting, but still, I agree it's a problem. As for the kosher concerns: I see nothing in the current product description for that thyroid support supplement making any claims about kosherness. On the whole, plenty of reasons to be suspicious 7-8 years ago, but fewer reasons today. My question would be: what supplement company does not suffer from such problems? TwinLAB maybe? By the way, has anyone gone through ConsumerLab's reviews in a systematic way to see which supplement companies consistently come up green on ConsumerLab's tests? I started doing that once, only getting as far as the Life-Extension Foundation (which, by the way, had a perfect score after having gone through around 15 supplements). Zeta
  10. [Note: I've moved this thread from the "Chit Chat" forum to "CR Practice", since it has useful information about food choice and supplements for CR practitioners. Thanks for starting it Greg! --Dean] I adhere to a low-fat vegan regimen. I'm looking for opinions on the advisability of taking the foods listed below. An example would be: - tempeh (for B12) possible response: recent studies indicate it might not be a good choice - some vegans who consumed plenty of tempeh were found to have low B12 levels. Food X (e.g. fortified yeast flakes) might be a better choice. Here is the list: - yeast flakes (for B12, since they are grown on a substrate with B12), e.g. Bob's Red Mill Yeast Flakes - brewer's yeast (for the variety of B vitamins other than B12) - flaxseed meal (for omega 3) - wheat bran - wheat germ I'm actually hoping that some members who know much more about nutrition than I do will advise me that some of these are really not necessary. The exception is the yeast flakes, since I don't know of a vegan alternative except capsules. Thank you.
  11. Strontium is one of the few supplements I still take, for bone health. But the new alert from Al Pater (thanks Al!) has got me wondering if this is wise. The news story (included below), talks about Canada putting warning labels on supplements and pharmaceuticals containing strontium. It cites [1], a European study that found increased risk of cardiovascular events in at-risk individuals taking strontium. On the other hand, the introduction of [1] points out that strontium really does appear pretty effective at building/maintaining bone health. Plus, from [1], it doesn't sound like someone WITHOUT CVD risk factors should be worried, but we're all a lot more paranoid about supplements in general these days, so I'm still a bit concerned. I take a 680/mg strontium capsule (as strontium citrate) per day. Study [1] talks about strontium ranelate, but I'm not sure if that makes any difference, since the Canadian authorities are talking about warnings for all strontium supplements, including strontium citrate. I'm hoping someone with deep expertise in supplements and nutrition (I'm looking at you Michael :-) ) will be able to shed some light on the wisdom or folly of strontium supplements for CR practitioners. Thanks! --Dean ---------------- http://www.cbc.ca/news/health/strontium-1.3284679 Strontium health products may carry heart risks: Health Canada Affected products products contain either strontium citrate, strontium gluconate or strontium lactate. CBC News Posted: Oct 22, 2015 5:23 PM ET| Last Updated: Oct 22, 2015 5:23 PM ET Health Canada has asked companies to strengthen their labels on natural health products containing strontium to warn of an increased risk of heart-related side-effects. The department said Thursday the label changes are for strontium-containing products with a daily dose between 4 mg and 682 mg, which are used to help support bone mineral density. Health Canada says findings in Europe led to restrictions for use of oral prescription drugs containing strontium at 680 mg/day, due to the increased risk of cardiovascular events seen in patients who have risk factors for heart or circulatory-related side-effects. (Sean Kilpatrick/Canadian Press) The products contain either strontium citrate, strontium gluconate or strontium lactate. Under the new directions, use of the products will be limited to people who have no history of, or risk factors for, heart disease, circulatory problems or blood clots. "While uncertainties remain, Health Canada is using a precautionary approach and considers that strontium, regardless of the form it comes in or dose taken, may have a potential risk of cardiovascular side-effects in people who are already at risk," it said. Health Canada recommends: Do not use a strontium-containing product if you have, or are at high risk for heart disease, circulatory problems, or blood clots. Risk factors include: a history of heart disease, heart attack, stroke, peripheral arterial disease, high blood pressure, high blood fat levels, diabetes, taking