Fruit and vegetable consumption and mortality from all causes, cardiovascular disease, and cancer: systematic review and dose-response meta-analysis of prospective cohort studies
BMJ 2014; 349 doi: https://doi.org/10.1136/bmj.g4490 (Published 29 July 2014) Cite this as: BMJ 2014;349:g4490
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The Journal wisely encourages the use of the “Number Needed to Treat” instead of “Relative Risk Reduction”.(1) Wang et al only provided hazard ratios when estimating risk for all cause, cardiovascular, and cancer mortality by levels of fruit and vegetable consumption.(2)
From the data provided by ref 42 one can calculate that the number needed to treat to avoid one death from ischemic heart disease during 8.4 years is 500 (6.7 deaths per 1000 persons consuming 3 portions of fruits and vegetables per day vs 4.7 deaths per 1000 persons consuming 8 portions per day).
Using the population attributable fraction (PAF) would have been even more appropriate to illustrate the true burden of poor diets. PAF is the proportional reduction in population disease or mortality that would occur if exposure to a risk factor were reduced to an alternative ideal exposure scenario.
Despite a weak association applied to the population may still be meaningful for public health, shifting to an herbivore or chimp diets is unlikely to be both enforceable and acceptable. Last, poor diet is simply a marker of more serious unhealthy behaviours and poor social determinants that influence cancer risk (alcohol, tobacco, lack of physical activity, obesity …).
1 Moore A, McQuay H. Numbers needed to treat derived from meta analysis. NNT is a tool, to be used appropriately. BMJ. 1999 Oct 30;319(7218):1200.
2 Wang X, Ouyang Y, Liu J et al. Fruit and vegetable consumption and mortality from all causes, cardiovascular disease, and cancer: systematic review and dose-response meta-analysis of prospective cohort studies. BMJ 2014;349:g4490.
Competing interests: No competing interests
The association between eating more fruit and vegetables and reduction in mortality, especially related to cancer and cardiovascular disease, is well established in this paper. One of the major challenges, however, is how we can translate this into practice.
With an increasing elderly population this poses difficulties for individuals who may no longer possess the physiological fitness required to source, prepare and consume fresh fruit and vegetables. More therefore needs to be done to help us understand how we can improve the diets of older people to prevent an increasing health burden which could be solved through simply eating more fruit and vegetables.
Competing interests: No competing interests
To the editor,
Although Dr Bao Wei et al. answered some of my questions (1), I still have concerns.
First, although the authors explained the reasons why three studies (2-4) we mentioned were excluded, it is still unclear why many studies on the relationship between fruit or vegetable intake and specific cancer mortality were finally excluded.
Second, as there was publication bias for their results, I still question whether the trim and fill method used by the authors can address the publication bias simply from a statistical perspective.
Zhihao
References
1. Authors' reply on the systematic review and does-response meta-analysis of fruit and vegetable consumption in relation to mortality.http://www.bmj.com/content/349/bmj.g4490/rr/762968
2. Mann JI, Appleby PN, Key TJ, Thorogood M. Dietary determinants of ischaemic heart disease in health conscious individuals. Heart. 1997;78:450-5.
3. Ness AR, Maynard M, Frankel S, Smith GD, Frobisher C, Leary SD, Emmett PM, Gunnell D. Diet in childhood and adult cardiovascular and all cause mortality: The boyd orr cohort. Heart. 2005;91:894-8.
4. Lo YT, Chang YH, Wahlqvist ML, Huang HB, Lee MS. Spending on vegetable and fruit consumption could reduce all-cause mortality among older adults. Nutr J. 2012;11:113.
Competing interests: No competing interests
I have read the response from Dr Wei Bao et al. about the publication on fruit and vegetable intake and mortality. However, two questions were not addressed.
Firat, the authors emphasized the linear dose-response association in their orginal publication but simply described the non-linear assocaiton in both the Abstract and Results section. In my opinion, it was wrong and the results on the linear dose-response association should be deleted as there was evidence of curvilinear associations between fruit and vegetable combined or alone and all cause, cardiovascular, and cancer mortality (all P less than 0.05 for non-linearity). However, in their response, the authors still stick with the results on linear dose-response association.
