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{{Fringe theories|date=August 2024}}

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'''Nutritional epigenetics''' is a science that studies the effects of nutrition on gene expression and [[chromatin]] accessibility.<ref name="Landecker_2011">{{cite journal | vauthors = Landecker H | title = Food as exposure: Nutritional epigenetics and the new metabolism | journal = BioSocieties | volume = 6 | issue = 2 | pages = 167–194 | date = June 2011 | pmid = 23227106 | pmc = 3500842 | doi = 10.1057/biosoc.2011.1 }}</ref><ref>{{cite book | vauthors = Skjærven KH, Adam AC, Takaya S, Waagbø R, Espe M | chapter =Chapter 5 - Nutritional epigenetics |date= January 2022 | title = Cellular and Molecular Approaches in Fish Biology |pages=161–192 | veditors = Monzón IF, Fernandes JM |publisher=Academic Press |language=en |isbn=978-0-12-822273-7 | doi = 10.1016/B978-0-12-822273-7.00006-9 | s2cid =245975506 }}</ref> It is a subcategory of [[nutritional genomics]] that focuses on the effects of [[Bioactive compound|bioactive]] food components on [[Epigenetics|epigenetic]] events.<ref name="Farhud_2010">{{cite journal | vauthors = Farhud D, Zarif Yeganeh M, Zarif Yeganeh M | title = Nutrigenomics and nutrigenetics | journal = Iranian Journal of Public Health | volume = 39 | issue = 4 | pages = 1–14 | date = 2010 | pmid = 23113033 | pmc = 3481686 }}</ref>
'''Nutritional epigenetics''' is a science that studies the effects of nutrition on gene expression and [[chromatin]] accessibility.<ref name="Landecker_2011">{{cite journal | vauthors = Landecker H | title = Food as exposure: Nutritional epigenetics and the new metabolism | journal = BioSocieties | volume = 6 | issue = 2 | pages = 167–194 | date = June 2011 | pmid = 23227106 | pmc = 3500842 | doi = 10.1057/biosoc.2011.1 }}</ref><ref>{{cite book | vauthors = Skjærven KH, Adam AC, Takaya S, Waagbø R, Espe M | chapter =Chapter 5 - Nutritional epigenetics |date= January 2022 | title = Cellular and Molecular Approaches in Fish Biology |pages=161–192 | veditors = Monzón IF, Fernandes JM |publisher=Academic Press |language=en |isbn=978-0-12-822273-7 | doi = 10.1016/B978-0-12-822273-7.00006-9 | s2cid =245975506 }}</ref> It is a subcategory of [[nutritional genomics]] that focuses on the effects of [[Bioactive compound|bioactive]] food components on [[Epigenetics|epigenetic]] events.<ref name="Farhud_2010">{{cite journal | vauthors = Farhud D, Zarif Yeganeh M, Zarif Yeganeh M | title = Nutrigenomics and nutrigenetics | journal = Iranian Journal of Public Health | volume = 39 | issue = 4 | pages = 1–14 | date = 2010 | pmid = 23113033 | pmc = 3481686 }}</ref>


== History ==
== History ==
Changes to children’s genetic profiles caused by fetal nutrition have been observed as early as the [[Dutch famine of 1944–1945|Dutch famine of 1944-1945]].<ref name="Roseboom_2011">{{cite journal | vauthors = Roseboom TJ, Painter RC, van Abeelen AF, Veenendaal MV, de Rooij SR | title = Hungry in the womb: what are the consequences? Lessons from the Dutch famine | journal = Maturitas | volume = 70 | issue = 2 | pages = 141–145 | date = October 2011 | pmid = 21802226 | doi = 10.1016/j.maturitas.2011.06.017 }}</ref><ref name="Franzek_2008">{{cite journal | vauthors = Franzek EJ, Sprangers N, Janssens AC, Van Duijn CM, Van De Wetering BJ | title = Prenatal exposure to the 1944-45 Dutch 'hunger winter' and addiction later in life | journal = Addiction | volume = 103 | issue = 3 | pages = 433–438 | date = March 2008 | pmid = 18190668 | doi = 10.1111/j.1360-0443.2007.02084.x }}</ref><ref name="Painter_2005">{{cite journal | vauthors = Painter RC, Roseboom TJ, Bleker OP | title = Prenatal exposure to the Dutch famine and disease in later life: an overview | journal = Reproductive Toxicology | volume = 20 | issue = 3 | pages = 345–352 | date = 2005 | pmid = 15893910 | doi = 10.1016/j.reprotox.2005.04.005 }}</ref> 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.<ref name="Roseboom_2011" /><ref name="Franzek_2008" /><ref name="Painter_2005" />
Changes to children’s genetic profiles caused by fetal nutrition have been observed as early as the [[Dutch famine of 1944–1945|Dutch famine of 1944-1945]].<ref name="Roseboom_2011">{{cite journal | vauthors = Roseboom TJ, Painter RC, van Abeelen AF, Veenendaal MV, de Rooij SR | title = Hungry in the womb: what are the consequences? Lessons from the Dutch famine | journal = Maturitas | volume = 70 | issue = 2 | pages = 141–145 | date = October 2011 | pmid = 21802226 | doi = 10.1016/j.maturitas.2011.06.017 }}</ref><ref name="Franzek_2008">{{cite journal | vauthors = Franzek EJ, Sprangers N, Janssens AC, Van Duijn CM, Van De Wetering BJ | title = Prenatal exposure to the 1944-45 Dutch 'hunger winter' and addiction later in life | journal = Addiction | volume = 103 | issue = 3 | pages = 433–438 | date = March 2008 | pmid = 18190668 | doi = 10.1111/j.1360-0443.2007.02084.x }}</ref><ref name="Painter_2005">{{cite journal | vauthors = Painter RC, Roseboom TJ, Bleker OP | title = Prenatal exposure to the Dutch famine and disease in later life: an overview | journal = Reproductive Toxicology | volume = 20 | issue = 3 | pages = 345–352 | date = 2005 | pmid = 15893910 | doi = 10.1016/j.reprotox.2005.04.005 }}</ref><ref name=":1">{{Cite journal |last=Tiffon |first=Céline |date=2018-11-01 |title=The Impact of Nutrition and Environmental Epigenetics on Human Health and Disease |journal=International Journal of Molecular Sciences |language=en |volume=19 |issue=11 |pages=3425 |doi=10.3390/ijms19113425 |doi-access=free |issn=1422-0067 |pmc=6275017 |pmid=30388784}}</ref><ref name="Liu_2020" /> 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.<ref name="Roseboom_2011" /><ref name="Franzek_2008" /><ref name="Painter_2005" />