prescription hormone drugs, or if you are temporarily or permanently immobilized. If you have any cardiovascular risk factors, read the label of products you are taking to know if they contain strontium. Consult a healthcare practitioner for use beyond six months. Talk to a healthcare practitioner if you have questions or if you are unsure whether these products are appropriate for you. ---------------------- [1] Expert Opin Drug Saf. 2014 September; 13(9): 1209–1213. Published online 2014 July 14. doi: 10.1517/14740338.2014.939169 PMCID: PMC4196504 Cardiac concerns associated with strontium ranelate Abstract Introduction Strontium ranelate is proven to reduce vertebral and non-vertebral fracture risk in osteoporosis. Concerns about cardiac safety have led to a new contraindication to strontium ranelate in patients with uncontrolled hypertension and/or current or past history of ischaemic heart disease, peripheral arterial disease and/or cerebrovascular disease. Areas covered A literature search was performed; data were also collected from the European Medicines Agency website. Randomised controlled trial (RCT) data indicate a higher incidence of non-adjudicated myocardial infarction (MI) with strontium ranelate versus placebo (1.7 vs 1.1%; odds ratio [OR]: 1.6; 95% CI: 1.07 – 2.38; p = 0.020) (Mantel-Haenzel estimate of the OR). There was no increase in cardiovascular mortality. MI risk was mitigated by excluding patients with cardiovascular contraindications (OR: 0.99; 95% CI: 0.48 – 2.04; p = 0.988). Three observational studies performed in the context of real-life medical practice in the UK and Denmark did not report a signal. Expert opinion The increased risk for cardiac events with strontium ranelate has been detected in RCTs but not in real life. Excluding patients with cardiovascular contraindications appears to be an effective measure for controlling the risk of MI. Strontium ranelate remains a useful therapeutic alternative in patients with severe osteoporosis without cardiovascular contraindications who are unable to take another osteoporosis treatment. Keywords: cardiac safety, myocardial infarction, osteoporosis, strontium ranelate Go to: 1.  Introduction Strontium ranelate, an osteoporosis medication registered in Europe in 2004, has been studied in a range of randomised controlled trials (RCTs) [1-6]. It was originally indicated for the treatment of women with postmenopausal osteoporosis to reduce the risk for vertebral and hip fracture. The efficacy of strontium ranelate for preventing fracture in osteoporosis is well established, having been demonstrated in two pivotal RCTs – Spinal Osteoporosis Therapeutic Intervention (SOTI) trial and TReatment Of Peripheral OSteoporosis (TROPOS) [2,3]. SOTI showed that, over 3 years, treatment with strontium ranelate 2 g/day reduced the risk of vertebral fracture in postmenopausal osteoporotic women and increased lumbar spine bone mineral density [2]. Strontium ranelate was demonstrated to have an effect on non-vertebral fracture (including hip) in postmenopausal osteoporotic women in TROPOS [3]. Strontium ranelate also increases bone mineral density in osteoporotic men [4], and there is evidence that its antifracture efficacy is maintained up to 10 years [5,6].
  12. Note: this guide was written over an extended period of time in 2009, and with one exception (the sections on choline and carnitine) has not been updated since. It is therefore probably in significant ways outdated on both current science and my own evolving understanding. Also, I am not a doctor or health professional. Information in this article is just that: information — not advice. Before taking up CR, veg(etari)anism, or using dietary supplements, consult a doctor or other licensed health professional. Neither I nor the CR Society provides any warranty is given or implied in relation to the information supplied in this article or on the website, and neither I nor CR Society accepts any liability in the event that a user suffers loss as a result of reliance upon the information. Finally: this is a multi-part article, and unlike posts on the old CR Society email distribution lists, it can be periodically updated thanks to the fine editability of the Forums. To avoid cluttering up the article, please post ask any questions or comments about the contents of this article in a new thread, rather than by hitting "reply" to posts in this one. I will make a good-faith effort to answer such and to update this article as appropriate. Part I: Principles and Strategies Records of groups practicing vegetarianism go back to ancient times, and while animal cruelty or religious purity have clearly been the dominant motivations, the belief that diets free of animal flesh were healthier has been and continues to