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  1. All, As discussed in this thread, research suggests that the gut microbiome can have a dramatic impact on physical, and even mental, health. But the relationship between the gut and health remains pretty murky, and research in the area is still in its infancy. Today everyone's favorite nutrition pundit, Dr. Greger had what I think even his skeptics will agree was a helpful video outlining one mechanistic account of how gut bacteria impact health via their influence on systemic inflammation, which itself has been implicated in most of the diseases of aging. In the video, he suggests that our body has a 'love/hate' relationship with the bacteria in our gut. On the one hand, some bacteria are quite helpful, turning what would otherwise be indigestible food (i.e. fiber) into useful metabolites, like short chain fatty acids that our body can burn as fuel. On the other hand, some bacteria like cholera or e. Coli are quite detrimental to our health, and can sometimes be fatal. So how does our immune system, which is tasked with coping with all these bacteria, handle the job? Specifically, how does it distinguish between the good bacteria which it should ignore and the bad bacteria which it should combat by triggering an inflammatory response? Dr. Greger points to research [see his citations at the bottom of this post] suggesting that the immune system uses the presence of a high level of the short chain fatty acid butyrate as the signal to distinguish between a gut populated with mostly 'good' vs. mostly 'bad' bacteria. More specifically, during our evolutionary heritage, when our ancestors were all eating a very high fiber (> 100g) diet, a healthy gut population would have generated a lot of butyrate, signally 'all clear' to the immune system, which would 'stand down' as a result. But when the gut became overgrown with 'bad' bacteria (which don't produce butyrate), the immune system would notice this lack of butyrate and swing into action, triggering a (systemic) inflammatory response to combat the bad bacteria. The problem is that today, people are eating a crappy, low-fiber, toxin-loaded Western diet, and as a result, even if a person has mostly 'good' bacteria in their gut, the bacteria don't have enough of their food (i.e. fiber) to produce much butyrate. The immune system interprets this lack of butyrate as a sign that the gut is infested with bad bacteria, and so triggers a persistent, systemic inflammatory response in order to fight the (non-existent) threat from the (non-existent) bad bacteria. This permanent inflammatory state in turn leads to all kinds of chronic disease outcomes, from cardiovascular disease, to inflammatory bowel disease, to neurodegenerative diseases like Alzheimer's. That's where Dr. Greger leaves the story, at least in this video. So which types of bacteria (as reported by uBiome) are the 'good', butyrate-producing guys that will signal our immune system that 'all is well'? According to [1]: Eighty percent of the butyrate-producing isolates [from a sample of human gut bacteria] fell within the XIVa cluster of gram-positive bacteria The common gram-positive bacteria reported at the highest level of the uBiome reports is the phylum "firmicutes". From the firmicutes wikipedia entry: The Firmicutes (Latin: firmus, strong, and cutis, skin, referring to the cell wall) are a phylum of bacteria, most of which have Gram-positive cell wall structure. In contrast, the other common high-level phylum of bacteria reported by uBiome are the gram-negative, non-butyrate-producing Bacteroides. From the microbiome wiki entry for Bacteriodes: Bacteroides are gram-negative, non-spore-forming, anaerobic, and rod-shaped bacteria. So overall, to first approximation, it appears preferable to have an abundance of firmicutes and a relative dearth of bacteroides on one's ubiome report of gut bacteria, at least from the perspective of avoiding the ill effects of systemic inflammation by maintaining a high level of butyrate. But it is undoubtedly not quite this simple. In fact I started down a rabbit hole of reading about gut bacteria that I can't entirely make heads or tails of, and that reinforced my belief that researchers a long way from understanding the impact of gut bacteria on human health - see Note 1 below for one such complication. If anyone has a different, better understanding of all of this, and wants to challenge Dr. Greger's account as an oversimplification, I'd love to hear about it! --Dean --------- Note 1: Perhaps paradoxically, vegetarians have been found to have relatively more non-butyrate producing bacteroides in their guts than omnivores, and the resulting relative dearth of energy-harvesting, butyrate-producing firmicutes in vegetarians has been used to explain the leanness of vegetarians compared to omnivores [2]. In other words, the obesogenic gut microbiome profile appears to be a higher ratio of firmicutes to bacteroides, since firmicutes are able to extract more calories from food by turning fiber into the short chain fatty acid butyrate which the body can metabolize for energy. So while firmicutes may be helpful for signalling the immune system that 'all is well' via butyrate production, the resulting abundance of butyrate produced by the firmicutes may increase one's tendency to gain weight by extracting more calories from food. But if this is true, why do firmicute-lacking vegetarians have lower levels of inflammation, and generally better health, than omnivores? Perhaps your average vegetarian doesn't actually eat that much fiber, so they aren't feeding their firmicutes sufficiently... As I said, it is complicated... ----------- [1] Appl Environ Microbiol. 2000 Apr;66(4):1654-61. Phylogenetic relationships of butyrate-producing bacteria from the human gut. Barcenilla A(1), Pryde SE, Martin JC, Duncan SH, Stewart CS, Henderson C, Flint HJ. Author information: (1)Rowett Research Institute, Bucksburn, Aberdeen AB21 9SB, United Kingdom. Butyrate is a preferred energy source for colonic epithelial cells and is thought to play an important role in maintaining colonic health in humans. In order to investigate the diversity and stability of butyrate-producing organisms of the colonic flora, anaerobic butyrate-producing bacteria were isolated from freshly voided human fecal samples from three healthy individuals: an infant, an adult omnivore, and an adult vegetarian. A second isolation was performed on the same three individuals 1 year later. Of a total of 313 bacterial isolates, 74 produced more than 2 mM butyrate in vitro. Butyrate-producing isolates were grouped by 16S ribosomal DNA (rDNA) PCR-restriction fragment length polymorphism analysis. The results indicate very little overlap between the predominant ribotypes of the three subjects; furthermore, the flora of each individual changed significantly between the two isolations. Complete sequences of 16S rDNAs were determined for 24 representative strains and subjected to phylogenetic analysis. Eighty percent of the butyrate-producing isolates fell within the XIVa cluster of gram-positive bacteria as defined by M. D. Collins et al. (Int. J. Syst. Bacteriol. 