Second, the marginal association (the upper limit of confidence interval for hazard ratios ranged from 0.98 to 0.99, approximately equal to 1. ) might be due to confounding factors or residual error. However, the authors did not mention this point in their response.
References
1. Authors' reply on the systematic review and does-response meta-analysis of fruit and vegetable consumption in relation to mortality.http://www.bmj.com/content/349/bmj.g4490/rr/762968
Competing interests: No competing interests
To the editor:
We appreciate very much the enormous interest from the globe in our recent study published in BMJ.1
We concur with Ellen M Storm2 that there were fewer studies evaluating the health benefits of fruit and vegetable consumption at the level of greater than 5 servings per day. Therefore, more studies are warranted in the future to confirm the association of fruit and vegetable consumption at levels of higher than 5 servings per day with risk of mortality. However, from public health point of view, the debate on the exact amount is not relevant at present, because the average consumption of fruit and vegetable is far below 5 servings per day in the general population.3 Consistent with our findings, the World Health Organization recommends 5 servings (400 g) of fruit and vegetables per day as the population goal for chronic disease prevention.4 Compared with the recommended level of fruit and vegetable consumption, the current average population level has much room to improve.
Both Liang Zhou5 and Zhihao Liu6 raised a concern of omitting a number of “eligible” studies in our meta-analysis. However, because Mann et al7 and Ness et al8 did not report data on person-years or total number of participants for each category of fruit and/or vegetable consumption, we were unable to include them in our dose-response meta-analysis using the generalized least squares trend estimation (GLST) method.9-11 The study by Lo et al12 was excluded because it reported daily expenditures on rather than consumption of fruit and vegetables.
Nechuta et al13 reported on the association between combined consumption of fruit and vegetable and mortality from the Shanghai Women’s Health Study. However, we did include a more recent article14 from the same cohort which examined the risk of mortality of fruit and vegetable separately. Including Nechuta et al13 in our meta-analysis did not materially alter our results or conclusions: the pooled hazard ratio (95% confidence interval) associated with each portion increase in fruit and vegetable consumption was 0.96 (0.94 to 0.97; P=0.001) for all-cause mortality. In addition, we still observed a threshold at around five servings daily consumption of fruit and vegetables, after which there was no further reduction in risk.
In our meta-analysis, two of the included studies reported fruit juice as part of fruit consumption.15 16 Liang Zhou5 argued that we should remove them from the analysis because there was evidence showing divergent associations of fruit and fruit juice consumption on type 2 diabetes.17 18 However, because there is no evidence showing any difference between fruit and fruit juice with regard to the risk of mortality, we do not believe there is sufficient rationale to exclude these two studies from our main analysis. Nonetheless, we conducted a sensitivity analysis by excluding these two studies and found almost identical results; the pooled hazard ratio of all-cause mortality was 0.94 (95% confidence interval 0.90 to 0.99; P=0.002) for each additional serving a day of fruit.
Suhail A. Doi19 questioned the random-effects models used in our meta-analysis, and suggested the use of the inverse variance heterogeneity (IVhet) and the quality effects (QE) models developed by the author. However, to our knowledge, the DerSimonian-Laird random-effects model20 21 is the standard method used in meta-analyses, and therefore it was used in our study.
We agree with Chibo Liu22 that the pooled HR associated with each unit increment of fruit and vegetable consumption may not be optimal in the context of curvilinear associations. Therefore, we presented both the dose-response curve plot and forest plot in our original paper.
We used the previously described definition23 for each serving of fruit (80 g) and vegetables (77 g), because these serving sizes were calculated on the basis of real weighting and averaging commonly consumed fruit and vegetables,23 rather than based on arbitrary numbers.
