Biology:Nutritional epigenetics

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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. ↑ 1.0 1.1 1.2 1.3 "Food as exposure: Nutritional epigenetics and the new metabolism". BioSocieties 6 (2): 167–194. June 2011. doi:10.1057/biosoc.2011.1. PMID 23227106. 
  2. ↑ "Chapter 5 - Nutritional epigenetics" (in en). Cellular and Molecular Approaches in Fish Biology. Academic Press. January 2022. pp. 161–192. doi:10.1016/B978-0-12-822273-7.00006-9. ISBN 978-0-12-822273-7. 
  3. ↑ 3.0 3.1 "Nutrigenomics and nutrigenetics". Iranian Journal of Public Health 39 (4): 1–14. 2010. PMID 23113033. 
  4. ↑ 4.0 4.1 "Hungry in the womb: what are the consequences? Lessons from the Dutch famine". Maturitas 70 (2): 141–145. October 2011. doi:10.1016/j.maturitas.2011.06.017. PMID 21802226. 
  5. ↑ 5.0 5.1 "Prenatal exposure to the 1944-45 Dutch 'hunger winter' and addiction later in life". Addiction 103 (3): 433–438. March 2008. doi:10.1111/j.1360-0443.2007.02084.x. PMID 18190668. 
  6. ↑ 6.0 6.1 "Prenatal exposure to the Dutch famine and disease in later life: an overview". Reproductive Toxicology 20 (3): 345–352. 2005. doi:10.1016/j.reprotox.2005.04.005. PMID 15893910. 
  7. ↑ "A Pregnant Mother's Diet May Turn the Genes Around" (in en-US). The New York Times. 2003-10-07. ISSN 0362-4331. https://www.nytimes.com/2003/10/07/science/a-pregnant-mother-s-diet-may-turn-the-genes-around.html. 
  8. ↑ 8.0 8.1 8.2 8.3 "Transposable elements: targets for early nutritional effects on epigenetic gene regulation". Molecular and Cellular Biology 23 (15): 5293–5300. August 2003. doi:10.1128/MCB.23.15.5293-5300.2003. PMID 12861015. 
  9. ↑ "Nutrigenomics 101: Understanding the Basics of DNA Diets" (in en-US). 2020-02-04. https://www.mygenefood.com/blog/what-is-nutrigenomics/. 
  10. ↑ "Epigenetics: A New Bridge between Nutrition and Health". Advances in Nutrition (Bethesda, Md.) 1 (1): 8–16. November 2010. doi:10.3945/an.110.1004. PMID 22043447. 
  11. ↑ "Nutrition & the Epigenome". Genetic Science Learning Center. University of Utah Genetics. 15 July 2013. https://learn.genetics.utah.edu/content/epigenetics/nutrition. 
  12. ↑ "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. March 2023. doi:10.5409/wjcp.v12.i2.25. PMID 37034430. 
  13. ↑ 13.0 13.1 "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. July 2021. doi:10.5662/wjm.v11.i4.144. PMID 34322366. 
  14. ↑ "What is Nutritional Genomics (Nutrigenomics)?" (in en). 2019-01-24. https://www.news-medical.net/life-sciences/What-is-Nutritional-Genomics.aspx. 
  15. ↑ "Nutritional Epigenetics and Phytochemicals in Cancer Formation". Journal of the American Nutrition Association 42 (7): 700–705. November 2022. doi:10.1080/27697061.2022.2147106. PMID 36416668. 
  16. ↑ "Nutrition, Epigenetics, and Major Depressive Disorder: Understanding the Connection". Frontiers in Nutrition 9: 867150. 2022. doi:10.3389/fnut.2022.867150. 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. PMID 18462782. 
  18. ↑ Goyal, Dipali; Limesand, Sean W.; Goyal, Ravi (2019-07-01). "Epigenetic responses and the developmental origins of health and disease" (in en-US). Journal of Endocrinology 242 (1): T105–T119. doi:10.1530/JOE-19-0009. ISSN 0022-0795. PMID 31091503. https://joe.bioscientifica.com/view/journals/joe/242/1/JOE-19-0009.xml. 
  19. ↑ Tang, Wan-yee; Ho, Shuk-mei (2007-06-01). "Epigenetic reprogramming and imprinting in origins of disease" (in en). Reviews in Endocrine and Metabolic Disorders 8 (2): 173–182. doi:10.1007/s11154-007-9042-4. ISSN 1573-2606. PMID 17638084. PMC 4056338. https://doi.org/10.1007/s11154-007-9042-4. 
  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. 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" (in en). The Journal of Nutrition 137 (9): 2087–2092. doi:10.1093/jn/137.9.2087. ISSN 0022-3166. PMID 17709447. PMC 2063452. https://www.sciencedirect.com/science/article/pii/S0022316622093658. 
  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. https://pubmed.ncbi.nlm.nih.gov/32124397/. 
  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. 
  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. 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. PMID 29026446. 
  26. ↑ "What is Nutritional Genomics (Nutrigenomics)?" (in en). 2019-01-24. https://www.news-medical.net/life-sciences/What-is-Nutritional-Genomics.aspx. 
  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. https://pubmed.ncbi.nlm.nih.gov/33502367/. 
  28. ↑ 28.0 28.1 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. https://pubmed.ncbi.nlm.nih.gov/16483706/. 
  29. ↑ MD, Claire McCarthy (2021-03-05). "Heavy metals in baby food? What parents should know and do" (in en). https://www.health.harvard.edu/blog/heavy-metals-in-baby-food-what-parents-should-know-and-do-2021030522088. 
  30. ↑ "New Disclosures Show Dangerous Levels of Toxic Heavy Metals in Even More Baby Foods". 2021-09-29. https://oversightdemocrats.house.gov/sites/democrats.oversight.house.gov/files/ECP%20Second%20Baby%20Food%20Report%209.29.21%20FINAL.pdf. 
  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. PMID 28396702. 



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