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.<ref>{{Cite news | vauthors = Blakeslee S |date=2003-10-07 |title=A Pregnant Mother's Diet May Turn the Genes Around |language=en-US |work=The New York Times |url=https://www.nytimes.com/2003/10/07/science/a-pregnant-mother-s-diet-may-turn-the-genes-around.html |access-date=2023-04-20 |issn=0362-4331}}</ref><ref name="Waterland_2003">{{cite journal | vauthors = Waterland RA, Jirtle RL | title = Transposable elements: targets for early nutritional effects on epigenetic gene regulation | journal = Molecular and Cellular Biology | volume = 23 | issue = 15 | pages = 5293–5300 | date = August 2003 | pmid = 12861015 | pmc = 165709 | doi = 10.1128/MCB.23.15.5293-5300.2003 }}</ref>
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.<ref>{{Cite news | vauthors = Blakeslee S |date=2003-10-07 |title=A Pregnant Mother's Diet May Turn the Genes Around |language=en-US |work=The New York Times |url=https://www.nytimes.com/2003/10/07/science/a-pregnant-mother-s-diet-may-turn-the-genes-around.html |access-date=2023-04-20 |issn=0362-4331}}</ref><ref name="Waterland_2003">{{cite journal | vauthors = Waterland RA, Jirtle RL | title = Transposable elements: targets for early nutritional effects on epigenetic gene regulation | journal = Molecular and Cellular Biology | volume = 23 | issue = 15 | pages = 5293–5300 | date = August 2003 | pmid = 12861015 | pmc = 165709 | doi = 10.1128/MCB.23.15.5293-5300.2003 }}</ref>


== Research ==
== Research ==
Researchers in nutritional epigenetics study the interaction between [[molecule]]s in food and molecules that control [[gene expression]], which leads to areas of focus such as dietary methyl groups and [[DNA methylation]].<ref name="Waterland_2003" /><ref>{{Cite web | vauthors = Gardner A |date=2020-02-04 |title=Nutrigenomics 101: Understanding the Basics of DNA Diets |url=https://www.mygenefood.com/blog/what-is-nutrigenomics/ |access-date=2023-04-20 |website=Gene Food |language=en-US}}</ref> Nutrients and [[Bioactive compound|bioactive]] food components affect epigenetics by inhibiting [[Enzyme|enzymatic]] activity related to DNA methylation and [[histone]] modifications.<ref name="pmid22043447">{{cite journal | vauthors = Choi SW, Friso S | title = Epigenetics: A New Bridge between Nutrition and Health | journal = Advances in Nutrition | volume = 1 | issue = 1 | pages = 8–16 | date = November 2010 | pmid = 22043447 | pmc = 3042783 | doi = 10.3945/an.110.1004 }}</ref> 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.<ref>{{Cite web |title=Nutrition & the Epigenome |url=https://learn.genetics.utah.edu/content/epigenetics/nutrition |access-date=2023-04-20 | work = Genetic Science Learning Center | date = 15 July 2013 | publisher = University of Utah Genetics }}</ref> 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.<sup><ref name="Landecker_2011" /></sup>
Researchers in nutritional epigenetics study the interaction between [[molecule]]s in food and molecules that control [[gene expression]], which leads to areas of focus such as dietary methyl groups and [[DNA methylation]].<ref name="Waterland_2003" /><ref>{{Cite web | vauthors = Gardner A |date=2020-02-04 |title=Nutrigenomics 101: Understanding the Basics of DNA Diets |url=https://www.mygenefood.com/blog/what-is-nutrigenomics/ |access-date=2023-04-20 |website=Gene Food |language=en-US}}</ref><ref name="Mazzio_2014" /> Nutrients and [[Bioactive compound|bioactive]] food components affect epigenetics by inhibiting [[Enzyme|enzymatic]] activity related to DNA methylation and [[histone]] modifications.<ref name="pmid22043447">{{cite journal | vauthors = Choi SW, Friso S | title = Epigenetics: A New Bridge between Nutrition and Health | journal = Advances in Nutrition | volume = 1 | issue = 1 | pages = 8–16 | date = November 2010 | pmid = 22043447 | pmc = 3042783 | doi = 10.3945/an.110.1004 }}</ref> 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.<ref>{{Cite web |title=Nutrition & the Epigenome |url=https://learn.genetics.utah.edu/content/epigenetics/nutrition |access-date=2023-04-20 | work = Genetic Science Learning Center | date = 15 July 2013 | publisher = University of Utah Genetics }}</ref> 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.<sup><ref name="Landecker_2011" /></sup>

