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User:Boydak13/Environmental Epigenetics - Nutrition

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Overview

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Epigenetics is the study of how outside factors can influence the expression of certain genes to create a variation of phenotypes (physical attributes/characteristics) without affecting the organism's DNA.[1] The base pair nucleotides (Adenine, Thymine, Guanine, and Cytosine) pair together to form DNA structures. The environment can change how many organisms such as plants, animals, bacteria, and even humans, develop and continue to grow. The three environmental agents that can cause phenotypes to be altered, including Direct Transcriptional Regulation, Neuroendocrine system, and Direct Induction. The most influential factors that affect environmental epigenetics are behaviors, nutrition, and chemical exposure.

Nutrition is one of the factors that most commonly affects organisms, especially humans. The development of a fetus, especially during utero, is heavily affected by the mother's intake of nutrients[2]. The nervous system receives signals from the environment to release chemical signals, altering the hormone production within organisms. The production of these hormones then causes changes in the phenotype of the animal.

Mechanisms of Epigenetics

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The main mechanisms of epigenetics include, DNA Methylation, Histone Modifications, and Non-coding RNAs. DNA Methylation occurs when a methyl group is added to a DNA cytosine base; this usually happens at CpG sites. Because methylation patterns change DNA's accessibility to transcription factors and other regulatory proteins, they can affect how genes are expressed. Proteins called histones wrap DNA to form chromatin. Histone tails can undergo a variety of chemical modifications, including acetylation, methylation, phosphorylation, and ubiquitination, which can affect chromatin structure and gene expression. Non-coding RNA molecules regulate the expression of genes but do not encode proteins. Examples include small interfering RNAs (siRNAs), long non-coding RNAs (lncRNAs), and microRNAs (miRNAs) that might affect gene expression by blocking translation or aiming to degrade messenger RNAs (mRNAs).[3]

Examples of Nutritional Epigenetics

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Royal Jelly

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[4] Developing queen larvae surrounded by royal jelly

Honeybee phenotype is influenced by the epigenome, which is influenced by their early nutrition. With identical genomes, two distinct female castes are produced: a long-lived queen with fully developed ovaries and a short-lived, functionally sterile worker. A queen-destined female larva is given enormous quantities of royal jelly. Queen structure, including the fully developed ovaries required to lay eggs, develops as a result of the royal jelly. The hypopharyngeal and mandibular glands of nurse honeybees create royal jelly.[5]

A male dung beetle with large horns

Horn Length of the Male Dung Beetle

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The horn length of male dung beetle (Onthophagus acuminatus) is determined by how it eats while in the larval stage. Male larvae that eat past a certain threshold are able to grow horns that are longer than their body. However, if the males do not meet this threshold or have less access to food; they will grow little to no horns[6]. The amount of food available to the larvae is what determines the amount of juvenile hormone in the beetle. Juvenile hormone directly correlates to horn growth. The size of the larvae at the last metamorphosis determines how large the horns can become.[1] Beetles with differing horn length exhibit different mating behaviors.

Nutritional Epigenetics and Diseases

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Obesity

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Obesity, including being overweight, is a common disease that affects more than 35% of the world's population[7]. You see obesity and overweight individuals all over America. These diseases can form during utero, in later life based on genes from your parents, and nutrition intake throughout life. Maternal obesity can affect the fetus by causing increased risk of obesity, heart diseases, diabetes, asthma, and CNS malformations (Congenital Central Nervous System). Obese mothers commonly have children that have CNS malformations including Spina Bifida, Anencephaly, and Isolated hydrocephaly[8].

Type 2 Diabetes

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Type 2 Diabetes is a condition where the body has problems regulating sugars and using them as fuel. The two main problems that people with this condition have are the pancreas not creating enough insulin for the body and their cells not responding to insulin. [9] Diet can influence the risk of getting diabetes. Specifically, the more an individual consumes unhealthy beverages, like sodas, vitamin waters, sweetened tea, the higher the chance of developing type 2 diabetes. [10] Managing the disease by implementing nutritional recommendations can help improve glucose in the blood[11]. Type 2 diabetes studies show that consuming certain fruits, like those in the citrus category, can help to reduce the risk of developing the disease.[12] Having more natural foods in the diets will also lessen the chances of developing this condition.