be a common belief amongst practitioners and advocates. And clearly there are reasons to expect that they might be. Vegetarian diets are lower in saturated fat and cholesterol, and vegetarians tend to have lower LDL (“bad”) cholesterol; they are free of the risks of the carcinogens present in highly-processed or overcooked meat; vegetarians tend to be slimmer; and the benefits of increasing one’s intake of fruits, vegetables, and whole grains are endorsed not only by academics and public health professionals, but by nearly every popular diet, from Atkins to Ornish. And yet, large-scale, prospective studies, in which the health of vegetarians is tracked over time with reference to the general population (and, more clearly, compared with other groups that include meat and/or seafood in their diets, but who otherwise lead similarly health-conscious lifestyles), fail to find an overall difference in the ultimate balance sheet of the health of a biological system: its life expectancy. Surprisingly, despite enjoying a reduction in risk of ischemic heart disease, vegetarians live about as long as similar omnivores do,[ii],[iii],[iv] – and, even when it comes to heart health, vegans (whose diets are the most restrictive of animal fat (and thus saturated fatty acids and cholesterol)) actually seem to have risks similar to have those of people who eat meat a few times a month, and are actually at higher risk than either ovolacto vegetarians (who get these nutrients from most dairy products and egg yolk), or eaters of fish but not terrestrial meat.4 And this is despite a lower rate of smoking and lighter bodies even in comparison with health-conscious omnivores.1 These findings are even more surprising when you consider one of its minor implications. Aside from the fact that the effects on heart disease are more modest than most of us would expect from the considerable reduction in the single most well-established dietary determinant of disease incidence, or the more surprising finding of a lack of overall benefit in cancer deaths, the only way that a group with a lower risk of death from one thing (heart disease) can wind up having no lower a risk of dying overall than members of another group, is if that group simultaneously suffers a commensurate increase in risk of death from one or more other causes. In other words, for every omnivore who dies early clutching hir heart and sprawled over the dining room table, there is a vegetarian out there dying from one of an unidentified spectrum of less common diseases than heart disease or major cancers. This should not trigger a massive research campaign to attempt to tease out the mystery illnesses cutting a swath through the ranks of vegetarians: most vegetarians are dying of exactly what’s killing the rest of the population, and as a corollary, an individual vegetarian’s risks of other diseases, even amongst vegetarians, remain low, and are more likely related to the biology of aging (which tends to dilute out the effects of risk factors for disease over time, as the intrinsic molecular decay that accumulates in the tissues of the body makes the organism more susceptible to insults of all kinds) than to some specific disease process. The more immediate question is, what’s wrong with a vegetarian diet that doesn’t allow us to reap the expected benefits of low intake of saturated fat and charred meat and high intake of plant-based foods? A number of certain and probable weaknesses of typical vegetarian diets have been identified in epidemiological and small cross-sectional studies, and for a number of them the potential health risks are reasonably clear, though the degree to which any of them actually contribute to risk of death and disease in vegetarians specifically has not been systematically tested with intervention trials (where one group of vegetarians would eat their normal, but typically nutritionally imperfect, diet, while another would have their diets improved in a way that actually brought one or more of these parameters more in line with typical omnivorous diets, and long-term health outcomes in the two groups would be compared). In addition to such limited information about the health effects that come somewhat inherently to a ‘default’ self-selected plant-based diet compared with one including a substantial amount of meat (and, for vegans, dairy and eggs), there is also the problem of failure, even by well-meaning vegetarian advocates, to correct these default deficiencies, for fear of making eating a healthy vegetarian diet seem more difficult and burdensome for most people to take up. And on top of that, there is a much higher level of sheer food faddism amongst vegetarians, resulting from a mixture of the perverse effect of many vegetarians being more health-conscious than