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Maugeri, A.; Barchitta, M. Diet and DNA Methylation. Encyclopedia. Available online: https://encyclopedia.pub/entry/2107 (accessed on 23 June 2024).
Maugeri A, Barchitta M. Diet and DNA Methylation. Encyclopedia. Available at: https://encyclopedia.pub/entry/2107. Accessed June 23, 2024.
Maugeri, Andrea, Martina Barchitta. "Diet and DNA Methylation" Encyclopedia, https://encyclopedia.pub/entry/2107 (accessed June 23, 2024).
Maugeri, A., & Barchitta, M. (2020, September 22). Diet and DNA Methylation. In Encyclopedia. https://encyclopedia.pub/entry/2107
Maugeri, Andrea and Martina Barchitta. "Diet and DNA Methylation." Encyclopedia. Web. 22 September, 2020.
Diet and DNA Methylation
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Over the past decades, DNA methylation has been proposed as a molecular mechanism underlying the positive or negative effects of diet on human health. Despite the number of studies on this topic is rapidly increasing, the relationship between dietary factors, changes in DNA methylation and health outcomes remains unclear. In this entry, we summarize the literature from observational studies which examined the association of dietary factors (nutrients, foods, and dietary patterns) with DNA methylation markers among diseased or healthy people during the lifetime.

DNA methylation Diet Nutritional Epidemiology Epigenetics Foods Nutrients

1. Introduction

‘Let food be thy medicine and medicine be thy food’—since ancient times this quote by Hippocrates has inspired humans to understand how foods could affect our health. However, in the last decades alone, research has revealed that dietary habits play a crucial role in maintaining health and in disease prevention [1]. More recently—especially through the Human Genome Project—it has become clearer how the interaction between genes and diet might influence human health, both positively and negatively. In this scenario, nutritional epigenomics elucidates what mechanisms are involved in the gene–diet interaction by investigating the effects of nutrients, foods and dietary patterns on DNA methylation, histone modifications, and non-coding RNAs [2]. As first defined by Conrad H. Waddington and later updated, these epigenetic mechanisms lead to heritable changes in gene expression that occur without modifications in DNA sequence [3]. Among these, DNA methylation is one of the most extensively studied and best characterized epigenetic mechanisms. In mammals, it is regulated by the activity of DNA methyltransferases (DNMT1, DNMT3a and DNMT3b) and ten-eleven translocation (TET) proteins [4]. DNA methylation almost exclusively occurs within CpG islands, short sequences that typically contain about 5–10 CpG dinucleotides per 100 bp [5]. Although some CpG islands are located within 60% of gene promoters in humans, the majority of them occur in repetitive sequences scattered throughout the genome [6]. In general, DNA methylation is involved in several key physiological processes (e.g., genomic imprinting, X-chromosome inactivation, regulation of gene expression, maintenance of chromosome integrity through chromatin modulation, DNA stabilization and DNA–protein interactions) [7], while aberrant DNMTs functions are associated with cardiovascular diseases, metabolic disorders, neurodegeneration, and cancers [8][9][10][11][12][13][14][15][16].

However, both environmental exposures and lifestyles can potentially modify DNA methylation, leading to genome reprogramming in exposed individuals and in future generations [17]. For instance, in vitro studies have demonstrated how several classes of nutrients modulated DNA methylation process via different mechanisms [18][19][20][21][22][23][24][25][26][27][28][29][30][31]. However, the relationship between the exposome—the sum of internal and external exposures of an individual in a lifetime—and DNA methylation is too complex to be investigated through in vitro models. For this reason, previous epidemiological studies began to focus on the effect of specific foods and nutrients on global and local DNA methylation. More recently, the research is approaching to the study of more complex dietary patterns to determine how they might affect epigenetic mechanisms in the lifetime. Here, we present current evidence obtained through observational research on the relationship between diet—in its broadest sense—and DNA methylation. Notably, findings summarized in this review come from studies conducted on “healthy” or diseased individuals during all stages of life. The search strategy and selection criteria are shown in Figure 1.Medicina 56 00374 g001 550

Figure 1. Search strategy and selection criteria of epidemiological studies examining the association between dietary factors and DNA methylation.

2. The Relationship between Dietary Factors and DNA Methylation in Mothers and Their Children

Another field of application of studying the interaction between dietary factors and DNA methylation regards the effect of maternal diet on pregnancy outcomes and newborns’ health. To our knowledge, the first evidence of this relationships comes from a study on people who were prenatally exposed to famine during the Dutch Hunger Winter in the middle of the 20th century. Indeed, sixty years later, study participants exhibited lower DNA methylation of the IGF2 gene when compared with unexposed individuals [32]. Further investigations on the same cohort revealed additional DNA methylation changes in genes implicated in metabolic disorders, such as INSIGF2, GNASAS1, MEG3, IL-10 and LEP [33]. More recently, findings from a genome-scale analysis confirmed that prenatal famine exposure was significantly associated with DNA methylation signatures in pathways related to growth and metabolism [34].