Human Lactation in Nutritional Epigenetics

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Lactation is one of the primary ways for mammals to optimize growth of their offspring. Through this process the infants are receiving essential nutrients required for healthy development. These inadequacies of micronutrients noted in the female’s diet can directly translate to congenital defects in their offspring. [13] Due to the early exposure of malnutrition in prenatal and postnatal fetal development, epigenetic changes in gene expression may occur in the form of DNA methylation, histone modification, and the interaction of ribonucleic acids for activation or silencing of genes. [14]

Although the exact mechanism of neural pathway of the infant’s development from maternal milk supplementation is unknown, conclusions have been reached that suggest the potential epigenetic effects of bioactive components such as growth factors, non-coding RNAs, stem cells, and early development of the fetal gut microbiome to be a major part of this process. [14]

Exosomes derived from human mammary glands possess the ability to cross the blood-brain barrier due to their extravesicular nature. This provides protection for the enclosed micro-ribonucleic acids (mRNAs) and long-non-coding ribonucleic acids (lncRNAs) that helps brain development and function by upregulation of associated genes. [14] As the exosomes are extremely stable vesicles, they have the capacity of preservation from digestive enzymes and are available for reuptake into the bloodstream via intestinal epithelial cells. [15] However These essential RNAs have been noted to be deficient in pregnant females with conditions such as diabetes with translation to obesity and even psychological factors. [16]

Stem cells from breast milk containing nestin, a neuroepithelial stem cell protein, have the ability to differentiate into neural cells or can perform as epigenetic regulators in the brain.[14] A study by Hosseini et al. [17] proved the human breast milk can have neural implications by their carried stem cells which can further progress into highly differentiated neural cells including oligodendrocytes and astrocytes. This association has proposed new pathways for explanation of the short- and long-term effects of human breast milk in fetal development.[14]

As for the microbiota located within breast milk, the different bacteria can help steer the infant’s development of their own gut microbiome. [18] Which is a known precursor for establishment of beneficial epigenetic modifications and neurodevelopment as shown in a study performed by Pannaraj et al. [19] that maternal breast milk performs contributions to the gut microbiome by promoting colonization of beneficial bacteria. Methods of exposure for allotment of the colonization of beneficial bacteria postnatally include the maternal flora, delivery of milk expression (breast pump or skin-to-skin), and the infant’s diet. [20] This accumulation of microbiota can directly influence specific epigenetic patterns by the Gut-Brain Axis through interactions between the central nervous system and gastrointestinal tract. [21]