We conducted stratified analyses but did not perform a formal meta-regression to identify potential sources of heterogeneity because a robust conclusion from meta-regression requires a large number of included studies.24 Also, for the evaluation of publication bias, we were actually short of statistical power because of the limited number of included studies.25 In addition, the Egger’s test, which is based on regression method, may have a high false positive rate.25 26
Finally, we have been informed about a slight error in our paper. From one of the studies (Leenders et al, Am J Epidemiol 2013;178:590-602) included in the meta-analysis we inadvertently used data on fruit consumption and all cause mortality for women only rather than for the whole population. We have re-run the analyses using the correct hazard ratio for overall mortality of 1.00 (95% confidence interval 0.99 to 1.01) for 100 g/day fruit consumption. The revised pooled hazard ratio for all cause mortality should be 0.94 (0.89 to 0.98; P=0.006) for an increment of one serving of fruit a day, which is almost identical to that reported in the paper (0.94, 0.90 to 0.98; P=0.002) and hence does not affect the conclusions.
Wang Xia, Department of Maternal and Child Health Care, School of Public Health, Shandong University, Jinan, China
Wei Bao, Epidemiology Branch, Division of Intramural Population Health Research, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Rockville, MD 20852, USA
Frank B. Hu, Departments of Nutrition and Epidemiology, Harvard School of Public Health, Boston, MA 02115, USA
References
1. Wang X, Ouyang Y, Liu J, Zhu M, Zhao G, Bao W, et al. Fruit and vegetable consumption and mortality from all causes, cardiovascular disease, and cancer: systematic review and dose-response meta-analysis of prospective cohort studies. BMJ 2014;349:g4490.
2. Storm EM. Re: Fruit and vegetable consumption and mortality from all causes, cardiovascular disease, and cancer: systematic review and dose-response meta-analysis of prospective cohort studies. 2014. http://www.bmj.com/content/349/bmj.g4490/rr/761891.
3. Hall JN, Moore S, Harper SB, Lynch JW. Global variability in fruit and vegetable consumption. Am J Prev Med 2009;36:402-09 e5.
4. World Health Organization. Promoting fruit and vegetable consumption around the world. http://www.who.int/dietphysicalactivity/fruit/en/index2.html.
5. Zhou L. The omission of eligible publications may bias the conclusions. 2014. http://www.bmj.com/content/349/bmj.g4490/rr/762437.
6. Liu Z. Insufficient literature was included in the meta-analysis by Wang et al. 2014. http://www.bmj.com/content/349/bmj.g4490/rr/762200.
7. Mann JI, Appleby PN, Key TJ, Thorogood M. Dietary determinants of ischaemic heart disease in health conscious individuals. Heart 1997;78:450-5.
8. Ness AR, Maynard M, Frankel S, Smith GD, Frobisher C, Leary SD, et al. Diet in childhood and adult cardiovascular and all cause mortality: the Boyd Orr cohort. Heart 2005;91:894-8.
9. Berlin JA, Longnecker MP, Greenland S. Meta-analysis of epidemiologic dose-response data. Epidemiology 1993:218-28.
10. Greenland S, Longnecker MP. Methods for trend estimation from summarized dose-response data, with applications to meta-analysis. American journal of epidemiology 1992;135:1301-09.
11. Orsini N, Bellocco R, Greenland S. Generalized least squares for trend estimation of summarized dose-response data. Stata J 2006;6:40-57.
12. Lo YT, Chang YH, Wahlqvist ML, Huang HB, Lee MS. Spending on vegetable and fruit consumption could reduce all-cause mortality among older adults. Nutr J 2012;11:113.
13. Nechuta SJ, Shu XO, Li HL, Yang G, Xiang YB, Cai H, et al. Combined impact of lifestyle-related factors on total and cause-specific mortality among Chinese women: prospective cohort study. PLoS Med 2010;7:e1000339.
14. Zhang X, Shu XO, Xiang YB, Yang G, Li H, Gao J, et al. Cruciferous vegetable consumption is associated with a reduced risk of total and cardiovascular disease mortality. Am J Clin Nutr 2011;94:240-6.