DNA methylation is the addition of a methyl group on a cytosine ring of DNA.<ref name=":2">{{Cite journal |last1=Jin |first1=Bilian |last2=Li |first2=Yajun |last3=Robertson |first3=Keith |date=June 2011 |title=DNA Methylation |url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3174260/#:~:text=DNA%20methylation%20is%20a%20heritable,T%2C%20or%20C)%20contexts. |access-date=7 April 2024 |journal=Genes & Cancer|volume=2 |issue=6 |pages=607–617 |doi=10.1177/1947601910393957 |pmid=21941617 |pmc=3174260 }}</ref> Without methylation, issues could arise regarding genomic imprinting, X-chromosome inactivation, and suppression of transcription and transposition.<ref name=":2" /> When methylation is not present to suppress transcription and transposition, the lack thereof can contribute to the development of [[cancer]].


[[Bioactive compound|Bioactive]] food components that influence epigenetic processes range from vitamins such as [[Vitamin A|A]], [[Vitamin b6|B6]], and [[Vitamin B12|B12]] to alcohol and elements such as [[arsenic]], [[cadmium]], and [[selenium]].<ref name="Farhud_2010" /> Dietary methyl supplements such as extra [[folic acid]] and [[choline]] can also have adverse effects on epigenetic gene regulation.<ref name="Landecker_2011" /><ref name="Waterland_2003" />
[[Bioactive compound|Bioactive]] food components that influence epigenetic processes range from vitamins such as [[Vitamin A|A]], [[Vitamin b6|B6]], and [[Vitamin B12|B12]] to alcohol and elements such as [[arsenic]], [[cadmium]], and [[selenium]].<ref name="Farhud_2010" /> Dietary methyl supplements such as extra [[folic acid]] and [[choline]] can also have adverse effects on epigenetic gene regulation.<ref name="Landecker_2011" /><ref name="Waterland_2003" />