the general population, but no more scientifically literate in nutrition (hence the widespread citation of John Robbins, John MacDougall, and even the authors of Skinny Bitch on the health benefits of vegetarianism), leading to a dangerous susceptibility to convincing-sounding but scientifically groundless arguments on the subject. Additionally, I personally suspect that, once immersed into a subculture (including online vegetarian communities) where an already-unusual dietary practice is the norm, vegetarians find it all the easier to begin walking down a slippery slope into increasingly unsafe or untested dietary practices. A recent study[v] finding that current and former adolescent vegetarians and semivegetarians are more prone to clearly pathological eating patterns (such as binge eating, use of laxatives for weight control) may support this idea, although it’s possible that some of this represents young people using “vegetarianism” as a camouflage for an eating disorder, or that all of their food relationships were in an unhealthy flux during their teen years. But there is a fair bit that we can say about the composition of meat-centered vs. plant-centered diets, and about observations of the nutritional statuses of vegetarians in the real world. And so we can say a fair amount about some of the more common deficiencies and imbalances built into typical vegetarian lifestyles – and, therefore, of what dietary adjustments or (as necessary) dietary supplements might at least help to correct them. So most of this article will be devoted to the well-established weaknesses in typical vegetarian diets, and some of the known or probable risks associated with letting those problems go uncorrected – but I emphatically do not intend this to be a boilerplate set of supplements and dietary modifications that should be adopted ‘as is’ by all vegetarians. Instead, the focus of the article will be on getting a handle on your own, unique dietary patterns and needs, and then giving some further insight on problems you’re likely to encounter, and the whys and hows of getting around them. Know Thy Diet In order to know what changes and additions are needed to your existing pattern, you’ll have to have a good handle on what, exactly, that pattern is, how it breaks down nutritionally, and where its weaknesses lie. Broad-stroke dietary advice inevitably misses this factor: even eating diets that are otherwise very healthy, almost everyone has a variety of mild deficiencies and imbalances in their day-to-day eating pattern, and the special strictures of a vegetarian diet tend to take away some of the wiggle room that omnivores have to fill in gaps in their nutritional pattern. Moreover, people’s understanding and characterization of their own diets tend to be quite mistaken: they come into their dietary habits by a lifelong mixture of culture, habit, availability, and taste that they’ve never deeply analyzed and haven’t compared to any Platonic standard, with the result that they really don’t know what they’re eating or how it compares to average diets or dietary guidelines. Worse, when they try to evaluate what they’re eating, they still get it wrong:[vi] they usually aren’t fully paying attention as they grab small snacks here and there through the day, can’t eyeball serving sizes (and indeed don’t really grasp what a ‘serving’ of a given food is), and frankly sometimes engage in self-deception, telling themselves white lies about the amount of poor-quality food they eat or (less commonly) indulging a tendency toward self-flagellation by exaggerating minor dietary infractions. So I’m going to strongly recommend that you spend a few dollars and some time doing something that my fellow practitioners of Calorie restriction do every day, which is to record and quantitate everything you eat for a few typical days – not days when you’re ‘being good,’ but a genuinely representative sample. If you don’t have them already, pick up a set of measuring cups (for liquids and solids) and spoons; also spend some money on a digital food scale accurate to 1 gram (postal scales are an easier-to-find and usually less expensive route to the same end). When you make food for yourself, weigh or measure it out; when you eat pre-packaged foods, carefully record the relevant information; keep a PDA or small pad of paper with you, and carefully evaluate small snacks and drinks eaten out. Plug all this information into nutritional software, such as CRON-O-Meter (on whose design I consulted), which is an excellent tool for nutritional analysis, is free (though the developer takes donations, and there are some nifty features for the inexpensive upgrade to "Gold" membership), or NutritionData.com. If a food isn’t on the list, you can use the Command-F (or Food > New Food) function to enter it, from the package or online sources like The Daily Plate and Calorie King; Google searches for the food name plus “nutrition facts” or (calories protein calcium) are also often successful. One significant challenge here is restaurants. Studies show that almost nobody – including postgraduate academic and professional nutritionists[viii] – can accurately estimate the Caloric or saturated fat content of restaurant meals, and almost always underestimate these values.