44:812-826, 1994) and A. Willems et al. (Int. J. Syst. Bacteriol. 46:195-199, 1996), with the most abundant group (10 of 24 or 42%) clustering with Eubacterium rectale, Eubacterium ramulus, and Roseburia cecicola. Fifty percent of the butyrate-producing isolates were net acetate consumers during growth, suggesting that they employ the butyryl coenzyme A-acetyl coenzyme A transferase pathway for butyrate production. In contrast, only 1% of the 239 non-butyrate-producing isolates consumed acetate. PMID: 10742256 ------------ [2] Ann Nutr Metab. 2009;54(4):253-7. doi: 10.1159/000229505. Epub 2009 Jul 27. Characterization of bacteria, clostridia and Bacteroides in faeces of vegetarians using qPCR and PCR-DGGE fingerprinting. Liszt K(1), Zwielehner J, Handschur M, Hippe B, Thaler R, Haslberger AG. Author information: (1)Department of Nutritional Sciences, University of Vienna, Vienna, Austria. BACKGROUND/AIMS: This study aimed to investigate the quantitative and qualitative changes of bacteria, Bacteroides, Bifidobacterium and Clostridium cluster IV in faecal microbiota associated with a vegetarian diet. METHODS: Bacterial abundances were measured in faecal samples of 15 vegetarians and 14 omnivores using quantitative PCR. Diversity was assessed with PCR-DGGE fingerprinting, principal component analysis (PCA) and Shannon diversity index. RESULTS: Vegetarians had a 12% higher abundance of bacterial DNA than omnivores, a tendency for less Clostridium cluster IV (31.86 +/- 17.00%; 36.64 +/- 14.22%) and higher abundance of Bacteroides (23.93 +/- 10.35%; 21.26 +/- 8.05%), which were not significant due to high interindividual variations. PCA suggested a grouping of bacteria and members of Clostridium cluster IV. Two bands appeared significantly more frequently in omnivores than in vegetarians (p < 0.005 and p < 0.022). One was identified as Faecalibacterium sp. and the other was 97.9% similar to the uncultured gut bacteriumDQ793301. CONCLUSIONS: A vegetarian diet affects the intestinal microbiota, especially by decreasing the amount and changing the diversity of Clostridium cluster IV. It remains to be determined how these shifts might affect the host metabolism and disease risks. Copyright 2009 S. Karger AG, Basel. PMID: 19641302 Dr Greger Video References: C J North, C S Venter, J C Jerling. The effects of dietary fibre on C-reactive protein, an inflammation marker predicting cardiovascular disease. Eur J Clin Nutr. 2009 Aug;63(8):921-33. J R Goldsmith, R B Sartor. The role of diet on intestinal microbiota metabolism: downstream impacts on host immune function and health, and therapeutic implications. J Gastroenterol. 2014 May;49(5):785-98. S M Kuo. The interplay between fiber and the intestinal microbiome in the inflammatory response. Adv Nutr. 2013 Jan 1;4(1):16-28. J M Harig, K H Soergel, R A Komorowski, C M Wood. Treatment of diversion colitis with short-chain-fatty acid irrigation. N Engl J Med. 1989 Jan 5;320(1):23-8. D M Saulnier, S Kolida, G R Gibson. Microbiology of the human intestinal tract and approaches for its dietary modulation. Curr Pharm Des. 2009;15(13):1403-14. J Tan, C McKenzie, M Potamitis, A N Thorburn, C R Mackay, L Macia. The role of short-chain fatty acids in health and disease. Adv Immunol. 2014;121:91-119. P V Chang, L Hao, S Offermanns, R Medzhitov. The microbial metabolite butyrate regulates intestinal macrophage function via histone deacetylase inhibition. Proc Natl Acad Sci U S A. 2014 Feb 11;111(6):2247-52. R Peltonen, J Kjeldsen-Kragh, M Haugen, J Tuominen, P Toivanen, O Førre, E Eerola. Changes of faecal flora in rheumatoid arthritis during fasting and one-year vegetarian diet. Br J Rheumatol.1994 Jul;33(7):638-43.
  2. All, Dr. Greger has an interesting video out today on "Paleo-Poop", discussing the evidence from fossilized human feces that our ancestors ate a very high fiber diet, > 100g of fiber per day vs. < 20g for most people today eating a standard American diet. This wasn't particularly new news to me, or to anyone reading this I suspect. But what I found most interesting about the video was at 2:30, where he discusses what was the likely source of all that fiber. In particular, whether ancestral humans were folivores (foliage / vegetable eaters), frugivores (fruit eaters) or faunivores (meat eaters). Its pretty clear from lots of evidence that we're not primarily meat eaters, and it has only been relatively recently in our evolutionary heritage that meat and other animal products became a large part of our diet. So we can knock faunivores out of the running - at least when considering deep evolutionary time. What was most interesting was the distinction between the other two categories - folivores vs. frugivores. The evidence he shows in the video is from [1], and it is a plot of organism body size (x-axis) vs. density of gut mucosa (y-axis). Apparently the three categories (folivores, frugivores and faunivores) fall into distinct clusters. Here is the graph, with the range at which humans fall as the intersection of the horizontal and vertical lines with the label "Homo Sapiens": As you can see, humans of today fall squarely in the cluster of frugivores, which the authors interpret to indicate that our distant ancestors were primarily fruit eaters. Obviously we're omnivorous now, and have been for quite a while, especially since we expanded out of Africa into environments where fruit isn't readily available in large quantities or year-round, and since we develop cooking and other processing techniques to make meat (as well as other parts of plants) more digestible, and more palatable! But being a fruit-lover myself, I thought it interesting to know that at least our distant ancestors appear to have been heavy fruit eaters like orangutan (who apparently also love durian!), rather than folivores like gorillas. --Dean --------- [1] Claude Marcel Hladik, Patrick Pasquet. The human adaptations to meat eating: a reappraisal. Human Evolution, Springer Verlag, 2002, 17, pp.199-206. Free full text Abstract In this paper we discuss the hypothesis, proposed by some authors, that man is a habitual meat-eater. Gut measurements of primate species do not support the contention that human digestive tract is specialized for meat-eating, especially when taking into account allometric factors and their variations between folivores, frugivores and meat-eaters. The dietary status of the human species is that of an unspecialized frugivore, having a flexible diet that includes seeds and meat (omnivorous diet). Throughout the various time periods, our human ancestors could have mostly consumed either vegetable, or large amounts of animal matter (with fat and/or carbohydrate as a supplement), depending on the availability and nutrient content of food resources. Some formerly adaptive traits (e. g. the “thrifty genotype”) could have resulted from selective pressure during transitory variations of feeding behavior linked to environmental constraints existing in the past. Key Words: meat eating, hominids, gut allometry, thrifty genotype