Accordingly, several observational studies evaluated the effect of dietary factors (i.e., nutrients, foods, and dietary patterns) on DNA methylation using data and sample from mother–child pairs (Table 1). In 2013, Boeke and colleagues failed in demonstrating an association of maternal intake of methyl donor nutrients with maternal and cord blood LINE-1 methylation [35]. Dietary cadmium, instead, was positively associated with maternal LINE-1 methylation at the first trimester of pregnancy, and negatively with cord blood methylation at birth [35]. Consistently, the study by Taylor and colleagues did not find a significant effect of one-carbon metabolism nutrients on global DNA methylation in cord blood or buccal cells of children [36]. In contrast, Haggarty and colleagues demonstrated that folate intake and use of folic acid supplements were associated with low LINE-1 methylation in the offspring. The authors also observed that folate intake positively associated with IGF2 and negatively with PEG3 methylation [37]. With respect to IGF2, Rijlaarsdam and colleagues found that maternal diet high in fat and carbohydrates before pregnancy was positively associated with IGF2 methylation in offspring [38]. Pauwels and colleagues evaluated the effect of maternal dietary factors before and during pregnancy on DNA methylation of RXRA, LEP, DNMT1, and IGF2. Interestingly, intake of betaine and methionine before pregnancy was positively associated with DNMT and LEP methylation; methyl group donor intake in the second trimester was negatively associated with LEP and DNMT methylation; intake of choline and folate in the third trimester was positively associated with DNMT methylation, and negatively with RXRA methylation [39]. To the best of our knowledge, only the study by McCullough and colleagues investigated the effect of complex dietary patterns rather than specific foods or nutrients. However, the authors demonstrated that a pro-inflammatory diets increased cytokine levels, but no effect on DNA methylation of nine genes was evident (i.e., IGF2, H19, MEG3, MEG3-IG, PEG3, MEST, SGCE/PEG10, NNAT, PLAGL1) [40].

Table 1. Summary of studies examining the relationship between dietary factors and DNA methylation in pregnant women and their children.

First Author and Year of Publication Country Study Design Study Population Dietary Factors DNA Methylation Markers Sample Type DNA Methylation Method Main Findings
Boeke et al. 2012 [35] USA Prospective 830 mother–child pairs Vitamin B12, betaine, choline, folate, cadmium, zinc and iron LINE-1 Maternal and infant cord blood Pyrosequencing No association of maternal intake of methyl donor nutrients with maternal and cord blood methylation. Periconceptional betaine intake was inversely associated with cord blood methylation; dietary cadmium was positively associated with first trimester methylation and inversely with cord blood methylation
Haggarty et al. 2013 [37] United Kingdom Prospective 913 mother–child pairs Folate intake PEG3, IGF2, small nuclear ribonucleoprotein polypeptide N, and LINE-1 Infant cord blood Pyrosequencing Folate intake was positively associated with IGF2 methylation and negatively with PEG3 and LINE-1 methylation in the offspring
McCullough et al. 2017 [40] USA Prospective 338 mother–child pairs from the NEST cohort Dietary inflammatory potential IGF2, H19, MEG3, MEG3-IG, PEG3, MEST, SGCE/PEG10, NNAT, PLAGL1 Infant cord blood Pyrosequencing Pro-inflammatory diets increased cytokine levels, but no association between dietary inflammatory potential and DNA methylation was evident
Pauwels et al. 2017 [39] Belgium Prospective 115 mother–child pairs from the Maternal Nutrition
and Offspring’s Epigenome study
Betaine, choline, folate, and methionine Global DNA methylation and RXRA, LEP, DNMT1, and IGF2 Infant cord blood Liquid chromatography–tandem mass spectrometry and Pyrosequencing Before pregnancy, intakes of betaine and methionine were positively associated with DNMT and LEP methylation. In the second trimester, methyl group donor intake was negatively associated with LEP and DNMT methylation. In the last trimester, intake of choline and folate was positively associated with DNMT methylation and negatively with RXRA methylation
Rijlaarsdam et al. 2017 [38] UK Prospective 346 mother–child pairs from the Avon Longitudinal Study of Parents and Children Dietary patterns IGF2 Infant cord blood and blood at 7 years Infinium Illumina Human Methylation 450 k BeadChip arrays Maternal diet high in fat and carbohydrates before pregnancy was positively associated with IGF2 methylation at birth
Taylor et al. 2017 [36] Australia Prospective 73 children from the WATCH study Methionine, folate, vitamins B2, B6 and B12 and choline Global DNA methylation Buccal cells Enzyme-linked immunosorbent assay No association between one-carbon metabolism nutrient intake and global DNA methylation levels was evident