[ix],[x] My anecdotal experience as an individual vegetarian with a fair number of vegetarian friends suggests that this was once less of a problem for vegetarians than for the general population, as they long seemed to eat relatively few meals out for the unpleasant reason of sheer lack of options, beyond vegetable side-dishes, salads, and a few pasta dishes. But times have changed, and for better and for worse, it’s become easier and easier for vegetarians to find real meals out at the same moment that there has been a significant increase in the percentage (and total!) of Calories eaten out in the culture at large, and a ballooning of portion sizes and Caloric densities of restaurant meals. The result is that most vegetarians have a reasonable range of restaurant meals available to them, and appear, anecdotally, to be taking advantage of the changes in the industry – and it is taking advantage of them. Certainly, there is always coffee (which can run 800 Calories at Starbucks these days) and bagels and cream cheese (or mustard and tomato for the vegans). If you mostly eat in major chain restaurants, you can likely get nutritional information online; if not, and if the Mysore Masala Dosai at the local Indian place is a part of your Friday ritual with your lover, you can’t just pretend it isn’t. Do your best to find a comparable dish at a large restaurant chain with nutritional information, or at least enter in a recipe for the same dish from online or other sources. Yes, this is a lot of work! But most people’s diets are fairly well-worn, happy ruts, and eating food you prepare yourself is a good and increasingly-rare pattern to be in, so you ought to be able to get away with doing it for a week or so, and then perhaps once a weeks or so for a few weeks thereafter. Again, I guarantee you that you will find some significant holes and ‘overgrowths’ in your diet, no matter how fundamentally healthy it may be. Do yourself the favor of investing the time and trouble: knowledge is power, and your health really shouldn’t rely on guesswork. The Benchmarks Now that you know what you’re eating, how do you identify and correct the imbalances? What are the standards? Most people, if they think about it at all, would first turn to the government’s nutrition experts, but such bodies are viewed with great suspicion by many health-conscious people. Advocates of vitamin and mineral supplementation believe that the RDAs only protect against frank, acute deficiency state, and don’t take account of the long-term impacts of a kind of chronic, low-level, suboptimal intake, whose correction requires supplemental intakes anywhere from a few to a hundred multiples of the RDA. Supporters of organic agriculture argue that our soils have become so depleted, and our plants first bred to be convenient for agribusiness production and distribution chains, and then forced to grow so quickly by synthetic fertilizers and ‘spoiled’ by pesticides that prevent the formation of secondary metabolites, that it has drained them dramatically of nutritional content. And vegetarians often point to the institutional conflict-of-interest inherent to having the USDA both make dietary recommendations and be responsible for supporting American agrobusiness as leading to flawed nutritional advice – especially when it comes to the consumption of animal products. But while there is some truth in all of these critiques, over time a healthy suspicion of authority has for many people slowly slid over time into uncritical, blanket derision, or closed-system conspiracy theory, to the point that no such guidance can be taken seriously. Worse, too many people concerned about their health have simply replaced highly-qualified government and academic authorities with alternative ‘authorities’ that are actually far less qualified, less grounded in the body of nutritional science, and more driven by outside agendas – and too often, by sheer nutritional superstition. While it’s heresy to say so in many health-driven communities, the government’s nutrition experts really do know what they’re talking about, and when they do make mistakes, they tend to be based on drawing conservative conclusions in the face of a limited amount of high-quality information, instead of making Olympian leaps from a few evidential