[[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.<ref>{{Cite web |title=Office of Dietary Supplements - Folate |url=https://ods.od.nih.gov/factsheets/Folate-HealthProfessional/ |access-date=2024-04-07 |website=ods.od.nih.gov |language=en}}</ref> 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.<ref>{{Cite journal |last=Nutrition |first=Center for Food Safety and Applied |date=March 25, 2024 |title=Folate and Folic Acid on the Nutrition and Supplement Facts Labels |url=https://www.fda.gov/food/nutrition-facts-label/folate-and-folic-acid-nutrition-and-supplement-facts-labels |journal=FDA |language=en}}</ref> In DNA methylation, folate serves as a source of carbon/ methyl group.<ref name=":12">{{Cite journal |last1=Crider |first1=Krista |last2=Yang |first2=Thomas |last3=Berry |first3=Robert |last4=Bailey |first4=Lynn |date=5 Jan 2012 |title=Folate and DNA Methylation: A Review of Molecular Mechanisms and the Evidence for Folate's Role |journal=Advances in Nutrition |volume=3 |issue=1 |pages=21–38 |doi=10.3945/an.111.000992 |pmid=22332098 |pmc=3262611 }}</ref>
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Researchers have considered dietary exposure to heavy metals such as [[Mercury (element)|mercury]] and [[lead]] primary epigenetic factors leading to increased [[Autism spectrum|autism]] and [[attention deficit hyperactivity disorder]].<ref>{{cite journal | vauthors = Dufault RJ, Crider RA, Deth RC, Schnoll R, Gilbert SG, Lukiw WJ, Hitt AL | title = Higher rates of autism and attention deficit/hyperactivity disorder in American children: Are food quality issues impacting epigenetic inheritance? | journal = World Journal of Clinical Pediatrics | volume = 12 | issue = 2 | pages = 25–37 | date = March 2023 | pmid = 37034430 | pmc = 10075020 | doi = 10.5409/wjcp.v12.i2.25 | doi-access = free }}</ref><ref name="Dufault_2021">{{cite journal | vauthors = Dufault RJ, Wolle MM, Kingston HM, Gilbert SG, Murray JA | title = Connecting inorganic mercury and lead measurements in blood to dietary sources of exposure that may impact child development | journal = World Journal of Methodology | volume = 11 | issue = 4 | pages = 144–159 | date = July 2021 | pmid = 34322366 | pmc = 8299913 | doi = 10.5662/wjm.v11.i4.144 | doi-access = free }}</ref> High-fat and low-protein diets during pregnancy can also increase the risk of obesity in infants.<ref>{{Cite web | vauthors = Greenwood M | veditors = Surat P |date=2019-01-24 |title=What is Nutritional Genomics (Nutrigenomics)? |url=https://www.news-medical.net/life-sciences/What-is-Nutritional-Genomics.aspx |access-date=2023-04-20 |website=News-Medical.net |language=en}}</ref> The consumption of [[phytochemical]]s can also positively affect epigenetic-based mechanisms that inhibit [[cancer cell]]s.<ref>{{cite journal | vauthors = Açar Y, Akbulut G | title = Nutritional Epigenetics and Phytochemicals in Cancer Formation | journal = Journal of the American Nutrition Association | volume = 42 | issue = 7 | pages = 700–705 | date = November 2022 | pmid = 36416668 | doi = 10.1080/27697061.2022.2147106 | s2cid = 253800920 }}</ref> Research has also suggested a link between nutritional epigenetics and the [[pathophysiology]] of major [[depressive disorder]].<ref>{{cite journal | vauthors = Ortega MA, Fraile-Martínez Ó, García-Montero C, Alvarez-Mon MA, Lahera G, Monserrat J, Llavero-Valero M, Mora F, Rodríguez-Jiménez R, Fernandez-Rojo S, Quintero J, Alvarez De Mon M | title = Nutrition, Epigenetics, and Major Depressive Disorder: Understanding the Connection | journal = Frontiers in Nutrition | volume = 9 | pages = 867150 | date = 2022 | pmid = 35662945 | pmc = 9158469 | doi = 10.3389/fnut.2022.867150 | doi-access = free }}</ref>


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.<ref>{{Cite journal |last1=Korsmo |first1=Hunter W. |last2=Dave |first2=Bhoomi |last3=Trasino |first3=Steven |last4=Saxena |first4=Anjana |last5=Liu |first5=Jia |last6=Caviglia |first6=Jorge Matias |last7=Edwards |first7=Kaydine |last8=Dembitzer |first8=Moshe |last9=Sheeraz |first9=Shameera |last10=Khaldi |first10=Sarah |last11=Jiang |first11=Xinyin |date=2022 |title=Maternal Choline Supplementation and High-Fat Feeding Interact to Influence DNA Methylation in Offspring in a Time-Specific Manner |journal=Frontiers in Nutrition |volume=9 |doi=10.3389/fnut.2022.841787 |doi-access=free |pmid=35165655 |issn=2296-861X|pmc=8837519 }}</ref> Choline can be found in animal products such as meat, eggs, poultry, fish and dairy as well as potatoes and green leafy vegetables.<ref>{{Cite web |title=Office of Dietary Supplements - Choline |url=https://ods.od.nih.gov/factsheets/Choline-Consumer/ |access-date=2024-04-12 |website=ods.od.nih.gov |language=en}}</ref>
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== Nutritional-Environmental Signals ==
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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.<ref name="Mazzio_2014">{{cite journal | vauthors = Mazzio EA, Soliman KF | title = Epigenetics and nutritional environmental signals | journal = Integrative and Comparative Biology | volume = 54 | issue = 1 | pages = 21–30 | date = July 2014 | pmid = 24861811 | pmc = 4072902 | doi = 10.1093/icb/icu049 }}</ref>  The [[epigenome]] of an organism can be triggered by just about any environmental signal, including climate change, food/water supply, plant nutrient, temperature and etc.


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Researchers have considered that high-fat and low-protein diets during pregnancy can increase the risk of obesity in infants.<ref>{{Cite web | vauthors = Greenwood M | veditors = Surat P |date=2019-01-24 |title=What is Nutritional Genomics (Nutrigenomics)? |url=https://www.news-medical.net/life-sciences/What-is-Nutritional-Genomics.aspx |access-date=2023-04-20 |website=News-Medical.net |language=en}}</ref> The consumption of [[phytochemical]]s can also positively affect epigenetic-based mechanisms that inhibit [[cancer cell]]s.<ref>{{cite journal | vauthors = Açar Y, Akbulut G | title = Nutritional Epigenetics and Phytochemicals in Cancer Formation | journal = Journal of the American Nutrition Association | volume = 42 | issue = 7 | pages = 700–705 | date = November 2022 | pmid = 36416668 | doi = 10.1080/27697061.2022.2147106 | s2cid = 253800920 }}</ref> Research has also suggested a link between nutritional epigenetics and the [[pathophysiology]] of major [[depressive disorder]].<ref>{{cite journal | vauthors = Ortega MA, Fraile-Martínez Ó, García-Montero C, Alvarez-Mon MA, Lahera G, Monserrat J, Llavero-Valero M, Mora F, Rodríguez-Jiménez R, Fernandez-Rojo S, Quintero J, Alvarez De Mon M | title = Nutrition, Epigenetics, and Major Depressive Disorder: Understanding the Connection | journal = Frontiers in Nutrition | volume = 9 | pages = 867150 | date = 2022 | pmid = 35662945 | pmc = 9158469 | doi = 10.3389/fnut.2022.867150 | doi-access = free }}</ref>
It has been estimated that more than 60% of deaths in humans are related to nutritional or dietary factors rather than environmental triggers.<ref name="Mazzio_2014" /><ref name="Liu_2020" />