3. Methodological Pitfalls and Future Challenges

An evaluation of studies included in the present review revealed some similarities but also great differences in study designs and methods. We noted that most studies had a cross-sectional design (65%), while only 13.9% and 20.9% were case-control or prospective studies, respectively. This did not allow us to understand the causal relationship between dietary factors and changes in DNA methylation, especially for studies on diseased patients. For this reason, further large-scale prospective research is encouraged to uncover the complex relationship of diet with DNA methylation among healthy people, but also to understand whether changes in DNA methylation could represent a molecular mechanism underlying the protective or risky effect of dietary factors against cancer and other diseases.With respect to dietary assessment, almost all studies (90.7%) collected data using Food Frequency Questionnaire (FFQ), which currently represents the gold standard in nutritional epidemiology. Although this method does not preclude errors and inaccuracies of its measurements, other tools for dietary assessment (e.g., weighted records and 24-h recalls) are also prone to misreporting [41]. In fact, the development of novel dietary assessment tools could help to overcome limitations of traditional assessments [42], however, their costs and unresolved intrinsic problems related to self-reporting prevent their extensive use in epidemiological research. Moreover, only a few studies (25.6%) evaluated the complex mixture of foods into a dietary pattern rather than the consumption of specific foods or nutrients. Indeed, nutritional research is generally moving towards the study of dietary patterns using both a priori (e.g., predefined dietary indexes) or a posteriori (i.e., dimensionality reduction techniques) approaches [43][44][45][46][47][48][49][50][51][52].Differences between studies also regarded methods used for DNA methylation analysis. Indeed, most studies applied methylation-specific PCR and pyrosequencing of bisulfite-treated DNA (37.2% and 34.9%, respectively), while 16.3% used alternative methods (e.g., enzyme-linked immunosorbent assay, Methylight assay, and mass spectrometry methods). The choice between these techniques followed the strides forward in DNA methylation profiling, but also depended on studies’ objectives, sample size and associated costs. Only in recent years, instead, some studies (11.6%) started applying DNA methylation microarrays based on the Illumina Beadchip technology to analyze more than 450,000 CpG sites. Each of the abovementioned techniques presented strengths and weaknesses that were systematically evaluated by Laird [53]. Nowadays, however, advances in DNA methylation microarrays along with reduction in their costs make them a versatile approach to explore the association between dietary factors and DNA methylation status, also in large-size studies [54].Another issue to be considered when interpreting findings of this kind of study regards the significance of DNA methylation changes observed. While for many genes and genomic sequences it is clear their function and probable association with health and diseases, for others—especially for DMRs identified by epigenome-wide association studies—it is necessary to understand what they exactly entail. Indeed, the biological effect of a particular DNA methylation change is often unknown and unpredictable based on our current knowledge. In support of this, functional studies using in vivo models might help to investigate the significance of DNA methylation changes and to solve controversies on the effect of specific nutrients and foods. For instance, examining studies included in the current review, it was not clear if folate intake was positively or negatively associated with DNA methylation. In fact, it is likely that folates—as well as other methyl donors—are important for DNA methylation maintenance, while other nutrients and/or bioactive foods exert their influence directly on enzymes involved in the methylation process. In fact, several reviews properly summarized evidence of this influence coming from in vivo studies [55][56]. Thus, in addition to investigate the association between dietary factors and DNA methylation, a deeper insight into the consequences of epigenetic changes on physiological and pathological events should be recommended. Studies on LINE-1 methylation represented a prime example of this need. Indeed, while methylation status of LINE-1 sequences could be considered a surrogate marker of global DNA methylation [13], the impacts of both hypo-and hyper-methylation should be considered. Indeed, aberrant methylation of LINE-1 sequences was previously associated with aging, cancer, neurodegeneration, metabolic disorders, and obesity by affecting genome and chromosome stability [13][14][16][24][57][58][59][60][61]. Moreover, since DNA methylation is highly cell-and tissue-specific, differences in tissue samples or blood cell composition should be addressed when comparing results from different studies. Last but not least, DNA methylation is highly sensitive to environmental exposure-in its broadest and most comprehensive meaning–and genetic factors [17][20][62][63][64][65][66][67][68][69]. For this reason, future studies should comprehensively evaluate not only dietary factors and their relationship with DNA methylation, but also the effects of other lifestyles, social determinants, environmental exposures, and genetic variants that might affect the methylation process. Finally, investments are necessary to promote studies able to assess the potential applications of genome knowledge into clinical practice to improve public health [70].

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