straws – and such errors tend to work themselves out over time and with scientific peer-review. This is particularly true when we turn away from the intentionally vague and highly politicized guidance offered by the USDA in the form of the ‘Food Pyramid’ (now ‘My Pyramid’) and similar efforts[xi] to the much more specific and independent guidance on nutritional science embodied in the National Academies of Science’s Institute of Medicine (IOM) reports on nutrient requirements, which for the basis for later Dietary Reference Intakes (DRIs), a panel of parameters that includes the Recommended Dietary Allowances (RDAs) by age, and which are different from the values promulgated by the FDA and USDA in the form of the US RDA (perversely, not the same as the IOM RDA) and such complementary indexes as the Daily Value and Reference Daily Intakes (RDIs). Broadly speaking, nearly all of the current DRIs are excellent, or at least within the right ballpark, especially for the general populace to which they are primarily addressed. There is a large (but fortunately shrinking) constituency in the life extension community whose knee-jerk reaction is assume that everything that Authority says about nutrition is wrong, and in particular that the RDAs are orders of magnitude too low; these opinions are largely based in honest ignorance, by folks who have been convinced by sloppy arguments, mostly advanced by supplement pushers (I speak as a notorious, but hopefully relatively intellectually honest and sophisticated, former supplement pusher myself), and who (crucially) have simply not read the enormous and normally quite well-presented documentation that form the basis of the IOM's recommendations, and usually lack the scientific background to do so. For those interested, the mammoth tomes that summarize the evidence underlying the IOM's current RDAs are available for free online[xii]; click on the photo of a given volume, and then scroll down to read the individual chapters (you have to go page-by-page, alas). But for bottom-line purposes, the latest iteration of the DRIs are also tabulated on the IOM website.[xiii] In addition to these guidelines for essential nutrients, there are a variety of ‘conditionally essential’ nutrients whose intake is much lower in vegetarians than in omnivores. “Conditionally essential” nutrients are substances that play an essential role in physiological function, are available in (and absorbable from) the diet, but are not strictly ‘essential’ because they can be biosynthesized from their precursors in the body. Many of these nutrients are present in animal products and not plant-based ones, so vegetians certainly have a lower intake of these nutrients, but because people can in principle synthesize these substances from other nutrients that are in their diets, and because experimental animals given diets free of these nutrients don’t suffer any obvious impairments in growth or fertility, long led to the assumption that there was no need to get them from the diet. However, as we’ll see, there are many cases where vegetarians’ levels of these nutrients are, in fact, lower than those of omnivores, and where evidence exists that their health is not as good as it could be because of it. How’s That Workin’ for you? In many health-conscious circles, it’s a commonplace that everyone has hir own unique nutritional needs: that genetic, age, and lifestyle variations in absorption, utilization, biotransformation, storage, enzymatic affinity, etc. ensure that the RDA will not provide the right dose for many people. And indeed, despite my previously-stated confidence in the RDAs, the fact is that even a benchmark set to cover the nutritional requirements for 95% of the population will, by mathematical necessity, mean that 5% of the population will actually not have their needs met at that level – even if the original RDA were set in perfect scientific knowledge of the range of needs and long-term impacts of a given dose of a particular nutrient, which of course it is not. But too often, this emphasis of “biochemical individuality” is ironically used to justify blanket, population-wide recommendations that everyone should engage in high-dose supplementation of everything, as if no essential nutrient (or combination of such nutrients) could be harmful in high doses. As we’ve learned from the miserable history of supplement trials for everything except vitamin D for fractures, this advice has turned out to be unhelpful at best, and occasionally fatal at worst, with multiple large, long-term, carefully-controlled trials of megadose supplements documenting possible marginal increases in cancer rates from ‘antioxidants,’ heart disease from B vitamins, and in diabetes from selenium. No, you want to determine and meet your particular