15. Sahyoun NR, Jacques PF, Russell RM. Carotenoids, vitamins C and E, and mortality in an elderly population. Am J Epidemiol 1996;144:501-11.
16. Whiteman D, Muir J, Jones L, Murphy M, Key T. Dietary questions as determinants of mortality: the OXCHECK experience. Public Health Nutr 1999;2:477-87.
17. Xi B, Li S, Liu Z, Tian H, Yin X, Huai P, et al. Intake of fruit juice and incidence of type 2 diabetes: a systematic review and meta-analysis. PLoS One 2014;9:e93471.
18. Li S, Miao S, Huang Y, Liu Z, Tian H, Yin X, et al. Fruit intake decreases risk of incident type 2 diabetes: an updated meta-analysis. Endocrine 2014.
19. Doi SA. Re: Fruit and vegetable consumption and mortality from all causes. 2014. http://www.bmj.com/content/349/bmj.g4490/rr/761969.
20. DerSimonian R, Laird N. Meta-analysis in clinical trials. Control Clin Trials 1986;7:177-88.
21. Jackson D, White IR, Thompson SG. Extending DerSimonian and Laird's methodology to perform multivariate random effects meta-analyses. Stat Med 2010;29:1282-97.
22. Liu C. Fruit and vegetable consumption and mortality. 2014. http://www.bmj.com/content/349/bmj.g4490/rr/762303.
23. He FJ, Nowson CA, MacGregor GA. Fruit and vegetable consumption and stroke: meta-analysis of cohort studies. Lancet 2006;367:320-6.
24. Thompson SG, Higgins JP. How should meta-regression analyses be undertaken and interpreted? Stat Med 2002;21:1559-73.
25. Sterne JA, Gavaghan D, Egger M. Publication and related bias in meta-analysis: power of statistical tests and prevalence in the literature. J Clin Epidemiol 2000;53:1119-29.
26. Harbord RM, Egger M, Sterne JA. A modified test for small-study effects in meta-analyses of controlled trials with binary endpoints. Stat Med 2006;25:3443-57.
Competing interests: No competing interests
Liang Zhou
Department of Sports Physiology, Hunan University of Science and Technology, Xiangtan, Hunan, China
In the recent issue of BMJ, Wang et al. (1) used a meta-analysis to examine the association between fruit and vegetable intake and risk of total, cardiovascular, and cancer mortality. They found that intake of fruits and vegetables for one serving per day may slightly decrease the risk of all cause, cardiovascular, and cancer mortality.
However, they omitted a number of eligible publications that may bias the conclusions. For total mortality and intake of fruit and vegetable combined, they at least omitted one eligible publication (2). For total mortality and intake of fruit alone, at least three eligible publications (3-5) have been missed. In addition, they included two ineligible publications (6,7) and both studies investigated the association between fruit and juices in combination and risk of total mortality. Based on the recent findings (8,9), fruits and fruit juices have different effect on human health. For total mortality and intake of vegetable alone, also at least at least three eligible publications (3-5) have been omitted.
In conclusions, the omission of eligible studies and inclusion of ineligible ones might have biased their conclusions. The authors have reported publication bias for their meta-analysis and we guess the publication bias may be due to the omission of eligible publications.
References
1. Wang X, Ouyang Y, Liu J, Zhu M, Zhao G, Bao W, Hu FB. Fruit and vegetable consumption and mortality from all causes, cardiovascular disease, and cancer: systematic review and dose-response meta-analysis of prospective cohort studies. BMJ 2014;349:g4490.
2. Nechuta SJ, Shu XO, Li HL, Yang G, Xiang YB, Cai H, Chow WH, Ji B, Zhang X, Wen W, Gao YT, Zheng W. Combined impact of lifestyle-related factors on total and cause-specific mortality among Chinese women: prospective cohort study. PLoS Med. 2010 Sep 14;7. pii: e1000339.
