Nutritional epigenetics is a science that studies the effects of nutrition on gene expression and chromatin accessibility.[1][2] It is a subcategory of nutritional genomics that focuses on the effects of bioactive food components on epigenetic events.[3]

History

Changes to children’s genetic profiles caused by fetal nutrition have been observed as early as the Dutch famine of 1944-1945.[4][5][6] Due to malnutrition in pregnant mothers, children born during this famine were more likely to exhibit health issues such as heart disease, obesity, schizophrenia, depression, and addiction.[4][5][6]

Biologists Randy Jirtle and Robert A. Waterland became early pioneers of nutritional epigenetics after publishing their research on the effects of a pregnant mother’s diet on her offspring’s gene functions in the research journal Molecular and Cellular Biology in 2003.[7][8]

Research

Researchers in nutritional epigenetics study the interaction between molecules in food and molecules that control gene expression, which leads to areas of focus such as dietary methyl groups and DNA methylation.[8][9] Nutrients and bioactive food components affect epigenetics by inhibiting enzymatic activity related to DNA methylation and histone modifications.[10] Because methyl groups are used for suppression of undesirable genes, a mother’s level of dietary methyl consumption can significantly alter her child’s gene expression, especially during early development.[11] Furthermore, nutrition can affect methylation as the process continues throughout an individual’s adult life. Because of this, nutritional epigeneticists have studied food as a form of molecular exposure.[1]

Bioactive food components that influence epigenetic processes range from vitamins such as A, B6, and B12 to alcohol and elements such as arsenic, cadmium, and selenium.[3] Dietary methyl supplements such as extra folic acid and choline can also have adverse effects on epigenetic gene regulation.[1][8]

Researchers have considered dietary exposure to heavy metals such as mercury and lead primary epigenetic factors leading to increased autism and attention deficit hyperactivity disorder.[12][13] High-fat and low-protein diets during pregnancy can also increase the risk of obesity in infants.[14] The consumption of phytochemicals can also positively affect epigenetic-based mechanisms that inhibit cancer cells.[15] Research has also suggested a link between nutritional epigenetics and the pathophysiology of major depressive disorder.[16]

Epigenetic Stressors

Evidence of the generational transmission of epigenetic mechanisms in humans was first discussed by Champagne in 2008 in the context of maternal stress with food insecurity being one type of stressor that can impact gene expression via changes in DNA methylation patterns.[17] Another type of stressor is a poor prenatal diet that results in nutritional insufficiency and fetal epigenetic reprogramming that creates the blueprint for the development of diseases later in a child’s life.[18][19] Depending on geographical region, food quality issues may impact epigenetic inheritance via changes in methylation patterns associated with dietary heavy metal exposures, especially in the case of autism and attention deficit hyperactivity disorders (ADHD).[20]

Food insecurity

Food insecurity refers to the inability to access enough food to meet basic needs and is associated with an increased risk of birth defects associated with DNA methylation patterns.[21][22] An expectant mother who is food insecure will likely be under financial stress and unable to secure enough food to meet her nutritional needs. Her geographical location may be in a food desert where she is unable to access enough safe and nutritious food. Food deserts are linked to food insecurity and defined as areas of high-density fast-food restaurants and corner stores offering only unhealthy highly processed foods at low prices.[23]

Poor prenatal diet

Poor prenatal diet or unhealthy diet has been shown to affect DNA methylation patterns and contribute to the development of type 2 diabetes, ADHD, and early onset conduct problems in children.[24][25]  Characteristics of an unhealthy prenatal diet leading to changes in DNA methylation patterns include the increased intake of high fat/sugar ultra-processed food products along with the inadequate intake of nutrient rich whole foods (e.g. fruits and vegetables). High-fat and low-protein diets during pregnancy can also increase the risk of obesity in infants.[26] Dietary methyl supplements such as extra folic acid and choline can also have adverse effects on epigenetic gene regulation.[1][8] The current global food system is plagued by issues that adversely affect human health through multiple pathways with contaminated, unsafe, and altered foods being one of the most common factors associated with unhealthy diet.[27]

Food quality

Food quality issues vary from one geographic region to the next depending on country, food safety practices, and manufacturing and agricultural regulations regarding heavy metal, pesticide residues, and other hazardous exposures of concern.[28] To reduce exposures to chemical hazards such as pesticide and heavy metal residues, the World Trade Organization (WTO) sponsored agreements between countries to establish codes of best practices, issued by the Codex Alimentarius Commission, that attempt to guarantee the trade of safe food.[28]  Despite the best practices in use, heavy metal and pesticide residues are still found in the food supply.[29][30]  Pre-natal and post-natal dietary exposures to inorganic mercury and lead residues resulting from unhealthy diets have been shown to consistently impact important gene behaviors in children with autism and ADHD.[13] Prenatal organophosphate pesticide exposure has been shown to impact DNA methylation in genes associated with the development of cardio-metabolic diseases.[31]