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== Nutritional-environmental signals ==
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=== Epigenetic Stressors ===
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All life on Earth is influenced by the different flows of its environment, yet in humans, different environmental conditions such as [[poverty]], [[Alcoholism|alcohol]], [[Stress (biology)|stress]], malnutrition, exposure to [[Pollutant|pollutants]], man-made chemicals, and [[Synthetic drug|synthetic drugs]] can lead to epigenetic-related illnesses/diseases with certain disease-specific genes typically being activated or deactivated.<ref name="Mazzio_2014">{{cite journal | vauthors = Mazzio EA, Soliman KF | title = Epigenetics and nutritional environmental signals | journal = Integrative and Comparative Biology | volume = 54 | issue = 1 | pages = 21–30 | date = July 2014 | pmid = 24861811 | pmc = 4072902 | doi = 10.1093/icb/icu049 }}</ref>  The [[epigenome]] of an organism can be triggered by just about any environmental signal, including [[climate change]], food/water supply, plant nutrient, temperature etc.
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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.<ref>{{cite journal | vauthors = Champagne FA | title = Epigenetic mechanisms and the transgenerational effects of maternal care | journal = Frontiers in Neuroendocrinology | volume = 29 | issue = 3 | pages = 386–397 | date = June 2008 | pmid = 18462782 | pmc = 2682215 | doi = 10.1016/j.yfrne.2008.03.003 }}</ref> 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.<ref>{{cite journal | vauthors = Goyal D, Limesand SW, Goyal R | title = Epigenetic responses and the developmental origins of health and disease | language = en-US | journal = The Journal of Endocrinology | volume = 242 | issue = 1 | pages = T105–T119 | date = July 2019 | pmid = 31091503 | doi = 10.1530/JOE-19-0009 | s2cid = 155101302 | doi-access = free }}</ref><ref>{{cite journal | vauthors = Tang WY, Ho SM | title = Epigenetic reprogramming and imprinting in origins of disease | journal = Reviews in Endocrine & Metabolic Disorders | volume = 8 | issue = 2 | pages = 173–182 | date = June 2007 | pmid = 17638084 | pmc = 4056338 | doi = 10.1007/s11154-007-9042-4 }}</ref> 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 spectrum|autism]] and [[Attention deficit hyperactivity disorder|attention deficit hyperactivity disorders (ADHD)]].<ref>{{cite journal | vauthors = Dufault R, Lukiw WJ, Crider R, Schnoll R, Wallinga D, Deth R | title = A macroepigenetic approach to identify factors responsible for the autism epidemic in the United States | journal = Clinical Epigenetics | volume = 4 | issue = 1 | pages = 6 | date = April 2012 | pmid = 22490277 | pmc = 3378453 | doi = 10.1186/1868-7083-4-6 | doi-access = free }}</ref>

It has been estimated that more than 60% of deaths in humans are related to nutritional or dietary factors rather than environmental triggers.<ref name="Mazzio_2014" /><ref name="Liu_2020" /> 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 2 diabetes|type II diabetes mellitus]], [[cardiovascular disease]], [[metabolic disorder]]s and decreased cognitive functions later in life.<ref name=":1"/>

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|spermatozoa's]] nucleus.<ref name=":1"/> An example of this is [[Transgenerational epigenetic inheritance|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.<ref name=":1" /><ref name="Mazzio_2014" />

