Wikipedia

Nutritional epigenetics

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

edit

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][7][8] 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.[9][10]

Research

edit

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.[10][11][12] Nutrients and bioactive food components affect epigenetics by inhibiting enzymatic activity related to DNA methylation and histone modifications.[13] 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.[14] 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]

DNA methylation is the addition of a methyl group on a cytosine ring of DNA.[15] Without methylation, issues could arise regarding genomic imprinting, X-chromosome inactivation, and suppression of transcription and transposition.[15] When methylation is not present to suppress transcription and transposition, the lack thereof can contribute to the development of cancer.

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][10]

Folate is an essential water soluble vitamin that is naturally occurring in some foods. Folate can be found naturally at high levels in dark green leafy vegetables such as spinach, brussels sprouts and asparagus, as well as in liver.[16] Folic acid is a man made form used to supplement certain foods. Enriched breads, flours, pastas, rice, and breakfast cereals are commonly supplemented with folic acid.[17] In DNA methylation, folate serves as a source of carbon/ methyl group.[18]

Choline is a semi-essential nutrient that can be oxidized to betaine. The betaine then functions as a methyl group donor in the process of DNA methylation.[19] Choline can be found in animal products such as meat, eggs, poultry, fish and dairy as well as potatoes and green leafy vegetables.[20]

Researchers have considered that high-fat and low-protein diets during pregnancy can increase the risk of obesity in infants.[21] The consumption of phytochemicals can also positively affect epigenetic-based mechanisms that inhibit cancer cells.[22] Research has also suggested a link between nutritional epigenetics and the pathophysiology of major depressive disorder.[23]

Nutritional-environmental signals

edit

All life on Earth is influenced by the different flows of its environment, yet in humans, different environmental conditions such as poverty, alcohol, stress, malnutrition, exposure to pollutants, man-made chemicals, and synthetic drugs can lead to epigenetic-related illnesses/diseases with certain disease-specific genes typically being activated or deactivated.[12]  The epigenome of an organism can be triggered by just about any environmental signal, including climate change, food/water supply, plant nutrient, temperature etc.

It has been estimated that more than 60% of deaths in humans are related to nutritional or dietary factors rather than environmental triggers.[12][8] Based on a couple of studies from the Dutch Famine of 1944-1945, it is stated that starvation during pregnancy and subsequent health can result in, but not limited to a some health risks including type II diabetes mellitus, cardiovascular disease, metabolic disorders and decreased cognitive functions later in life.[7]

The maternal lineage or mother's health and nutritional habits during pregnancy isn't the only influence on the offspring's overall health. Further transmission via the paternal line is highly likely to occur by epigenetic modulation of the spermatozoa's nucleus.[7] An example of this is transgenerational transmission by the paternal lineage. There is evidence that both the paternal and maternal diets influence metabolic phenotypes in the offspring through epigenetic information transmission.[7][12]

Epigenetic stressors

edit

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.[24] 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.[25][26] 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).[27]

Food insecurity

edit

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.[28][8] 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.[29]

Poor prenatal diet

edit

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.[30][31]  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.[32] Dietary methyl supplements such as extra folic acid and choline can also have adverse effects on epigenetic gene regulation.[1][10] 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.[33] Low iron diets, or women who suffer from an iron deficiency, have been shown to increase the likelihood of a premature birth, low birth weight, and the increased possibility of postpartum depression.[34]

Food quality

edit

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.[35] 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.[35]  Despite the best practices in use, heavy metal and pesticide residues are still found in the food supply.[36][37]  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.[38] Prenatal organophosphate pesticide exposure has been shown to impact DNA methylation in genes associated with the development of cardio-metabolic diseases.[39] Infection from food is a serious factor during pregnancy. Not in particular of what the mother eats, but that is just as important, but the way the food is prepared. A mother should cook all of the food thoroughly, especially meats. All of the produce should be washed well after washing hands. Pasteurized dairy products should be the type of dairy being consumed by the mother.[40]