  3. All, Al Pater posted this paper [1] on the mortality rates of meat-eaters vs. vegetarians (and vegans) among participates in the EPIC-Oxford study of diet and health. The results were disappointing for us vegans (and vegetarians): There was no significant difference in overall (all-cause) mortality between the diet groups: HRs in low meat eaters, fish eaters, and vegetarians compared with regular meat eaters were 0.93 (95% CI: 0.86, 1.00), 0.96 (95% CI: 0.86, 1.06), and 1.02 (95% CI: 0.94, 1.10), respectively; P-heterogeneity of risks = 0.082. In a separate sub-analysis of the vegan's in the study, they found the same thing - no difference in all-cause mortality between vegans and any of the other diets. Given the distinct longevity advantage for vegans and vegetarians seen in the Adventists Health Study [2], what's the deal with these British vegans and vegetarians? One possible reason is social support. From the demographics in Table 1 of the full text of [1], the UK vegans and vegetarians were significantly less likely to be married or cohabitating than meat eaters (60.8% vs. 75.5%), and less likely to have kids (41.5% vs. 77.2%). Loneliness and social isolation are well-known contributors to ill-health and early mortality. In contrast, from the full text of [2], the Adventist vegans were slightly more likely to be married than the meat-eaters (75.6% vs. 70.3%). In addition, study [3] found the vegetarians and especially vegans in the Epic-Oxford study have significantly lower levels of vitamin B12 than meat-eaters, to the point of outright deficiency: Half of the vegans were categorized as vitamin B12 deficient and would be expected to have a higher risk of developing clinical symptoms related to vitamin B12 deficiency. Here is the graph of B12 levels in meat-eaters (open circles at top), vegetarians (closed circles in middle) and vegans (open triangles at bottom): So perhaps it is low B12 and/or other specific vitamin deficiencies among poorly planned diets of the EPIC-Oxford vegan / vegetarian participants that make them more prone to dying than the Adventists. Or perhaps it is simply overall diet quality that is worse in the UK vegans/vegetarians relative to the Adventists that makes them shorter-lived. Here is the table with diet information for the EPIC-Oxford cohort from [1]: As you can see from the highlights in yellow, the vegans/vegetarians aren't much better than the meat eaters in terms of dietary saturated fat, fiber, fruit or vegetable intake. This contrasts markedly with the Adventists dietary data, from [4], shown in tabular form below: Notice among the Adventists, the vegans consumed 50% more fiber and about have the saturated fat compared with the Adventist meat-eaters, and over twice as much fiber as the vegans/vegetarians in the EPIC-Oxford cohort. Unfortunately, the table does not have explicit data on fruit or vegetable consumption, but the fiber numbers and higher Vitamin C numbers of vegans are probably a pretty good indication of higher consumption of fruits/veggies among the vegans. Also notice that B12 intake is actually higher for vegans than for meat-eaters among the Adventist, presumably due to supplementation by the vegans. So overall, it looks the the answer to the question in the title of this post, "Why Don't UK Vegans/Vegetarians Live Longer?", is likely to be that they have much lower overall diet quality than more carefully planned vegan and vegetarian diets, like those of the Adventists, and (hopefully) all of us CR practitioners! This comparison could also be thought of as support for the idea that dietary quality may be as important or more important for health and longevity than dietary quantity (i.e. CR), which I posted about yesterday, and previously in the context of comparing the Okinawans with the Adventists. --Dean ------ [1] Mortality in vegetarians and comparable nonvegetarians in the United Kingdom. Appleby PN, Crowe FL, Bradbury KE, Travis RC, Key TJ. Am J Clin Nutr. 2015 Dec 9. pii: ajcn119461. [Epub ahead of print] PMID: 26657045 Free Article http://ajcn.nutrition.org/content/early/2015/12/07/ajcn.115.119461.long Abstract BACKGROUND: Vegetarians and others who do not eat meat have been observed to have lower incidence rates than meat eaters of some chronic diseases, but it is unclear whether this translates into lower mortality. OBJECTIVE: The purpose of this study was to describe mortality in vegetarians and comparable nonvegetarians in a large United Kingdom cohort. DESIGN: The study involved a pooled analysis of data from 2 prospective studies that included 60,310 persons living in the United Kingdom, comprising 18,431 regular meat eaters (who ate meat =5 times/wk on average), 13,039 low (less-frequent) meat eaters, 8516 fish eaters (who ate fish but not meat), and 20,324 vegetarians (including 2228 vegans who did not eat any animal foods). Mortality by diet group for each of 18 common causes of death was estimated with the use of Cox proportional hazards models. RESULTS: There were 5294 deaths before age 90 in >1 million y of follow-up. There was no significant difference in overall (all-cause) mortality between the diet groups: HRs in low meat eaters, fish eaters, and vegetarians compared with regular meat eaters were 0.93 (95% CI: 0.86, 1.00), 0.96 (95% CI: 0.86, 1.06), and 1.02 (95% CI: 0.94, 1.10), respectively; P-heterogeneity of risks = 0.082. There were significant differences in risk compared with regular meat eaters for deaths from circulatory disease [higher in fish eaters (HR: 1.22; 95% CI: 1.02, 1.46)]; malignant cancer [lower in fish eaters (HR: 0.82; 95% CI: 0.70, 0.97)], including pancreatic cancer [lower in low meat eaters and vegetarians (HR: 0.55; 95% CI: 0.36, 0.86 and HR: 0.48; 95% CI: 0.28, 0.82, respectively)] and cancers of the lymphatic/hematopoietic tissue [lower in vegetarians (HR: 0.50; 95% CI: 0.32, 0.79)]; respiratory disease [lower in low meat eaters (HR: 0.70; 95% CI: 0.53, 0.92)]; and all other causes [lower in low meat eaters (HR: 0.74; 95% CI: 0.56, 0.99)]. Further adjustment for body mass index left these associations largely unchanged. CONCLUSIONS: United Kingdom-based vegetarians and comparable nonvegetarians have similar all-cause mortality. Differences found for specific causes of death merit further investigation. KEYWORDS: diet; mortality; nonvegetarian; vegan; vegetarian -------- [2] [2] JAMA Intern Med.. 2013 Jul 8;173(13):1230-8.. doi: 10.1001/jamainternmed.2013.6473. Vegetarian dietary patterns and mortality in Adventist Health Study 2. Orlich MJ(1), Singh PN, Sabaté J, Jaceldo-Siegl K, Fan J, Knutsen S, Beeson WL, Fraser GE. Author information: (1)School of Public Health, Loma Linda University, Loma Linda, CA 92350, USA. morlich@llu.edu Comment in JAMA Intern Med.. 2014 Jan;174(1):168-9. JAMA Intern Med.. 2014 Jan;174(1):169. JAMA Intern Med.. 2013 Jul 8;173(13):1238-9. Dtsch Med Wochenschr.. 