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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: (Published 29 July 2014) Cite this as: BMJ 2014;349:g4490

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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:

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

29 September 2014
Celia M. Ross
Delaware, USA