References

edit
  1. ^ a b c d 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. ^ a b 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. ^ a b 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. ^ a b 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. ^ a b 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. ^ a b c d Tiffon C (2018-11-01). "The Impact of Nutrition and Environmental Epigenetics on Human Health and Disease". International Journal of Molecular Sciences. 19 (11): 3425. doi:10.3390/ijms19113425. ISSN 1422-0067. PMC 6275017. PMID 30388784.
  8. ^ a b c Liu HY, Liu SM, Zhang YZ (April 2020). "Maternal Folic Acid Supplementation Mediates Offspring Health via DNA Methylation". Reproductive Sciences. 27 (4): 963–976. doi:10.1007/s43032-020-00161-2. PMID 32124397. S2CID 211729425.
  9. ^ 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.
  10. ^ a b c d 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.
  11. ^ Gardner A (2020-02-04). "Nutrigenomics 101: Understanding the Basics of DNA Diets". Gene Food. Retrieved 2023-04-20.
  12. ^ a b c d Mazzio EA, Soliman KF (July 2014). "Epigenetics and nutritional environmental signals". Integrative and Comparative Biology. 54 (1): 21–30. doi:10.1093/icb/icu049. PMC 4072902. PMID 24861811.
  13. ^ Choi SW, Friso S (November 2010). "Epigenetics: A New Bridge between Nutrition and Health". Advances in Nutrition. 1 (1): 8–16. doi:10.3945/an.110.1004. PMC 3042783. PMID 22043447.
  14. ^ "Nutrition & the Epigenome". Genetic Science Learning Center. University of Utah Genetics. 15 July 2013. Retrieved 2023-04-20.
  15. ^ a b Jin B, Li Y, Robertson K (June 2011). "DNA Methylation". Genes & Cancer. 2 (6): 607–617. doi:10.1177/1947601910393957. PMC 3174260. PMID 21941617. Retrieved 7 April 2024.
  16. ^ "Office of Dietary Supplements - Folate". ods.od.nih.gov. Retrieved 2024-04-07.
  17. ^ Nutrition Cf (March 25, 2024). "Folate and Folic Acid on the Nutrition and Supplement Facts Labels". FDA.
  18. ^ Crider K, Yang T, Berry R, Bailey L (5 Jan 2012). "Folate and DNA Methylation: A Review of Molecular Mechanisms and the Evidence for Folate's Role". Advances in Nutrition. 3 (1): 21–38. doi:10.3945/an.111.000992. PMC 3262611. PMID 22332098.
  19. ^ Korsmo HW, Dave B, Trasino S, Saxena A, Liu J, Caviglia JM, et al. (2022). "Maternal Choline Supplementation and High-Fat Feeding Interact to Influence DNA Methylation in Offspring in a Time-Specific Manner". Frontiers in Nutrition. 9. doi:10.3389/fnut.2022.841787. ISSN 2296-861X. PMC 8837519. PMID 35165655.
  20. ^ "Office of Dietary Supplements - Choline". ods.od.nih.gov. Retrieved 2024-04-12.
  21. ^ Greenwood M (2019-01-24). Surat P (ed.). "What is Nutritional Genomics (Nutrigenomics)?". News-Medical.net. Retrieved 2023-04-20.
  22. ^ 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.
  23. ^ 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.
  24. ^ Champagne FA (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. PMC 2682215. PMID 18462782.
  25. ^ Goyal D, Limesand SW, Goyal R (July 2019). "Epigenetic responses and the developmental origins of health and disease". The Journal of Endocrinology. 242 (1): T105–T119. doi:10.1530/JOE-19-0009. PMID 31091503. S2CID 155101302.
  26. ^ Tang WY, Ho SM (June 2007). "Epigenetic reprogramming and imprinting in origins of disease". Reviews in Endocrine & Metabolic Disorders. 8 (2): 173–182. doi:10.1007/s11154-007-9042-4. PMC 4056338. PMID 17638084.
  27. ^ Dufault R, Lukiw WJ, Crider R, Schnoll R, Wallinga D, Deth R (April 2012). "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. PMC 3378453. PMID 22490277.
  28. ^ Carmichael SL, Yang W, Herring A, Abrams B, Shaw GM (September 2007). "Maternal food insecurity is associated with increased risk of certain birth defects". The Journal of Nutrition. 137 (9): 2087–2092. doi:10.1093/jn/137.9.2087. PMC 2063452. PMID 17709447.
  29. ^ Di Renzo GC, Tosto V (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. PMID 34918992. S2CID 245262917.
  30. ^ Rijlaarsdam J, Cecil CA, Walton E, Mesirow MS, Relton CL, Gaunt TR, et al. (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. PMC 5161647. PMID 27535767.
  31. ^ Nilsson E, Ling C (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. PMC 5627472. PMID 29026446.
  32. ^ "What is Nutritional Genomics (Nutrigenomics)?". News-Medical.net. 2019-01-24. Retrieved 2023-05-13.
  33. ^ Yambi O, Rocha C, Jacobs N (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. PMID 33502367. S2CID 226421936.
  34. ^ "Prevent iron deficiency anemia during pregnancy". Mayo Clinic.
  35. ^ a b Aruoma OI (April 2006). "The impact of food regulation on the food supply chain". Toxicology. 221 (1): 119–127. doi:10.1016/j.tox.2005.12.024. PMID 16483706.
  36. ^ McCarthy C (2021-03-05). "Heavy metals in baby food? What parents should know and do". Harvard Health. Retrieved 2023-05-13.
  37. ^ "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.
  38. ^ 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.
  39. ^ Declerck K, Remy S, Wohlfahrt-Veje C, Main KM, Van Camp G, Schoeters G, et al. (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. PMC 5382380. PMID 28396702.
  40. ^ "What are the most common pregnancy complications?". 7 February 2022.
Retrieved from "https://en.wikipedia.org/w/index.php?title=Nutritional_epigenetics&oldid=1251436297"