2013 Sep;138(39):1930. IMPORTANCE: Some evidence suggests vegetarian dietary patterns may be associated with reduced mortality, but the relationship is not well established. OBJECTIVE: To evaluate the association between vegetarian dietary patterns and mortality. DESIGN: Prospective cohort study; mortality analysis by Cox proportional hazards regression, controlling for important demographic and lifestyle confounders. SETTING: Adventist Health Study 2 (AHS-2), a large North American cohort. PARTICIPANTS: A total of 96,469 Seventh-day Adventist men and women recruited between 2002 and 2007, from which an analytic sample of 73,308 participants remained after exclusions. EXPOSURES: Diet was assessed at baseline by a quantitative food frequency questionnaire and categorized into 5 dietary patterns: nonvegetarian, semi-vegetarian, pesco-vegetarian, lacto-ovo-vegetarian, and vegan. MAIN OUTCOME AND MEASURE: The relationship between vegetarian dietary patterns and all-cause and cause-specific mortality; deaths through 2009 were identified from the National Death Index. RESULTS: There were 2570 deaths among 73,308 participants during a mean follow-up time of 5.79 years.. The mortality rate was 6.05 (95% CI, 5.82-6.29) deaths per 1000 person-years.. The adjusted hazard ratio (HR) for all-cause mortality in all vegetarians combined vs nonvegetarians was 0.88 (95% CI, 0.80-0.97).. The adjusted HR for all-cause mortality in vegans was 0.85 (95% CI, 0.73-1.01); in lacto-ovo-vegetarians, 0.91 (95% CI, 0.82-1.00); in pesco-vegetarians, 0.81 (95% CI, 0.69-0.94); and in semi-vegetarians, 0.92 (95% CI, 0.75-1.13) compared with nonvegetarians.. Significant associations with vegetarian diets were detected for cardiovascular mortality, noncardiovascular noncancer mortality, renal mortality, and endocrine mortality.. Associations in men were larger and more often significant than were those in women. CONCLUSIONS AND RELEVANCE: Vegetarian diets are associated with lower all-cause mortality and with some reductions in cause-specific mortality.. Results appeared to be more robust in males.. These favorable associations should be considered carefully by those offering dietary guidance. PMCID: PMC4191896 PMID: 23836264 ----------- [3] Eur J Clin Nutr. 2010 Sep;64(9):933-9. doi: 10.1038/ejcn.2010.142. Epub 2010 Jul 21. Serum concentrations of vitamin B12 and folate in British male omnivores, vegetarians and vegans: results from a cross-sectional analysis of the EPIC-Oxford cohort study. Gilsing AM(1), Crowe FL, Lloyd-Wright Z, Sanders TA, Appleby PN, Allen NE, Key TJ. Author information: (1)Cancer Epidemiology Unit, Nuffield Department of Clinical Medicine, University of Oxford, Oxford, UK. BACKGROUND/OBJECTIVES: Vegans, and to a lesser extent vegetarians, have low average circulating concentrations of vitamin B12; however, the relation between factors such as age or time on these diets and vitamin B12 concentrations is not clear. The objectives of this study were to investigate differences in serum vitamin B12 and folate concentrations between omnivores, vegetarians and vegans and to ascertain whether vitamin B12 concentrations differed by age and time on the diet. SUBJECTS/METHODS: A cross-sectional analysis involving 689 men (226 omnivores, 231 vegetarians and 232 vegans) from the European Prospective Investigation into Cancer and Nutrition Oxford cohort. RESULTS: Mean serum vitamin B12 was highest among omnivores (281, 95% CI: 270-292 pmol/l), intermediate among vegetarians (182, 95% CI: 175-189 pmol/l) and lowest among vegans (122, 95% CI: 117-127 pmol/l). In all, 52% of vegans, 7% of vegetarians and one omnivore were classified as vitamin B12 deficient (defined as serum vitamin B12 <118 pmol/l). There was no significant association between age or duration of adherence to a vegetarian or a vegan diet and serum vitamin B12. In contrast, folate concentrations were highest among vegans, intermediate among vegetarians and lowest among omnivores, but only two men (both omnivores) were categorized as folate deficient (defined as serum folate <6.3 nmol/l). CONCLUSION: Vegans have lower vitamin B12 concentrations, but higher folate concentrations, than vegetarians and omnivores. Half of the vegans were categorized as vitamin B12 deficient and would be expected to have a higher risk of developing clinical symptoms related to vitamin B12 deficiency. PMCID: PMC2933506 PMID: 20648045 ------------ [4] J Acad Nutr Diet. 2013 Dec;113(12):1610-9. doi: 10.1016/j.jand.2013.06.349. Epub 2013 Aug 27. Nutrient profiles of vegetarian and nonvegetarian dietary patterns. Rizzo NS, Jaceldo-Siegl K, Sabate J, Fraser GE. Comment in J Acad Nutr Diet. 2014 Feb;114(2):197-8. J Acad Nutr Diet. 2014 Feb;114(2):197. BACKGROUND: Differences in nutrient profiles between vegetarian and nonvegetarian dietary patterns reflect nutritional differences that can contribute to the development of disease. OBJECTIVE: Our aim was to compare nutrient intakes between dietary patterns characterized by consumption or exclusion of meat and dairy products. DESIGN: We conducted a cross-sectional study of 71,751 subjects (mean age=59 years) from the Adventist Health Study 2. Data were collected between 2002 and 2007. Participants completed a 204-item validated semi-quantitative food frequency questionnaire. Dietary patterns compared were nonvegetarian, semi-vegetarian, pesco vegetarian, lacto-ovo vegetarian, and strict vegetarian. Analysis of covariance was used to analyze differences in nutrient intakes by dietary patterns and was adjusted for age, sex, and race. Body mass index and other relevant demographic data were reported and compared by dietary pattern using χ(2) tests and analysis of variance. RESULTS: Many nutrient intakes varied significantly between dietary patterns. Nonvegetarians had the lowest intakes of plant proteins, fiber, beta carotene, and magnesium compared with those following vegetarian dietary patterns, and the highest intakes of saturated, trans, arachidonic, and docosahexaenoic fatty acids. The lower tails of some nutrient distributions in strict vegetarians suggested inadequate intakes by a portion of the subjects. Energy intake was similar among dietary patterns at close to 2,000 kcal/day, with the exception of semi-vegetarians, who had an intake of 1,707 kcal/day. Mean body mass index was highest in nonvegetarians (mean=28.7 [standard deviation=6.4]) and lowest in strict vegetarians (mean=24.0 [standard deviation=4.8]). CONCLUSIONS: Nutrient profiles varied markedly among dietary patterns that were defined by meat and dairy intakes. These differences are of interest in the etiology of obesity and chronic diseases. Copyright © 2013 Academy of Nutrition and Dietetics. Published by Elsevier Inc. All rights reserved. PMCID: PMC4081456 PMID: 23988511