needs – no more, no less. To do this, you’ll certainly want to start with the IOM RDAs – but where you can, you won’t want to stay there. Instead, it’s best to get yourself functionally tested, to see if the enzymes and biochemical pathways that rely on a given nutrient are functioning as they would if the supply of that nutrient were adequate. Many people (including many health providers, especially in the ‘alternative’ medicine fields) rely on blood levels to determine adequacy, but these are almost never a good guide to functional status. For some nutrients, blood levels are held within strict limits that are maintained by either furiously working to metabolize the excess away in a not-always-helpful way, or by drawing down long-term body stores to make up a deficiency, which if not replaced by future dietary intake creates (and masks) a creeping systemic deficiency. In other cases, blood levels fluctuate with recent intake, and tell you more about what you had for dinner the night before than about your day-to-day health status. And in still other cases, a level in the blood that would be quite adequate to saturate enzyme activity in most people is insufficient for you as an individual, because a minor typo in your genetic code makes the enzyme require a bit higher concentration of the nutrient to squeeze a molecule of it into a slightly resistant binding site. And in the end, most blood level guidance is based on the level that is ‘normal’ in the population, or (in a closed-loop) on people already following a given nutritionally-minded health care provider’s dietary recommendations, and not on any evidence that the target level actually meets metabolic demand. Unfortunately, for many essential nutrients (especially minerals), no reliable test exists, or is only available in a few research labs instead of from commercial testing laboratories. But where your own body’s biochemical soup can tell you how you’re doing, you’ll want to hear what its saying. Another Tool As we go along, and as you find the need to boost intake of some nutrients and avoid overdosing on others, you’ll often want to find foods high in some nutrient – and generally, low in others. Lists of ‘foods rich in …’ are often misleading, because they’re based on a serving size that can be quite arbitrary, and because they don’t help you to tailor a food in to other priorities, such as keeping Calories low or avoiding common ‘fellow traveller’ nutrients (such as high copper levels in most zinc-rich vegan foods). A good tool for this is the "Oracle" function on CRON-O-Meter; NutritionData.com’s Nutrient Search tool can also allow you to look for foods high in one or more nutrients, but high or low in other nutrients at the same time. Combined with an analysis of your full diet, good guidance for intake, and testing where good functional assays are available, this will let you bring your diet closer to its health-supporting best. In Part II of this article, we’ll tackle the essential vitamins, minerals, and amino acids, with a focus on nutrients typically lacking or overrepresented in a vegetarian diet; in Part III, we’ll more gingerly approach the more limited information about the ‘conditionally essential’ nutrients. Next: Part II: Essential Nutrients Remember, please post ask any questions or comments about the contents of this article in a new thread, rather than by hitting "reply" to posts in this one. 1: Bor MV, Lydeking-Olsen E, Møller J, Nexø E. A daily intake of approximately 6 microg vitamin B-12 appears to saturate all the vitamin B-12-related variables in Danish postmenopausal women. Am J Clin Nutr. 2006 Jan;83(1):52-8. Eussen SJ, de Groot LC, Clarke R, Schneede J, Ueland PM, Hoefnagels WH, van Staveren WA. Oral cyanocobalamin supplementation in older people with vitamin B12 deficiency: a dose-finding trial. Arch Intern Med. 2005 May 23;165(10):1167-72. “Daily doses of 647 to 1032 mug of cyanocobalamin were associated with 80% to 90% of the estimated maximum reduction in the plasma methylmalonic acid concentration.” ,[xxvi],[xxvii], McDougall J. Optimal diets to prevent heart disease. JAMA. 2003 Mar 26;289(12):1509. Key TJ, Appleby PN, Spencer EA, Travis RC, Roddam AW, Allen NE. Mortality in British vegetarians: results from the European Prospective Investigation into Cancer and Nutrition (EPIC-Oxford). Am J Clin Nutr. 2009 Mar 18. doi:10.3945/ajcn.2009.26736L [ii] 1: Singh PN, Sabaté J, Fraser GE. Does low meat consumption increase life expectancy in humans?. Am J Clin Nutr. 2003 Sep;78(3 Suppl):526S-532S. [iii] 1: Chang-Claude J, Hermann S, Eilber U, Steindorf K. Lifestyle determinants and mortality in German vegetarians and health-conscious persons: results of a 21-year follow-up. Cancer Epidemiol Biomarkers Prev. 2005 Apr;14(4):963-8. [iv] Key TJ, Fraser GE, Thorogood M, Appleby PN, Beral V, Reeves G, Burr ML, Chang-Claude J, Frentzel-Beyme R, Kuzma JW, Mann J, McPherson K. Mortality in vegetarians and nonvegetarians: detailed findings from a collaborative analysis of 5 prospective studies. Am J Clin Nutr. 1999 Sep;70(3 Suppl):516S-524S. [v] Robinson-O'Brien R, Perry CL, Wall MM, Story M, Neumark-Sztainer D. Adolescent and young adult vegetarianism: better dietary intake and weight outcomes but increased risk of disordered eating behaviors. J Am Diet Assoc. 