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=== Epigenetic stressors ===
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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.<ref>{{cite journal | vauthors = Champagne FA | title = Epigenetic mechanisms and the transgenerational effects of maternal care | journal = Frontiers in Neuroendocrinology | volume = 29 | issue = 3 | pages = 386–397 | date = June 2008 | pmid = 18462782 | pmc = 2682215 | doi = 10.1016/j.yfrne.2008.03.003 }}</ref> 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.<ref>{{cite journal | vauthors = Goyal D, Limesand SW, Goyal R | title = Epigenetic responses and the developmental origins of health and disease | language = en-US | journal = The Journal of Endocrinology | volume = 242 | issue = 1 | pages = T105–T119 | date = July 2019 | pmid = 31091503 | doi = 10.1530/JOE-19-0009 | s2cid = 155101302 | doi-access = free }}</ref><ref>{{cite journal | vauthors = Tang WY, Ho SM | title = Epigenetic reprogramming and imprinting in origins of disease | journal = Reviews in Endocrine & Metabolic Disorders | volume = 8 | issue = 2 | pages = 173–182 | date = June 2007 | pmid = 17638084 | pmc = 4056338 | doi = 10.1007/s11154-007-9042-4 }}</ref> 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 spectrum|autism]] and [[Attention deficit hyperactivity disorder|attention deficit hyperactivity disorders (ADHD)]].<ref name="A macroepigenetic approach to ident">{{cite journal | vauthors = Dufault R, Lukiw WJ, Crider R, Schnoll R, Wallinga D, Deth R | title = A macroepigenetic approach to identify factors responsible for the autism epidemic in the United States | journal = Clinical Epigenetics | volume = 4 | issue = 1 | pages = 6 | date = April 2012 | pmid = 22490277 | pmc = 3378453 | doi = 10.1186/1868-7083-4-6 | doi-access = free }}</ref>


=== Food insecurity ===
=== Food insecurity ===
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=== Poor prenatal diet ===
=== Poor prenatal diet ===
Poor [[Prenatal development|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.<ref>{{cite journal | vauthors = Rijlaarsdam J, Cecil CA, Walton E, Mesirow MS, Relton CL, Gaunt TR, McArdle W, Barker ED | title = 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 = Journal of Child Psychology and Psychiatry, and Allied Disciplines | volume = 58 | issue = 1 | pages = 19–27 | date = January 2017 | pmid = 27535767 | pmc = 5161647 | doi = 10.1111/jcpp.12589 | author5-link = Caroline Relton }}</ref><ref>{{cite journal | vauthors = Nilsson E, Ling C | title = DNA methylation links genetics, fetal environment, and an unhealthy lifestyle to the development of type 2 diabetes | journal = Clinical Epigenetics | volume = 9 | pages = 105 | date = 2017 | pmid = 29026446 | pmc = 5627472 | doi = 10.1186/s13148-017-0399-2 | doi-access = free }}</ref>  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.<ref>{{Cite web |date=2019-01-24 |title=What is Nutritional Genomics (Nutrigenomics)? |url=https://www.news-medical.net/life-sciences/What-is-Nutritional-Genomics.aspx |access-date=2023-05-13 |website=News-Medical.net |language=en}}</ref> Dietary methyl supplements such as extra [[folic acid]] and [[choline]] can also have adverse effects on epigenetic gene regulation.<ref name="Landecker_2011" /><ref name="Waterland_2003" /> 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.<ref>{{cite journal | vauthors = Yambi O, Rocha C, Jacobs N | title = Unravelling the Food-Health Nexus to Build Healthier Food Systems | journal = World Review of Nutrition and Dietetics | volume = 121 | pages = 1–8 | date = 2020 | pmid = 33502367 | doi = 10.1159/000507497 | isbn = 978-3-318-06697-5 | s2cid = 226421936 }}</ref> 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.<ref>https://www.mayoclinic.org/healthy-lifestyle/pregnancy-week-by-week/in-depth/anemia-during-pregnancy/art-20114455#:~:text=Severe%20iron%20deficiency%20anemia%20during,weight%20baby%20and%20postpartum%20depression.</ref>
Poor [[Prenatal development|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.<ref>{{cite journal | vauthors = Rijlaarsdam J, Cecil CA, Walton E, Mesirow MS, Relton CL, Gaunt TR, McArdle W, Barker ED | title = 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 = Journal of Child Psychology and Psychiatry, and Allied Disciplines | volume = 58 | issue = 1 | pages = 19–27 | date = January 2017 | pmid = 27535767 | pmc = 5161647 | doi = 10.1111/jcpp.12589 | author5-link = Caroline Relton }}</ref><ref>{{cite journal | vauthors = Nilsson E, Ling C | title = DNA methylation links genetics, fetal environment, and an unhealthy lifestyle to the development of type 2 diabetes | journal = Clinical Epigenetics | volume = 9 | pages = 105 | date = 2017 | pmid = 29026446 | pmc = 5627472 | doi = 10.1186/s13148-017-0399-2 | doi-access = free }}</ref>  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.<ref>{{Cite web |date=2019-01-24 |title=What is Nutritional Genomics (Nutrigenomics)? |url=https://www.news-medical.net/life-sciences/What-is-Nutritional-Genomics.aspx |access-date=2023-05-13 |website=News-Medical.net |language=en}}</ref> Dietary methyl supplements such as extra folic acid and choline can also have adverse effects on epigenetic gene regulation.<ref name="Landecker_2011" /><ref name="Waterland_2003" /> 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.<ref>{{cite journal | vauthors = Yambi O, Rocha C, Jacobs N | title = Unravelling the Food-Health Nexus to Build Healthier Food Systems | journal = World Review of Nutrition and Dietetics | volume = 121 | pages = 1–8 | date = 2020 | pmid = 33502367 | doi = 10.1159/000507497 | isbn = 978-3-318-06697-5 | s2cid = 226421936 }}</ref> Low iron diets, or women who suffer from an [[iron deficiency]], have been shown to increase the likelihood of a [[Preterm birth|premature birth]], [[low birth weight]], and the increased possibility of [[postpartum depression]].<ref>{{cite web | url=https://www.mayoclinic.org/healthy-lifestyle/pregnancy-week-by-week/in-depth/anemia-during-pregnancy/art-20114455#:~:text=Severe%20iron%20deficiency%20anemia%20during,weight%20baby%20and%20postpartum%20depression | title=Prevent iron deficiency anemia during pregnancy | website=[[Mayo Clinic]] }}</ref>