  4. All, There hasn't been much talk around here lately directly related to CR - so I figured now is a good time to bring up a topic I've been puzzling over for a while now. I wonder if anyone else is feeling the same cognitive dissonance that I am. It involves the apparent health benefits of fiber on the one-hand, and the so-called "Hunger Hypothesis" (HH) on the other. In a nutshell, the HH is the idea that experiencing hunger may be important (some say critical) for manifesting the benefits of CR. The benefits of fiber were highlighted recently by this study [1]. It followed 1600+ older adults (49 years and older) for 10 years using repeated food frequency questionnaires to assess diet and it's relationship to "healthy aging", defined as "absence of disability, depressive symptoms, cognitive impairment, respiratory symptoms, and chronic diseases (eg, cancer and coronary artery disease)." It found that folks in the highest quartile of fiber intake were nearly 80% more likely to age successfully than those in the lowest quartile. Interestingly, vegetable fiber wasn't as protective as fiber from fruit or grains/cereal. But if we know anything, we know that a high fiber, high volume, low-GI diet is a great way to reduce the hunger that accompanies CR, and that some say, may be required for CR to be beneficial - the so-called "Hunger Hypothesis". Michael discusses the HH in his comprehensive SENS blog post on the Primate CR studies - suggesting it might be an explanation for the disappointing monkey results based on the fact that over the years the monkeys in the NIA's CR group appeared to become less motivated by food [3], suggesting they weren't experiencing much hunger. He suggests neuropeptide Y (NPY) or ghrelin as two potential candidate signalling molecules associated with hunger that might mediate the HH effect on longevity. He focuses a lot on NPY, since it seems to be elevated both by acute fasting and at least by several months of chronic CR - which makes it unusual among hormones and neuropeptides involved in energy homeostasis, which generally tend to return to baseline after a few week or months of chronic energy restriction. But the evidence he provides in that blog post to support the involvement of NPY (or ghrelin for that matter) in the longevity benefits of CR seems to me to be pretty scant. He suggests the lack of a drop blood pressure in the CR monkeys is suggestive of a low NPY level, since both CR and elevated NPY are usually accompanied by a drop in blood pressure. But there are lots of things affect BP besides NPY, so his reasoning seems like a pretty big stretch. And even if it were a lack of elevated NPY that explained why the CR monkey's BP didn't drop, that still doesn't say anything (directly at least) about whether elevated NPY (a surrogate for hunger) has anything to do with the lifespan effects of CR. Although high BP is the world's #1 cause of early preventable death, ahead of tobacco and alcohol use [2], I don't think anyone (esp. Michael) would claim that you can gain CR lifespan benefits simply by reducing your BP, e.g. through sodium restriction or blood pressure medication. So if NPY is going to affect longevity, it probably isn't through its BP-lowering effect. The evidence he provide to suggest a direct link between hunger (and esp, elevated NPY) and longevity seems similarly weak and tenuous. He cites [5] which found reducing NPY via lesion or genetic mutation prevents CR from protecting mice against skin cancer. He also cites [6], a study of a drug that, among several effects relating to serotonin, may possibly (Michael's word) block the effect of NPY. Rats given the drug ate 10% less food when fed ad lib than rats not given the drug, but didn't live any longer (except for the male rats on a medium dose, who did live longer). As I said, pretty tenuous evidence for a link between NPY and longevity if you ask me. If it were just Michael and the dubious evidence he provides, I think the HH could be pretty easily dismissed. But he's not the only one who advocates for it. TomB's been promoting the HH idea for a while, and even claims to be its originator. In that post he says: Tom - care to back up that bold claim with an argument and citations that are more convincing than what Michael points to? But it's not just amateur scientists like Michael and Tom promoting the HH. Dr. Speakman (who spoke at our recent CR Conference) is also an advocate for the HH. As exhibit A, he says rodents remain hungry when subjected to prolonged CR [7], which by itself is neither surprising nor especially strong evidence in favor of the HH. But in [8] (discussed here) he goes more or less all-in for the HH. In it he calls a high fiber diet "calorie dilution" rather than "calorie restriction". He claims rodents allowed to eat as much as they want of a high fiber diet become satiated and therefore stop eating voluntarily before consuming as many calories as a rodents fed normal chow ad lib. He suggests in [8] that this calorie dilution effect is the explanation for the recent, blasphemous Solon-Biet study [9]. Solon-Biet et al suggest that it is protein restriction (PR), and not calorie restriction, that mediates the observed benefits of CR via a PR-induced induced reduction in mTOR activity, saying in [9] that: Longevity and health were optimized when protein was replaced with carbohydrate to limit compensatory feeding for protein and suppress protein intake. These consequences are associated with hepatic mammalian target of rapamycin (mTOR) activation and mitochondrial function and, in turn, related to circulating branched-chain amino acids and glucose. Calorie restriction achieved by high-protein diets or dietary dilution had no beneficial effects on lifespan. The results suggest that longevity can be extended in ad libitum-fed animals by manipulating the ratio of macronutrients to inhibit mTOR activation. Speakman begs to differ. He suggests in [8] that Solon-Biet et al employed a calorie dilution paradigm, feeding all their mice ad lib, but adding fiber to modulate calorie intake on the different diet. Speakman says this is a bad idea. In his view, rodents need to be hungry to live longer as a result of CR, and so diluting their food with non-nutritive fiber so they are satisfied eating fewer calories won't trigger CR benefits. Maybe I'm missing something, but Speakman's claim about [9] puzzles me. Why? Because in [9] the mice fed a low-protein, high-carb diet ate more (both volume-wise and calorie-wise), and got fatter as a result, but did in fact live