3. Mann JI, Appleby PN, Key TJ, Thorogood M. Dietary determinants of ischaemic heart disease in health conscious individuals. Heart. 1997;78:450-5.
4. Ness AR, Maynard M, Frankel S, Smith GD, Frobisher C, Leary SD, Emmett PM, Gunnell D. Diet in childhood and adult cardiovascular and all cause mortality: The boyd orr cohort. Heart. 2005;91:894-8.
5. Lo YT, Chang YH, Wahlqvist ML, Huang HB, Lee MS. Spending on vegetable and fruit consumption could reduce all-cause mortality among older adults. Nutr J. 2012;11:113.
6. Sahyoun NR, Jacques PF, Russell RM. Carotenoids, vitamins C and E, and mortality in an elderly population. Am J Epidemiol. 1996;144:501-11.
7. Whiteman D, Muir J, Jones L, Murphy M, Key T. Dietary questions as determinants of mortality: the OXCHECK experience. Public Health Nutr. 1999;2:477-87.
8. Xi B, Li S, Liu Z, Tian H, Yin X, Huai P, Tang W, Zhou D, Steffen LM. Intake of fruit juice and incidence of type 2 diabetes: a systematic review and meta-analysis. PLoS One. 2014;9:e93471.
9. Li S, Miao S, Huang Y, Liu Z, Tian H, Yin X, Tang W, Steffen LM, Xi B. Fruit intake decreases risk of incident type 2 diabetes: an updated meta-analysis. Endocrine. 2014 Jul 30. [Epub ahead of print].
Competing interests: No competing interests
Wang et al. 1 performed a meta-analysis to investigate the association between fruit and vegetable consumption and mortality from all causes, cardiovascular disease and cancer. However, I have three different opinions.
First, they described that “Pooled hazard ratios of all-cause mortality were 0.95 (95% confidence interval 0.92 to 0.98) for an increment of one serving a day of fruit and vegetables (P=0.001), 0.94 (0.90 to 0.98) for fruit (P=0.002), and 0.95 (0.92 to 0.99) for vegetables (P=0.006)”. In my opinion, those descriptions above are incorrect. The authors used generalized least squares trend estimation method developed by Greenland and Longnecker2,3 to estimate the dose-response relationship. Based on their results, there was evidence of curvilinear associations between fruit and vegetable combined or alone and all cause, cardiovascular, and cancer mortality (all P less than 0.05 for non-linearity). Thus, it is wrong to further emphasize the linear dose-response associations and present pooled relative risk for an increment of one serving a day of fruit and vegetable combined, fruit and vegetable alone since those associations did not conform to linear dose-response relationship. And the authors should describe the curvilinear associations in detail.
Second, I noted that the protective effects of fruit and vegetable consumption on risk of total, cardiovascular, and cancer mortality were very small, the decreased risk ranging from 5% to 6%. In addition, the upper limit of confidence interval ranged from 0.98 to 0.99, approximately equal to 1. Thus, the significant association might be due to confounding factors or residual error.
Third, I also query about the use of 77 g for vegetables and 80 g for fruits to define one serving or each time intake. Wang et al. 1 cited the article by He FJ et al.4 to support their definition, but to my knowledge, 80 g for vegetables and 100 g for fruits were more widely accepted to quantify one serving or each time intake 5.
References
1. Wang X, Ouyang Y, Liu J, Zhu M, Zhao G, Bao W, Hu FB. Fruit and vegetable consumption and mortality from all causes, cardiovascular disease, and cancer: systematic review and dose-response meta-analysis of prospective cohort studies. BMJ 2014;349:g4490.
2. Greenland S, Longnecker MP. Methods for trend estimation from summarizeddose-response data, with applications to meta-analysis. Am J Epidemiol1992;135:1301-9.
3. Orsini N, Bellocco R, Greenland S. Generalized least squares for trend estimation ofsummarized dose-response data. Stata J 2006;6:40-57.
4. He FJ, Nowson CA, MacGregor GA. Fruit and vegetable consumption and stroke: meta-analysis of cohort studies. Lancet 2006;367:320-6.