=== Food quality ===
=== 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.<ref name="Aruoma_2006">{{cite journal | vauthors = Aruoma OI | title = The impact of food regulation on the food supply chain | journal = Toxicology | volume = 221 | issue = 1 | pages = 119–127 | date = April 2006 | pmid = 16483706 | doi = 10.1016/j.tox.2005.12.024 }}</ref> 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.<ref name="Aruoma_2006" />  Despite the best practices in use, heavy metal and pesticide residues are still found in the food supply.<ref>{{Cite web | vauthors = McCarthy C |date=2021-03-05 |title=Heavy metals in baby food? What parents should know and do |url=https://www.health.harvard.edu/blog/heavy-metals-in-baby-food-what-parents-should-know-and-do-2021030522088 |access-date=2023-05-13 |website=Harvard Health |language=en}}</ref><ref>{{Cite web |date=2021-09-29 |title=New Disclosures Show Dangerous Levels of Toxic Heavy Metals in Even More Baby Foods |url= https://oversightdemocrats.house.gov/sites/democrats.oversight.house.gov/files/ECP%20Second%20Baby%20Food%20Report%209.29.21%20FINAL.pdf |access-date=2023-05-12 |website=US House of Representatives}}</ref>  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.<ref name="Dufault_2021" /> Prenatal organophosphate pesticide exposure has been shown to impact [[DNA methylation]] in genes associated with the development of cardio-metabolic diseases.<ref>{{cite journal | vauthors = Declerck K, Remy S, Wohlfahrt-Veje C, Main KM, Van Camp G, Schoeters G, Vanden Berghe W, Andersen HR | title = Interaction between prenatal pesticide exposure and a common polymorphism in the <i>PON1</i> gene on DNA methylation in genes associated with cardio-metabolic disease risk-an exploratory study | journal = Clinical Epigenetics | volume = 9 | pages = 35 | date = 2017 | pmid = 28396702 | pmc = 5382380 | doi = 10.1186/s13148-017-0336-4 | doi-access = free }}</ref>
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 (elements)|heavy metal]], [[Pesticide residue|pesticide residues]], and other [https://www.who.int/tools/occupational-hazards-in-health-sector/exposure-to-hazardous-chemicals hazardous exposures of concern].<ref name="Aruoma_2006">{{cite journal | vauthors = Aruoma OI | title = The impact of food regulation on the food supply chain | journal = Toxicology | volume = 221 | issue = 1 | pages = 119–127 | date = April 2006 | pmid = 16483706 | doi = 10.1016/j.tox.2005.12.024 }}</ref> 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.<ref name="Aruoma_2006" />  Despite the best practices in use, heavy metal and pesticide residues are still found in the food supply.<ref>{{Cite web | vauthors = McCarthy C |date=2021-03-05 |title=Heavy metals in baby food? What parents should know and do |url=https://www.health.harvard.edu/blog/heavy-metals-in-baby-food-what-parents-should-know-and-do-2021030522088 |access-date=2023-05-13 |website=Harvard Health |language=en}}</ref><ref>{{Cite web |date=2021-09-29 |title=New Disclosures Show Dangerous Levels of Toxic Heavy Metals in Even More Baby Foods |url= https://oversightdemocrats.house.gov/sites/democrats.oversight.house.gov/files/ECP%20Second%20Baby%20Food%20Report%209.29.21%20FINAL.pdf |access-date=2023-05-12 |website=US House of Representatives}}</ref>  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.<ref name="Dufault_2021">{{cite journal |vauthors=Dufault RJ, Wolle MM, Kingston HM, Gilbert SG, Murray JA |date=July 2021 |title=Connecting inorganic mercury and lead measurements in blood to dietary sources of exposure that may impact child development |journal=World Journal of Methodology |volume=11 |issue=4 |pages=144–159 |doi=10.5662/wjm.v11.i4.144 |pmc=8299913 |pmid=34322366 |doi-access=free}}</ref> Prenatal organophosphate pesticide exposure has been shown to impact [[DNA methylation]] in genes associated with the development of cardio-metabolic diseases.<ref>{{cite journal | vauthors = Declerck K, Remy S, Wohlfahrt-Veje C, Main KM, Van Camp G, Schoeters G, Vanden Berghe W, Andersen HR | title = 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 | journal = Clinical Epigenetics | volume = 9 | pages = 35 | date = 2017 | pmid = 28396702 | pmc = 5382380 | doi = 10.1186/s13148-017-0336-4 | doi-access = free }}</ref> 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.<ref>{{cite web | url=https://www.invitra.com/en/pregnancy-complications/ | title=What are the most common pregnancy complications? | date=7 February 2022 }}</ref>