References

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  1. ^ a b Gilbert, Scott. "Ecological Developmental Biology". reader.yuzu.com. Retrieved 2024-02-28.
  2. ^ Bazer, Fuller W.; Spencer, Thomas E.; Wu, Guoyao; Cudd, Timothy A.; Meininger, Cynthia J. (2004-09-01). "Maternal Nutrition and Fetal Development". The Journal of Nutrition. 134 (9): 2169–2172. doi:10.1093/jn/134.9.2169. ISSN 0022-3166.
  3. ^ Loscalzo, Joseph; Handy, Diane E. (2014-06). "Epigenetic Modifications: Basic Mechanisms and Role in Cardiovascular Disease (2013 Grover Conference Series)". Pulmonary Circulation. 4 (2): 169–174. doi:10.1086/675979. ISSN 2045-8940. PMC 4070783. PMID 25006435. {{cite journal}}: Check date values in: |date= (help)CS1 maint: PMC format (link)
  4. ^ Waugsberg (2008-05-11), Deutsch: Zwei Weiselzellen wurden von der Wabe entfernt und geöffnet, um die Entwicklung einer Bienenkönigin der Westlichen Honigbiene zu zeigen. Die Larven schwimmen zunächst, wie hier zu sehen, als Rundmaden waagrecht an der Unterseite des Königinfuttersafts (Gelée Royale), der sich oben in der anfangs nach unten offenen Zelle befindet. Wenn sich die Zellen in ihrer natürlichen Lage befänden, würde man die Larven so sehen, wenn man senkrecht nach oben blickt. Die Larven sind etwa vor 3 und 4 Tage aus dem Ei geschlüpft oder ab Eilage etwa 6 bzw. 7 Tage alt., retrieved 2024-03-04
  5. ^ Viuda-Martos, Manuel; Pérez-Alvarez, José A.; Fernández-López, Juana (2017), "Royal Jelly: Health Benefits and Uses in Medicine", Bee Products - Chemical and Biological Properties, Cham: Springer International Publishing, pp. 199–218, doi:10.1007/978-3-319-59689-1_10, ISBN 978-3-319-59688-4, retrieved 2024-03-11
  6. ^ Emlen, Douglas J. (1997). "Alternative Reproductive Tactics and Male-Dimorphism in the Horned Beetle Onthophagus acuminatus (Coleoptera: Scarabaeidae)". Behavioral Ecology and Sociobiology. 41 (5): 335–341. doi:10.1007/s002650050393. ISSN 0340-5443. JSTOR 4601395.
  7. ^ Sertie, Rogerio; Kang, Minsung; Antipenko, Jessica P.; Liu, Xiaobing; Maianu, Lidia; Habegger, Kirk; Garvey, W. Timothy (August 2020). "In utero nutritional stress as a cause of obesity: Altered relationship between body fat, leptin levels and caloric intake in offspring into adulthood". Life Sciences. 254: 117764. doi:10.1016/j.lfs.2020.117764. ISSN 0024-3205. PMC 8513136. PMID 32407841.
  8. ^ Anderson, James L.; Waller, D Kim; Canfield, Mark A.; Shaw, Gary M.; Watkins, Margaret L.; Werler, Martha M. (2005-01). "Maternal Obesity, Gestational Diabetes, and Central Nervous System Birth Defects:". Epidemiology. 16 (1): 87–92. doi:10.1097/01.ede.0000147122.97061.bb. ISSN 1044-3983. {{cite journal}}: Check date values in: |date= (help)
  9. ^ "Type 2 diabetes - Symptoms and causes". Mayo Clinic. Retrieved 2024-03-22.
  10. ^ Malik, Vasanti S.; Popkin, Barry M.; Bray, George A.; Després, Jean-Pierre; Willett, Walter C.; Hu, Frank B. (2010-11-01). "Sugar-Sweetened Beverages and Risk of Metabolic Syndrome and Type 2 Diabetes". Diabetes Care. 33 (11): 2477–2483. doi:10.2337/dc10-1079. ISSN 0149-5992. PMC 2963518. PMID 20693348.{{cite journal}}: CS1 maint: PMC format (link)
  11. ^ Salvia, Meg G.; Quatromoni, Paula A. (June 2023). "Behavioral approaches to nutrition and eating patterns for managing type 2 diabetes: A review". American Journal of Medicine Open. 9: 100034. doi:10.1016/j.ajmo.2023.100034. ISSN 2667-0364.
  12. ^ Visvanathan, Rizliya; Williamson, Gary (September 2021). "Effect of citrus fruit and juice consumption on risk of developing type 2 diabetes: Evidence on polyphenols from epidemiological and intervention studies". Trends in Food Science & Technology. 115: 133–146. doi:10.1016/j.tifs.2021.06.038. ISSN 0924-2244.