References

  1. 1 2 3 4 Landecker H (June 2011). "Food as exposure: Nutritional epigenetics and the new metabolism". BioSocieties. 6 (2): 167–194. doi:10.1057/biosoc.2011.1. PMC 3500842. PMID 23227106.
  2. ↑ Skjærven KH, Adam AC, Takaya S, Waagbø R, Espe M (January 2022). "Chapter 5 - Nutritional epigenetics". In Monzón IF, Fernandes JM (eds.). Cellular and Molecular Approaches in Fish Biology. Academic Press. pp. 161–192. doi:10.1016/B978-0-12-822273-7.00006-9. ISBN 978-0-12-822273-7. S2CID 245975506.
  3. 1 2 Farhud D, Zarif Yeganeh M, Zarif Yeganeh M (2010). "Nutrigenomics and nutrigenetics". Iranian Journal of Public Health. 39 (4): 1–14. PMC 3481686. PMID 23113033.
  4. 1 2 Roseboom TJ, Painter RC, van Abeelen AF, Veenendaal MV, de Rooij SR (October 2011). "Hungry in the womb: what are the consequences? Lessons from the Dutch famine". Maturitas. 70 (2): 141–145. doi:10.1016/j.maturitas.2011.06.017. PMID 21802226.
  5. 1 2 Franzek EJ, Sprangers N, Janssens AC, Van Duijn CM, Van De Wetering BJ (March 2008). "Prenatal exposure to the 1944-45 Dutch 'hunger winter' and addiction later in life". Addiction. 103 (3): 433–438. doi:10.1111/j.1360-0443.2007.02084.x. PMID 18190668.
  6. 1 2 Painter RC, Roseboom TJ, Bleker OP (2005). "Prenatal exposure to the Dutch famine and disease in later life: an overview". Reproductive Toxicology. 20 (3): 345–352. doi:10.1016/j.reprotox.2005.04.005. PMID 15893910.
  7. ↑ Blakeslee S (2003-10-07). "A Pregnant Mother's Diet May Turn the Genes Around". The New York Times. ISSN 0362-4331. Retrieved 2023-04-20.
  8. 1 2 3 4 Waterland RA, Jirtle RL (August 2003). "Transposable elements: targets for early nutritional effects on epigenetic gene regulation". Molecular and Cellular Biology. 23 (15): 5293–5300. doi:10.1128/MCB.23.15.5293-5300.2003. PMC 165709. PMID 12861015.
  9. ↑ Gardner A (2020-02-04). "Nutrigenomics 101: Understanding the Basics of DNA Diets". Gene Food. Retrieved 2023-04-20.
  10. ↑ Choi SW, Friso S (November 2010). "Epigenetics: A New Bridge between Nutrition and Health". Advances in Nutrition. Bethesda, Md. 1 (1): 8–16. doi:10.3945/an.110.1004. PMC 3042783. PMID 22043447.
  11. ↑ "Nutrition & the Epigenome". Genetic Science Learning Center. University of Utah Genetics. 15 July 2013. Retrieved 2023-04-20.
  12. ↑ Dufault RJ, Crider RA, Deth RC, Schnoll R, Gilbert SG, Lukiw WJ, Hitt AL (March 2023). "Higher rates of autism and attention deficit/hyperactivity disorder in American children: Are food quality issues impacting epigenetic inheritance?". World Journal of Clinical Pediatrics. 12 (2): 25–37. doi:10.5409/wjcp.v12.i2.25. PMC 10075020. PMID 37034430.
  13. 1 2 Dufault RJ, Wolle MM, Kingston HM, Gilbert SG, Murray JA (July 2021). "Connecting inorganic mercury and lead measurements in blood to dietary sources of exposure that may impact child development". World Journal of Methodology. 11 (4): 144–159. doi:10.5662/wjm.v11.i4.144. PMC 8299913. PMID 34322366.
  14. ↑ Greenwood M (2019-01-24). Surat P (ed.). "What is Nutritional Genomics (Nutrigenomics)?". News-Medical.net. Retrieved 2023-04-20.
  15. ↑ Açar Y, Akbulut G (November 2022). "Nutritional Epigenetics and Phytochemicals in Cancer Formation". Journal of the American Nutrition Association. 42 (7): 700–705. doi:10.1080/27697061.2022.2147106. PMID 36416668. S2CID 253800920.
  16. ↑ Ortega MA, Fraile-Martínez Ó, García-Montero C, Alvarez-Mon MA, Lahera G, Monserrat J, et al. (2022). "Nutrition, Epigenetics, and Major Depressive Disorder: Understanding the Connection". Frontiers in Nutrition. 9: 867150. doi:10.3389/fnut.2022.867150. PMC 9158469. PMID 35662945.
  17. ↑ Champagne, Frances A. (June 2008). "Epigenetic mechanisms and the transgenerational effects of maternal care". Frontiers in Neuroendocrinology. 29 (3): 386–397. doi:10.1016/j.yfrne.2008.03.003. ISSN 1095-6808. PMC 2682215. PMID 18462782.