longer, seemingly in contradiction to Speakman's claim that being satiated trounces longevity. Here is a handy graphical abstract of [9] to get a better feel for what I mean: See this post for more discussion of [9] and Speakman's interpretation of it. Overall, despite my respect for Michael, Tom and Dr. Speakman, I'm dubious. First, I'm dubious in general about the promise of serious (hunger-inducing) CR to extend lifespan significantly more than an obesity-avoiding diet and lifestyle. The full evidence can be found in this thread, but a big part of it is data from the vegan Adventists, who live longer, eat more and are a lot heavier than Okinawans, the latter of which following a traditional, much lower calorie diet. More to the point, vegan Adventists following a healthy diet and lifestyle live 10-14 years longer than the general population, and eat 3x as much fiber as the average American (46g vs. 15g). If a high fiber diet is so bad, why do the vegan Adventists do so well on it? The combination of the evidence from the Adventists and from [1] supporting the health and longevity promoting effects of fiber in humans, and the weak rodent evidence supporting the Hunger Hypothesis makes me pretty dubious about any deleterious effects of fiber or feeling satiated. But I've got an open mind on the subject. Would any of you HH advocates care to take a shot at convincing me and the rest of the fiber-munching CR folks around here of the validity of your perspective - namely that we we are deluding ourselves by diluting our diets and still hoping to enjoy CR benefits? Or put another way, that we need to be CRed and hungry to benefit from CR. --Dean ---------- [1] J Gerontol A Biol Sci Med Sci. 2016 Jun 1. pii: glw091. [Epub ahead of print] Association Between Carbohydrate Nutrition and Successful Aging Over 10 Years. Gopinath B(1), Flood VM(2), Kifley A(3), Louie JC(4), Mitchell P(3). Free full text: http://biomedgerontology.oxfordjournals.org/content/early/2016/05/23/gerona.glw091.full BACKGROUND: We prospectively examined the relationship between dietary glycemic index (GI) and glycemic load (GL), carbohydrate, sugars, and fiber intake (including fruits, vegetable of breads/cereals fiber) with successful aging (determined through a multidomain approach). METHODS: A total of 1,609 adults aged 49 years and older who were free of cancer, coronary artery disease, and stroke at baseline were followed for 10 years. Dietary data were collected using a semiquantitative Food Frequency Questionnaire. Successful aging status was determined through interviewer-administered questionnaire at each visit and was defined as the absence of disability, depressive symptoms, cognitive impairment, respiratory symptoms, and chronic diseases (eg, cancer and coronary artery disease). RESULTS: In all, 249 (15.5%) participants had aged successfully 10 years later. Dietary GI, GL, and carbohydrate intake were not significantly associated with successful aging. However, participants in the highest versus lowest (reference group) quartile of total fiber intake had greater odds of aging successfully than suboptimal aging, multivariable-adjusted odds ratio (OR), 1.79 (95% confidence interval [CI] 1.13-2.84). Those who remained consistently below the median in consumption of fiber from breads/cereal and fruit compared with the rest of cohort were less likely to age successfully, OR 0.53 (95% CI 0.34-0.84) and OR 0.64 (95% CI 0.44-0.95), respectively. CONCLUSIONS: Consumption of dietary fiber from breads/cereals and fruits independently influenced the likelihood of aging successfully over 10 years. These findings suggest that increasing intake of fiber-rich foods could be a successful strategy in reaching old age disease free and fully functional. PMID: 27252308 ---------- [1] Lancet. 2012 Dec 15;380(9859):2224-60. doi: 10.1016/S0140-6736(12)61766-8. A comparative risk assessment of burden of disease and injury attributable to 67 risk factors and risk factor clusters in 21 regions, 1990-2010: a systematic analysis for the Global Burden of Disease Study 2010. Lim SS, et al BACKGROUND: Quantification of the disease burden caused by different risks informs prevention by providing an account of health loss different to that provided by a disease-by-disease analysis. No complete revision of global disease burden caused by risk factors has been done since a comparative risk assessment in 2000, and no previous analysis has assessed changes in burden attributable to risk factors over time. METHODS: We estimated deaths and disability-adjusted life years (DALYs; sum of years lived with disability [YLD] and years of life lost [YLL]) attributable to the independent effects of 67 risk factors and clusters of risk factors for 21 regions in 1990 and 2010. We estimated exposure distributions for each year, region, sex, and age group, and relative risks per unit of exposure by systematically reviewing and synthesising published and unpublished data. We used these estimates, together with estimates of cause-specific deaths and DALYs from the Global Burden of Disease Study 2010, to calculate the burden attributable to each risk factor exposure compared with the theoretical-minimum-risk exposure. We incorporated uncertainty in disease burden, relative risks, and exposures into our estimates of attributable burden. FINDINGS: In 2010, the three leading risk factors for global disease burden were high blood pressure (7·0% [95% uncertainty interval 6·2-7·7] of global DALYs), tobacco smoking including second-hand smoke (6·3% [5·5-7·0]), and alcohol use (5·5% [5·0-5·9]). In 1990, the leading risks were childhood underweight (7·9% [6·8-9·4]), household air pollution from solid fuels (HAP; 7·0% [5·6-8·3]), and tobacco smoking including second-hand smoke (6·1% [5·4-6·8]). Dietary risk factors and physical inactivity collectively accounted for 10·0% (95% UI 9·2-10·8) of global DALYs in 2010, with the most prominent dietary risks being diets low in fruits and those high in sodium. Several risks that primarily affect childhood communicable diseases, including unimproved water and sanitation and childhood micronutrient deficiencies, fell in rank between 1990 and 2010, with unimproved water and sanitation accounting for 0·9% (0·4-1·6) of global DALYs in 2010. However, in most of sub-Saharan Africa childhood underweight, HAP, and non-exclusive and discontinued breastfeeding were the leading risks in 2010, while HAP was the leading risk in south Asia. The leading risk factor in Eastern Europe, most of Latin America, and southern sub-Saharan Africa in 2010 was alcohol use; in most of Asia, North Africa and Middle East, and central Europe it was high blood pressure. Despite declines, tobacco smoking including second-hand smoke remained the leading risk in high-income north America and western Europe. High body-mass index has increased globally and it is the leading risk in