  13. ^ Keats, Emily C.; Oh, Christina; Chau, Tamara; Khalifa, Dina S.; Imdad, Aamer; Bhutta, Zulfiqar A. (2021-06). "Effects of vitamin and mineral supplementation during pregnancy on maternal, birth, child health and development outcomes in low‐ and middle‐income countries: A systematic review". Campbell Systematic Reviews. 17 (2). doi:10.1002/cl2.1127. ISSN 1891-1803. {{cite journal}}: Check date values in: |date= (help)
  14. ^ a b c d e Gialeli, Giannoula; Panagopoulou, Ourania; Liosis, Georgios; Siahanidou, Tania (2023-08-17). "Potential Epigenetic Effects of Human Milk on Infants' Neurodevelopment". Nutrients. 15 (16): 3614. doi:10.3390/nu15163614. ISSN 2072-6643.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  15. ^ Shandilya, Shruti; Rani, Payal; Onteru, Suneel Kumar; Singh, Dheer (2017-11-01). "Small Interfering RNA in Milk Exosomes Is Resistant to Digestion and Crosses the Intestinal Barrier In Vitro". Journal of Agricultural and Food Chemistry. 65 (43): 9506–9513. doi:10.1021/acs.jafc.7b03123. ISSN 0021-8561.
  16. ^ Shah, Kruti B.; Fields, David A.; Pezant, Nathan P.; Kharoud, Harmeet K.; Gulati, Shelly; Jacobs, Katherine; Gale, Cheryl A.; Kharbanda, Elyse O.; Nagel, Emily M.; Demerath, Ellen W.; Tryggestad, Jeanie B. (2022-02). "Gestational Diabetes Mellitus Is Associated with Altered Abundance of Exosomal MicroRNAs in Human Milk". Clinical Therapeutics. 44 (2): 172–185.e1. doi:10.1016/j.clinthera.2022.01.005. ISSN 1879-114X. PMC 9089438. PMID 35090750. {{cite journal}}: Check date values in: |date= (help)
  17. ^ Hosseini, Seyed Mojtaba; Talaei-khozani, Tahere; Sani, Mahsa; Owrangi, Bahareh (2014). "Differentiation of Human Breast-Milk Stem Cells to Neural Stem Cells and Neurons". Neurology Research International. 2014: 1–8. doi:10.1155/2014/807896. ISSN 2090-1852.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  18. ^ Vuong, Helen E. (2022), "Intersections of the microbiome and early neurodevelopment", International Review of Neurobiology, vol. 167, Elsevier, pp. 1–23, doi:10.1016/bs.irn.2022.06.004., ISBN 978-0-323-99176-6, retrieved 2024-04-16 {{citation}}: Check |doi= value (help)
  19. ^ Pannaraj, Pia S.; Li, Fan; Cerini, Chiara; Bender, Jeffrey M.; Yang, Shangxin; Rollie, Adrienne; Adisetiyo, Helty; Zabih, Sara; Lincez, Pamela J.; Bittinger, Kyle; Bailey, Aubrey; Bushman, Frederic D.; Sleasman, John W.; Aldrovandi, Grace M. (2017-07-01). "Association Between Breast Milk Bacterial Communities and Establishment and Development of the Infant Gut Microbiome". JAMA Pediatrics. 171 (7): 647. doi:10.1001/jamapediatrics.2017.0378. ISSN 2168-6203.
  20. ^ Indrio, Flavia; Martini, Silvia; Francavilla, Ruggiero; Corvaglia, Luigi; Cristofori, Fernanda; Mastrolia, Salvatore Andrea; Neu, Josef; Rautava, Samuli; Russo Spena, Giovanna; Raimondi, Francesco; Loverro, Giuseppe (2017-08-22). "Epigenetic Matters: The Link between Early Nutrition, Microbiome, and Long-term Health Development". Frontiers in Pediatrics. 5. doi:10.3389/fped.2017.00178. ISSN 2296-2360.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  21. ^ Laue, Hannah E.; Coker, Modupe O.; Madan, Juliette C. (2022-03-07). "The Developing Microbiome From Birth to 3 Years: The Gut-Brain Axis and Neurodevelopmental Outcomes". Frontiers in Pediatrics. 10. doi:10.3389/fped.2022.815885. ISSN 2296-2360.{{cite journal}}: CS1 maint: unflagged free DOI (link)
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