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Dean Pomerleau posted a topic in CR PracticeAll, 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 . 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 , 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 , 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  which found reducing NPY via lesion or genetic mutation prevents CR from protecting mice against skin cancer. He also cites , 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 , which by itself is neither surprising nor especially strong evidence in favor of the HH. But in  (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  that this calorie dilution effect is the explanation for the recent, blasphemous Solon-Biet study . 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  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  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  puzzles me. Why? Because in  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  to get a better feel for what I mean: See this post for more discussion of  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  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 ----------  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 ----------  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 -----------  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.  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.  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.  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.  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. --------------  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 ----------------  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
drewab posted a topic in CR Science & TheoryI came across this gem - a cross sectional/correlational study on being a father and T levels. The reason I think it's important is that Tanzanian hunter gatherers are known to eat 100-150g of fibre daily, something many of us here do. In addition they have a low BMI and low energy intake. http://rspb.royalsocietypublishing.org/content/276/1655/347 I'm typing this from my phone so my response has to be limited, but here were some points I picked up on: -their T in general is far lower than Americans - 150 pmol vs Americans being 250-400pmol (I'm not familiar with this unit and google didn't help) -caring for offspring closely lowered AM T by 30% and PM T by 50% (same trend not seen in America) -more closely caring for children lowered T more, while distance parenting didn't -fidelity lowered T -T didn't vary by age in these groups, suggesting you can maintain some T as you age Maybe this is why some CR practitioners like Paul McGlothin are able to maintain youthful T levels. Thoughts?
Dean Pomerleau posted a topic in CR PracticeAll, 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 : 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 . 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... -----------  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 ------------  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.