Australasia and southern Latin America, and also ranks high in other high-income regions, North Africa and Middle East, and Oceania. INTERPRETATION: Worldwide, the contribution of different risk factors to disease burden has changed substantially, with a shift away from risks for communicable diseases in children towards those for non-communicable diseases in adults. These changes are related to the ageing population, decreased mortality among children younger than 5 years, changes in cause-of-death composition, and changes in risk factor exposures. New evidence has led to changes in the magnitude of key risks including unimproved water and sanitation, vitamin A and zinc deficiencies, and ambient particulate matter pollution. The extent to which the epidemiological shift has occurred and what the leading risks currently are varies greatly across regions. In much of sub-Saharan Africa, the leading risks are still those associated with poverty and those that affect children. FUNDING: Bill & Melinda Gates Foundation. Copyright © 2012 Elsevier Ltd. All rights reserved. PMCID: PMC4156511 PMID: 23245609 ----------- [3] Mattison JA, Black A, Huck J, Moscrip T, Handy A, Tilmont E, Roth GS, Lane MA, Ingram DK. Age-related decline in caloric intake and motivation for food in rhesus monkeys. Neurobiol Aging. 2005 Jul;26(7):1117-27. Epub 2004 Dec 10. PubMed PMID: 15748792. [4] Minor RK, Chang JW, de Cabo R. Hungry for life: How the arcuate nucleus and neuropeptide Y may play a critical role in mediating the benefits of calorie restriction. Mol Cell Endocrinol. 2009 Feb 5;299(1):79-88. doi: 10.1016/j.mce.2008.10.044. Epub 2008 Nov 11. Review. PubMed PMID: 19041366; PubMed Central PMCID: PMC2668104. [5] Minor RK, López M, Younts CM, Jones B, Pearson KJ, Anson RM, Diéguez C, de Cabo R. The arcuate nucleus and neuropeptide Y contribute to the antitumorigenic effect of calorie restriction. Aging Cell. 2011 Jun;10(3):483-92. doi: 10.1111/j.1474-9726.2011.00693.x. Epub 2011 Apr 5. PubMed PMID: 21385308; PubMed Central PMCID: PMC3094497. [6] Smith DL Jr, Robertson HT, Desmond RA, Nagy TR, Allison DB. No compelling evidence that sibutramine prolongs life in rodents despite providing a dose-dependent reduction in body weight. Int J Obes (Lond). 2011 May;35(5):652-7. doi: 10.1038/ijo.2010.247. Epub 2010 Nov 16. PubMed PMID: 21079617; PubMed Central PMCID: PMC3091992. [7] Hambly C, Mercer JG, Speakman JR. Hunger does not diminish over time in mice under protracted caloric restriction. Rejuvenation Res. 2007 Dec;10(4):533-42. PubMed PMID: 17990972. -------------- [8] Exp Gerontol. 2016 Mar 19. pii: S0531-5565(16)30069-9. doi: 10.1016/j.exger.2016.03.011. [Epub ahead of print] Calories or protein? The effect of dietary restriction on lifespan in rodents is explained by calories alone. Speakman JR(1), Mitchell SE(2), Mazidi M(3). Full text: http://sci-hub.cc/10...ger.2016.03.011 Almost exactly 100years ago Osborne and colleagues demonstrated that restricting the food intake of a small number of female rats extended their lifespan. In the 1930s experiments on the impact of diet on lifespan were extended by Slonaker, and subsequently McCay. Slonaker concluded that there was a strong impact of protein intake on lifespan, while McCay concluded that calories are the main factor causing differences in lifespan when animals are restricted (Calorie restriction or CR). Hence from the very beginning the question of whether food restriction acts on lifespan via reduced calorie intake or reduced protein intake was disputed. Subsequent work supported the idea that calories were the dominant factor. More recently, however, this role has again been questioned, particularly in studies of insects. Here we review the data regarding previous studies of protein and calorie restriction in rodents. We show that increasing CR (with simultaneous protein restriction: PR) increases lifespan, and that CR with no PR generates an identical effect. None of the residual variation in the impact of CR (with PR) on lifespan could be traced to variation in macronutrient content of the diet. Other studies show that low protein content in the diet does increase median lifespan, but the effect is smaller than the CR effect. We conclude that CR is a valid phenomenon in rodents that cannot be explained by changes in protein intake, but that there is a separate phenomenon linking protein intake to lifespan, which acts over a different range of protein intakes than is typical in CR studies. This suggests there may be a fundamental difference in the responses of insects and rodents to CR. This may be traced to differences in the physiology of these groups, or reflect a major methodological difference between 'restriction' studies performed on rodents and insects. We suggest that studies where the diet is supplied ad libitum, but diluted with inert components, should perhaps be called dietary or caloric dilution, rather than dietary or caloric restriction, to distinguish these potentially important methodological differences. Copyright © 2016 Elsevier Inc. All rights reserved. PMID: 27006163 ---------------- [9] Cell Metab. 2014 Mar 4;19(3):418-30. doi: 10.1016/j.cmet.2014.02.009. The ratio of macronutrients, not caloric intake, dictates cardiometabolic health, aging, and longevity in ad libitum-fed mice. Solon-Biet SM(1), McMahon AC(2), Ballard JW(3), Ruohonen K(4), Wu LE(5), Cogger VC(2), Warren A(2), Huang X(2), Pichaud N(3), Melvin RG(6), Gokarn R(7), Khalil M(8), Turner N(9), Cooney GJ(9), Sinclair DA(10), Raubenheimer D(11), Le Couteur DG(12), Simpson SJ(13). Free full text: http://www.cell.com/...4131(14)00065-5 Comment in Science. 2014 Mar 7;343(6175):1068. The fundamental questions of what represents a macronutritionally balanced diet and how this maintains health and longevity remain unanswered. Here, the Geometric Framework, a state-space nutritional modeling method, was used to measure interactive effects of dietary energy, protein, fat, and carbohydrate on food intake, cardiometabolic phenotype, and longevity in mice fed one of 25 diets ad libitum. Food intake was regulated primarily by protein and carbohydrate content. Longevity and health were optimized when protein was replaced with carbohydrate to limit compensatory feeding for protein and suppress protein intake. These consequences are associated with hepatic mammalian target of rapamycin (mTOR) activation and mitochondrial function and, in turn, related to circulating branched-chain amino acids and glucose. Calorie restriction achieved by high-protein diets or dietary dilution had no beneficial effects on lifespan. The results suggest that longevity can be extended in ad libitum-fed animals by manipulating the ratio of macronutrients to inhibit mTOR activation. Copyright © 2014 Elsevier Inc. All rights reserved. PMID: 24606899