5. Riboli E, Norat T. Epidemiologic evidence of the protective effect of fruit and vegetables on cancer risk. Am J Clin Nutr. 2003;78:559S-69S.
Competing interests: No competing interests
Dear editor,
We read with interest the meta-analysis by Wang et al. 1 published in a recent issue of BMJ. However, we found some problems in their meta-analysis that might have influenced their results.
First, their search items were insufficient. The keywords such as “cancer”,” tumor”, “cohort study”, “longitudinal study” also should be used.
Second, we found that the authors omitted many eligible studies that met their inclusion criteria. Taking the association of fruit consumption with health outcomes for example, we identified 21 studies for total mortality, 20 studies for cardiovascular mortality, and 25 studies for cancer mortality based on their search strategy. Surprisingly, the authors only identified 7, 6 and 7, for total, cardiovascular and cancer mortality, accordingly.
Third, there was significant between-study heterogeneity for associations with majority of health outcomes. The authors used subgroup analysis to examine the source of heterogeneity. In our opinion, it was not sufficient. Meta regression analysis should be performed firstly 2 and then the subgroup analysis.
Fourth, there was significant publication bias for the associations of total mortality with fruit and vegetable combined and fruit alone (p=0.006 and 0.02, respectively). The authors used trim and fill method to address the publication bias. In our opinion, this method may partially address the publication bias in statistical aspect, but it cannot overcome the inherent publication bias. Thus, the protective effect of fruit and vegetable combined or fruit alone on risk of total mortality should be interpreted with caution.
References
1. Wang X, Ouyang Y, Liu J, Zhu M, Zhao G, Bao W, Hu FB. Fruit and vegetable consumption and mortality from all causes, cardiovascular disease, and cancer: systematic review and dose-response meta-analysis of prospective cohort studies. BMJ 2014;349:g4490.
2. Martin B. Meta-analysis: Dealing with heterogeneity. York: University of York; 2006.
Competing interests: No competing interests
Many scientific contributions support the benefits of fruit and vegetables for Western “health and well-being” though few suggest mechanisms (1).
DP Burkitt’s observations in the 1970’s that Western stool weights and oro-anal, transit times show four-fold differences compared to those of Africans eating a high fibre diet, suggest remarkable physiological differences (2). KW Heaton’s observations in the 1990’s that 1% of an East Bristol population achieve successful defaecation once per week, but 0.1% only manage successful defaecation once per month, and, that 20-30% of all bowel movements are complicated by physical efforts during defaecation, is also important evidence (3). Physical efforts during defaecation at different times of life cause specific neuro-immunohistochemical signatures in many pelvic organs, and, may contribute to unexplained, extrapelvic denervation and reinnervation with diverse and varying consequences that we recognise as Western diseases (4).
Fruit and vegetables may protect us by many mechanisms but the present epidemic of obesity suggests that our deteriorating diets and bowel habits, are serving up a menu of Western diseases that will overwhelm health services throughout the developed, and developing, world. And, tragically, as Bdurkitt suggested in the 1970’s, they are entirely preventable (2).
(1) Wang X, Ouyang YY, Liu J, Zhu MM, Bao W, Hu FB
Fruit and vegetable consumption and mortality from all causes, cardiovascular disease, and cancer: systematic review and dose-response meta-analysis of prospective cohort studies
BMJ 2014; 349 doi: http://dx.doi.org/10.1136/bmj.g4490 (Published 29 July 2014)
(2) Burkitt DP, Trowell HC. Western diseases: their emergence and
prevention. London: Edward Arnold, 1981
(3) Heaton KW, Cripps HA.
Straining at stool and laxative taking in an English population.
Dis Dig Sci 1993 (Jun);38(6):1004-8.
(4) Quinn MJ.
Autonomic denervation and Western diseases.
Am J Med 2014 (Jan); 127(1):3-4.