2009 Apr;109(4):648-55. [vi] The foibles of our self-monitoring are cataloged extensively and entertainingly in Cornell University Professor of Consumer Behavior Brian Wansink’s excellent and revealing Mindless Eating: Why We Eat More Than We Think (2006; Bantam books, ISBN: 0-553-80434-0). [vii] http://spaz.ca/cronometer/ [viii] Food Commission. Which fast food meals are healthiest? Anyone’s guess! The Food Magazine. 2008 Jul/Aug:82. [ix] Burton S, Creyer EH, Kees J, Huggins K. Attacking the obesity epidemic: the potential health benefits of providing nutrition information in restaurants. Am J Public Health. 2006 Sep;96(9):1669-75. [x] Wansink B, Chandon P. Meal size, not body size, explains errors in estimating the calorie content of meals. Ann Intern Med. 2006 Sep 5;145(5):326-32. [xi] The corrupting influence of business interests on the media and much government (especially USDA) nutrition communication is very well covered in Marion Nestle’s excellent Food Politics: How the Food Industry Influences Nutrition and Health (2007; Univ of California Press, ISBN-10: 0520254031). [xii] http://www.nap.edu/catalog/dri/ [xiii] Food and Nutrition Board, Institute of Medicine, National Academies. Dietary Reference Intakes (DRIs): Recommended Intakes for Individuals, Vitamins. Online at http://www.iom.edu/File.aspx?ID=21372 ; accessed 2009-04-09. [xiv] McDougall J. Vitamin B12 Deficiency—the Meat-eaters’ Last Stand. McDougall Newsletter. 2007 Nov;6(11). Online at http://www.drmcdougall.com/misc/2007nl/nov/b12.htm , accessed 2009-04-06. [xv] McDougall J. Vegetarianism - An Offensive Stand. Pamphlet, ND. Box 14039, Santa Rosa, CA 95402. Copies posted online at http://old.animalsong.org/mcdougal.html , http://www.thisiscool.com/mohan/mcdougal.html , http://www.vegetarian1.net/Page2.htm#Vegetarianism%20-%20An%20Offensive%20Stand , and elsewhere. Accessed 200-04-06. [xvi] Herbert V. Vitamin B-12: plant sources, requirements, and assay. Am J Clin Nutr. 1988 Sep;48(3 Suppl):852-8. [xvii] Elmadfa I, Singer I. Vitamin B-12 and homocysteine status among vegetarians: a global perspective. Am J Clin Nutr. 2009 Apr 8. [Epub ahead of print] [xviii] Majchrzak D, Singer I, Männer M, Rust P, Genser D, Wagner KH, Elmadfa I. B-vitamin status and concentrations of homocysteine in Austrian omnivores, vegetarians and vegans. Ann Nutr Metab. 2006;50(6):485-91. [xix] Koebnick C, Hoffmann I, Dagnelie PC, Heins UA, Wickramasinghe SN, Ratnayaka ID, Gruendel S, Lindemans J, Leitzmann C. Long-term ovo-lacto vegetarian diet impairs vitamin B-12 status in pregnant women. J Nutr. 2004 Dec;134(12):3319-26. [xx] Herrmann W, Schorr H, Obeid R, Geisel J. Vitamin B-12 status, particularly holotranscobalamin II and methylmalonic acid concentrations, and hyperhomocysteinemia in vegetarians. Am J Clin Nutr. 2003 Jul;78(1):131-6. [xxi] Krajcovicová-Kudlácková M, Blazícek P, Kopcová J, Béderová A, Babinská K. Homocysteine levels in vegetarians versus omnivores. Ann Nutr Metab. 2000;44(3):135-8. [xxii] Mann NJ, Li D, Sinclair AJ, Dudman NP, Guo XW, Elsworth GR, Wilson AK, Kelly FD. The effect of diet on plasma homocysteine concentrations in healthy male subjects. Eur J Clin Nutr. 1999 Nov;53(11):895-9. [xxiii] Mezzano D, Muñoz X, Martínez C, Cuevas A, Panes O, Aranda E, Guasch V, Strobel P, Muñoz B, Rodríguez S, Pereira J, Leighton F. Vegetarians and cardiovascular risk factors: hemostasis, inflammatory markers and plasma homocysteine. Thromb Haemost. 1999 Jun;81(6):913-7. [xxiv] Kumar J, Garg G, Sundaramoorthy E, Prasad PV, Karthikeyan G, Ramakrishnan L, Ghosh S, Sengupta S. Vitamin B12 deficiency is associated with coronary artery disease in an Indian population. Clin Chem Lab Med. 2009 Mar; 47(3): 334-8. [xxv] Geisel J, Schorr H, Bodis M, Isber S, Hübner U, Knapp JP, Obeid R, Herrmann W. The vegetarian lifestyle and DNA methylation. Clin Chem Lab Med. 2005;43(10):1164-9. [xxvi] Karabudak E, Kiziltan G, Cigerim N. A comparison of some of the cardiovascular risk factors in vegetarian and omnivorous Turkish females. J Hum Nutr Diet. 2008 Feb;21(1):13-22. [xxvii] Chen CW, Lin YL, Lin TK, Lin CT, Chen BC, Lin CL. Total cardiovascular risk profile of Taiwanese vegetarians. Eur J Clin Nutr. 2008 Jan;62(1):138-44.
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