  5. Diet & Colon Cancer Prevention While researching the Adventists diet study for prostate cancer prevention, Al Pater kindly pointed me to a similar study [1] of diet and colon cancer risk among the Adventists in the AHS-2 study by the same authors (thanks Al!). It followed 96,000 Adventists of both genders for an average follow-up time of 7.3 years to see which diets were associated with a reduced risk of colon cancer. As expected, all vegetarians combined were 22% less likely than omnivores to develop any form of colon cancer during the follow-up (HR 0.78: 95% CI, 0.64-0.95). Here is the breakdown of colon cancer risk by various types of vegetarian diets, again relative to omnivores: Vegans 0.84 (95% CI, 0.59-1.19); lacto-ovo vegetarians 0.82 (95% CI, 0.65-1.02); pescovegetarians, 0.57 (95% CI, 0.40-0.82) semivegetarians, 0.92 (95% CI, 0.62-1.37) For colon cancer, it appears to be the pesky pesco-vegetarians who have the lowest risk of colon cancer. But vegans win overall, at least among this healthy Adventist population relative to all cancers (not just prostate or colon cancer), according to [2]. From the abstract: ... vegan diets showed statistically significant protection for overall cancer incidence (HR, 0.84; 95% CI, 0.72-0.99) in both genders combined. Here is the diagram from [2] comparing the overall cancer risk for different forms of vegetarian diets, relative to omnivores: If we look at the male & female line (first highlight) or the male-only line (second highlight) in the fully adjusted model (including adjusting for BMI), it is only the vegan dietary pattern that reaches the level of 0.05 significance, and is P < 0.05 for the combined gender group. The other vegetarian subgroups failed to show a statistically significant lower overall risk of cancer relative to omnivores. Go ahead - call my Dr. Greger. But thems the data... --Dean ----------- [1] JAMA Intern Med. 2015 May;175(5):767-76. doi: 10.1001/jamainternmed.2015.59. Vegetarian dietary patterns and the risk of colorectal cancers. Orlich MJ(1), Singh PN(2), Sabaté J(1), Fan J(2), Sveen L(2), Bennett H(2), Knutsen SF(1), Beeson WL(2), Jaceldo-Siegl K(1), Butler TL(2), Herring RP(2), Fraser GE(1). IMPORTANCE: Colorectal cancers are a leading cause of cancer mortality, and their primary prevention by diet is highly desirable. The relationship of vegetarian dietary patterns to colorectal cancer risk is not well established. OBJECTIVE: To evaluate the association between vegetarian dietary patterns and incident colorectal cancers. DESIGN, SETTING, AND PARTICIPANTS: The Adventist Health Study 2 (AHS-2) is a large, prospective, North American cohort trial including 96,354 Seventh-Day Adventist men and women recruited between January 1, 2002, and December 31, 2007. Follow-up varied by state and was indicated by the cancer registry linkage dates. Of these participants, an analytic sample of 77,659 remained after exclusions. Analysis was conducted using Cox proportional hazards regression, controlling for important demographic and lifestyle confounders. The analysis was conducted between June 1, 2014, and October 20, 2014. EXPOSURES: Diet was assessed at baseline by a validated quantitative food frequency questionnaire and categorized into 4 vegetarian dietary patterns (vegan, lacto-ovo vegetarian, pescovegetarian, and semivegetarian) and a nonvegetarian dietary pattern. MAIN OUTCOMES AND MEASURES: The relationship between dietary patterns and incident cancers of the colon and rectum; colorectal cancer cases were identified primarily by state cancer registry linkages. RESULTS: During a mean follow-up of 7.3 years, 380 cases of colon cancer and 110 cases of rectal cancer were documented. The adjusted hazard ratios (HRs) in all vegetarians combined vs nonvegetarians were 0.78 (95% CI, 0.64-0.95) for all colorectal cancers, 0.81 (95% CI, 0.65-1.00) for colon cancer, and 0.71 (95% CI, 0.47-1.06) for rectal cancer. The adjusted HR for colorectal cancer in vegans was 0.84 (95% CI, 0.59-1.19); in lacto-ovo vegetarians, 0.82 (95% CI, 0.65-1.02); in pescovegetarians, 0.57 (95% CI, 0.40-0.82); and in semivegetarians, 0.92 (95% CI, 0.62-1.37) compared with nonvegetarians. Effect estimates were similar for men and women and for black and nonblack individuals. CONCLUSIONS AND RELEVANCE: Vegetarian diets are associated with an overall lower incidence of colorectal cancers. Pescovegetarians in particular have a much lower risk compared with nonvegetarians. If such associations are causal, they may be important for primary prevention of colorectal cancers. PMCID: PMC4420687 PMID: 25751512 ------------ [2] Cancer Epidemiol Biomarkers Prev. 2013 Feb;22(2):286-94. doi: 10.1158/1055-9965.EPI-12-1060. Epub 2012 Nov 20. Vegetarian diets and the incidence of cancer in a low-risk population. Tantamango-Bartley Y(1), Jaceldo-Siegl K, Fan J, Fraser G. Author information: (1)Department of Epidemiology and Biostatistics, Loma Linda University, School of Public Health, Loma Linda, CA 92350, USA. ytantamango@hotmail.com BACKGROUND: Cancer is the second leading cause of death in the United States. Dietary factors account for at least 30% of all cancers in Western countries. As people do not consume individual foods but rather combinations of them, the assessment of dietary patterns may offer valuable information when determining associations between diet and cancer risk. METHODS: We examined the association between dietary patterns (non-vegetarians, lacto, pesco, vegan, and semi-vegetarian) and the overall cancer incidence among 69,120 participants of the Adventist Health Study-2. Cancer cases were identified by matching to cancer registries. Cox proportional hazard regression analysis was conducted to estimate hazard ratios, with "attained age" as the time variable. RESULTS: A total of 2,939 incident cancer cases were identified. The multivariate HR of overall cancer risk among vegetarians compared with non-vegetarians was statistically significant [hr, 0.92; 95% confidence interval (CI), 0.85-0.99] for both genders combined. Also, a statistically significant association was found between vegetarian diet and cancers of the gastrointestinal tract (HR, 0.76; 95% CI, 0.63-0.90). When analyzing the association of specific vegetarian dietary patterns, vegan diets showed statistically significant protection for overall cancer incidence (HR, 0.84; 95% CI, 0.72-0.99) in both genders combined and for female-specific cancers (HR, 0.66; 95% CI, 0.47-0.92). Lacto-ovo-vegetarians appeared to be associated with decreased risk of cancers of the gastrointestinal system (HR, 0.75; 95% CI, 0.60-0.92). CONCLUSION: Vegetarian diets seem to confer protection against cancer. IMPACT: Vegan diet seems to confer lower risk for overall and female-specific cancer than other dietary patterns. The lacto-ovo-vegetarian diets seem to confer protection from cancers of the gastrointestinal tract. PMCID: PMC3565018 PMID: 23169929
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