Competing interests: No competing interests
Re: Fruit and vegetable consumption and mortality from all causes, cardiovascular disease, and cancer: systematic review and dose-response meta-analysis of prospective cohort studies
Wang et al (2014) conducted an important meta-analysis study which showed that eating more fruits and vegetables appears to lower the risk of cardiovascular mortality (1). Wang et al (2014) point to the probability that multiple mechanisms could be involved in explaining this relationship. It might also be interesting to look at these results from the perspective of cardiovascular disease having epigenetic roots (2, 3). It should be noted that there is evidence that the epigenome is malleable throughout the lifespan (4). Researchers are looking at environmental variables that might affect disease risk by nudging the epigenome (5).
Fruits and vegetables might nudge the epigenome by a couple of mechanisms. First, phytochemicals found in fruits and vegetables may play a role in shaping the epigenome (6, 7). Since the natural diet for humans is one that is rich in produce, and thus phytochemicals, it is reasonable to hypothesize that our epigenomic system was formed on the assumption that abundant amounts of phytochemicals would be available (8). Second, fruits and vegetables support a healthy gut ecosystem (9). Gut microbiota are believed to influence the human epigenome through chemical signaling (10, 11, 12). Could the gut ecosystem influence cardiovascular health by epigenetic means?
About the author: www.CeliaMRoss.com
1. Wang X, Ouyang Y, Liu J, Zhu M, Zhao G, Bao W, Hu FB. Fruit and vegetable consumption and mortality from all causes, cardiovascular disease, and cancer: systematic review and dose-response meta-analysis of prospective cohort studies. BMJ. 2014 Jul 29;349:g4490.
2. Yamada Y, Nishida T, Horibe H, Oguri M, Kato K, Sawabe M. Identification of hypo- and hypermethylated genes related to atherosclerosis by a genome-wide analysis of DNA methylation. Int J Mol Med. 2014 May;33(5):1355-63.
3. Wang Y, Miao X, Liu F, Li F, Liu Q, Sun J, Cai L. Dysregulation of histone acetyltransferases and deacetylases in cardiovascular diseases. Oxid Med Cell Longev. 2014;2014:641979.
4. Fraga MF, et al. Epigenetic differences arise during the lifetime of monozygotic twins. Proceeding of the National Academy of Science U S A. 2005 Jul 26;102(30):10604-9.
5. Ordovás JM, Smith CE. Epigenetics and cardiovascular disease. Nat Rev Cardiol. 2010 Sep;7(9):510-9.
6. Blade C, Baselga-Escudero L, Arola-Amal A MicroRNAs as New Targets of Dietary Polyphenols. Curr Pharm Biotechnol. 2014 Jul 11. [Epub ahead of print]
7. Pan MH, Lai CS, Wu JC, Ho CT. Epigenetic and disease targets by polyphenols. Curr Pharm Des. 2013;19(34):6156-85.
8. Jew S, AduMweis SS, Jones PJ. Evolution of the human diet: linking our ancestral diet to modern functional foods as a means of chronic disease prevention. J Med Food. 2009 Oct;12(5):925-34.
9. Tuohy KM, Contemo L, Gasperotti M, Viola R. Up-regulating the human intestinal microbiome using whole plant foods, polyphenols, and/or fiber. J Agric Food Chem. 2012 Sep 12;60(36):8776-82.
10. Hullar MA, Fu BC. Diet, the gut microbiome, and epigenetics. Cancer J. 2014 May-Jun;20(3):170-5.
11. Nankova BB, Agarwal R, MacFabe DF, La Gamma EF. Enteric Bacterial Metabolites Propionic and Butyric Acid Modulate Gene Expression, Including CREB-Dependent Catecholaminergic Neurotransmission, in PC12 Cells - Possible Relevance to Autism Spectrum Disorders. PLoS One. 2014 Aug 29;9(8):e103740.
12. Berndt BE, et al. Butyrate increases IL-23 production by stimulated dendritic cells. Am J Physiol Gastrointest Liver Physiol. 2012 Dec 15;303(12):G1384-92.
Competing interests: No competing interests