== Nutritional Epigenetics Model for Autism and ADHD ==
'''[[Renee Dufault|R]]'''[[Renee Dufault|enee Dufault]] developed and published the first nutritional epigenetics model for autism which was initially known as the Mercury Toxicity Model in 2009.<ref name="Dufault_2009">{{cite journal | vauthors = Dufault R, Schnoll R, Lukiw WJ, Leblanc B, Cornett C, Patrick L, Wallinga D, Gilbert SG, Crider R | title = Mercury exposure, nutritional deficiencies and metabolic disruptions may affect learning in children | journal = Behavioral and Brain Functions | volume = 5 | pages = 44 | date = October 2009 | pmid = 19860886 | pmc = 2773803 | doi = 10.1186/1744-9081-5-44 | doi-access = free }}</ref> The model below shows the impact of dietary mercury (Hg) exposure on the [[metallothionein]] (MT) gene when the child is zinc (Zn) deficient.<ref name="Dufault_2009" />
[[File:Mercury Toxicity Model.jpg|right|frameless]]

In 2009, the [[United States Department of Agriculture]] (USDA) estimated the average American was consuming 30.4 pounds of [[High-fructose corn syrup|high fructose corn syrup]] (HFCS) each year.<ref>{{Cite web |title=USDA ERS - Food Availability (Per Capita) Data System |url=https://www.ers.usda.gov/data-products/food-availability-per-capita-data-system/ |access-date=2024-02-16 |website=www.ers.usda.gov}}</ref> Dufault linked the consumption of HFCS to zinc losses and the subsequent impairment of the MT gene which results in the [[bioaccumulation]] of mercury in blood and symptoms of autism. A recent clinical trial conducted on human subjects and published in 2020 further strengthens Dufault’s model as it verified the consumption of HFCS does in fact lead to significant [[zinc]] losses in Americans.<ref>{{cite journal | vauthors = Harder NH, Hieronimus B, Stanhope KL, Shibata NM, Lee V, Nunez MV, Keim NL, Bremer A, Havel PJ, Heffern MC, Medici V | title = Effects of Dietary Glucose and Fructose on Copper, Iron, and Zinc Metabolism Parameters in Humans | journal = Nutrients | volume = 12 | issue = 9 | page = 2581 | date = August 2020 | pmid = 32854403 | pmc = 7551875 | doi = 10.3390/nu12092581 | doi-access = free }}</ref>

The term “nutritional epigenetics” was coined one year after publication of Dufault’s “Mercury Toxicity Model.” Farhud et al. described mechanisms involved in “Nutritional epigenetics” in a paper published in 2010.<ref>{{cite journal | vauthors = Farhud D, Zarif Yeganeh M, Zarif Yeganeh M | title = Nutrigenomics and nutrigenetics | journal = Iranian Journal of Public Health | volume = 39 | issue = 4 | pages = 1–14 | date = 2010 | pmid = 23113033 | pmc = 3481686 }}</ref>
[[File:Nutritional Epigenetics Model for Autism and ADHD.png|right|frameless]]
Dufault’s updated nutritional epigenetics model featured in the image below incorporates the constructs of Dufault’s previous models that show the role dietary lead (Pb) and Hg exposures play in [[PON1]] gene inhibition which occurs in both autism and ADHD.<ref>{{cite journal | vauthors = Dufault R, Lukiw WJ, Crider R, Schnoll R, Wallinga D, Deth R | title = A macroepigenetic approach to identify factors responsible for the autism epidemic in the United States | journal = Clinical Epigenetics | volume = 4 | issue = 1 | pages = 6 | date = April 2012 | pmid = 22490277 | pmc = 3378453 | doi = 10.1186/1868-7083-4-6 | doi-access = free }}</ref>Dufault’s updated nutritional epigenetics model was recently used to test a successful intervention in a clinical trial with results published in 2024.<ref name="Dufault_2024">{{cite journal | vauthors = Dufault RJ, Adler KM, Carpenter DO, Gilbert SG, Crider RA | title = Nutritional epigenetics education improves diet and attitude of parents of children with autism or attention deficit/hyperactivity disorder | journal = World Journal of Psychiatry | volume = 14 | issue = 1 | pages = 159–178 | date = January 2024 | pmid = 38327893 | pmc = 10845225 | doi = 10.5498/wjp.v14.i1.159 | doi-access = free }}</ref> Parents of children with autism and ADHD who took part in the intervention improved their diets by significantly reducing their intake of ultra-processed foods and changed their attitude about the role of diet in controlling their child’s behaviors.<ref name="Dufault_2024" />


== References ==
== References ==

Latest revision as of 03:29, 16 October 2024

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.
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  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.
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