  18. ↑ Goyal, Dipali; Limesand, Sean W.; Goyal, Ravi (2019-07-01). "Epigenetic responses and the developmental origins of health and disease". Journal of Endocrinology. 242 (1): T105–T119. doi:10.1530/JOE-19-0009. ISSN 0022-0795. PMID 31091503. S2CID 155101302.
  19. ↑ Tang, Wan-yee; Ho, Shuk-mei (2007-06-01). "Epigenetic reprogramming and imprinting in origins of disease". Reviews in Endocrine and Metabolic Disorders. 8 (2): 173–182. doi:10.1007/s11154-007-9042-4. ISSN 1573-2606. PMC 4056338. PMID 17638084.
  20. ↑ Dufault, Renee; Lukiw, Walter J.; Crider, Raquel; Schnoll, Roseanne; Wallinga, David; Deth, Richard (2012-04-10). "A macroepigenetic approach to identify factors responsible for the autism epidemic in the United States". Clinical Epigenetics. 4 (1): 6. doi:10.1186/1868-7083-4-6. ISSN 1868-7083. PMC 3378453. PMID 22490277.
  21. ↑ Carmichael, Suzan L.; Yang, Wei; Herring, Amy; Abrams, Barbara; Shaw, Gary M. (2007-09-01). "Maternal Food Insecurity Is Associated with Increased Risk of Certain Birth Defects1,2". The Journal of Nutrition. 137 (9): 2087–2092. doi:10.1093/jn/137.9.2087. ISSN 0022-3166. PMC 2063452. PMID 17709447.
  22. ↑ Liu, Huan-Yu; Liu, Song-Mei; Zhang, Yuan-Zhen (April 2020). "Maternal Folic Acid Supplementation Mediates Offspring Health via DNA Methylation". Reproductive Sciences (Thousand Oaks, Calif.). 27 (4): 963–976. doi:10.1007/s43032-020-00161-2. ISSN 1933-7205. PMID 32124397. S2CID 211729425.
  23. ↑ Di Renzo, Gian Carlo; Tosto, Valentina (December 2022). "Food insecurity, food deserts, reproduction and pregnancy: we should alert from now". The Journal of Maternal-Fetal & Neonatal Medicine. 35 (25): 9119–9121. doi:10.1080/14767058.2021.2016052. ISSN 1476-4954. PMID 34918992. S2CID 245262917.
  24. ↑ Rijlaarsdam, Jolien; Cecil, Charlotte A. M.; Walton, Esther; Mesirow, Maurissa S. C.; Relton, Caroline L.; Gaunt, Tom R.; McArdle, Wendy; Barker, Edward D. (January 2017). "Prenatal unhealthy diet, insulin-like growth factor 2 gene (IGF2) methylation, and attention deficit hyperactivity disorder symptoms in youth with early-onset conduct problems". Journal of Child Psychology and Psychiatry, and Allied Disciplines. 58 (1): 19–27. doi:10.1111/jcpp.12589. ISSN 1469-7610. PMC 5161647. PMID 27535767.
  25. ↑ Nilsson, Emma; Ling, Charlotte (2017). "DNA methylation links genetics, fetal environment, and an unhealthy lifestyle to the development of type 2 diabetes". Clinical Epigenetics. 9: 105. doi:10.1186/s13148-017-0399-2. ISSN 1868-7083. PMC 5627472. PMID 29026446.
  26. ↑ "What is Nutritional Genomics (Nutrigenomics)?". News-Medical.net. 2019-01-24. Retrieved 2023-05-13.
  27. ↑ Yambi, Olivia; Rocha, Cecilia; Jacobs, Nicholas; International Panel of Experts on Sustainable Food Systems (IPES-Food) (2020). "Unravelling the Food-Health Nexus to Build Healthier Food Systems". World Review of Nutrition and Dietetics. 121: 1–8. doi:10.1159/000507497. ISBN 978-3-318-06697-5. ISSN 1662-3975. PMID 33502367. S2CID 226421936.
  28. 1 2 Aruoma, Okezie I. (2006-04-03). "The impact of food regulation on the food supply chain". Toxicology. 221 (1): 119–127. doi:10.1016/j.tox.2005.12.024. ISSN 0300-483X. PMID 16483706.
  29. ↑ MD, Claire McCarthy (2021-03-05). "Heavy metals in baby food? What parents should know and do". Harvard Health. Retrieved 2023-05-13.
  30. ↑ "New Disclosures Show Dangerous Levels of Toxic Heavy Metals in Even More Baby Foods" (PDF). US House of Representatives. 2021-09-29. Retrieved 2023-05-12.
  31. ↑ Declerck, Ken; Remy, Sylvie; Wohlfahrt-Veje, Christine; Main, Katharina M.; Van Camp, Guy; Schoeters, Greet; Vanden Berghe, Wim; Andersen, Helle R. (2017). "Interaction between prenatal pesticide exposure and a common polymorphism in the PON1 gene on DNA methylation in genes associated with cardio metabolic disease risk-an exploratory study". Clinical Epigenetics. 9: 35. doi:10.1186/s13148-017-0336-4. ISSN 1868-7083. PMC 5382380. PMID 28396702.
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