User:TabSpikes/Prenatal stress
Pathway
Another pathway that prenatal stress can interfere with fetal development is telomere length. A telomere is a structure of repetitive DNA sequences that can be found at the end of chromosomes.[1] They are made up of the same short DNA sequence that is repeated multiple times and serve to protect the ends of chromosomes so they do not become damaged.[2] Another function of telomeres is to allow chromosomes to properly function in the process of replication. However, each time a cell divides, the telomeres loses length and becomes shorter. After repeated replications they will eventually become so short that the cell is unable to divide any further and the cell will die.[1] When offspring are exposed to prenatal distress during development it can affect the length of the offspring's telomeres, more specifically it can result in shortened telomeres.[3] Shortened telomeres have been linked to multiple issues including shortened lifespan and increased risk of diseases.[4] Typically, telomeres shorten substantially with increasing age, and telomere length is thus a bioindicator of aging. However, prenatal stress puts offspring at an increased state of vulnerability by shortening the telomeres and leaving less room for shortening as the offspring age.[3]
Impact of development
Prenatal distress has been shown to increase the risk that the offspring will experience a mental disorder as well as the severity of some symptoms. Typical disorders that are increased due to prenatal distress include autism, the severity of ADHD, and the development of mood disorders.[5]Prenatal stress disrupts multiple developmental systems within the individual carrying offspring. One of the disrupted processes is hormone production. Maternal exposure to excess dihydrotestosterone, progestin, and norethindrone have been linked to a higher risk of offspring developing ASD.[6] A 2008 study found that children whose mothers experienced moderate to severe stress during their pregnancy tended to develop symptoms that more frequently fell on the severe side of the ADHD severity spectrum. This distinction was made in comparison to those with ADHD whose mothers were not exposed to prenatal stressors.[7] This increased development of ADHD from heightened prenatal distress can be due to many factors, one of the more popular and founded claims being the neurological development of the offspring. Exposure to stress during the process of pregnancy affects fetal brain development and predisposes offspring to the development of a multitude of mental disorders.[8] Many studies have found that there is an association between ADHD and lessened functioning within the prefrontal cortex (PFC). This area of the brain plays a crucial role in attention regulation as well as behavioral and emotional control. The PFC right hemisphere in particular has been linked to decreased size in individuals who have ADHD.[9] This is notable due to the important role of the PFC right hemisphere which is behavioral inhibition, a common struggle for individuals with ADHD. Prenatal distress has also been linked to the development of mood disorders such as depression or anxiety. A 2019 study found that prenatal distress, specifically during the first 20 weeks of gestation, was linked to higher mood dysregulation and lower grey matter (GM) volume. [10] The lessening of grey matter volume is a detrimental loss because of the multitude of functions that this structure is essential for. Grey matter is found throughout the central nervous system and is crucial for motor function, memory, and emotions.[11] The reduction of GM volume is impactful in many negative ways which is another contributing factor that can lead to the development of mental disorders in children that experience in utero stress.
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[edit]References
[edit]- ^ a b "Telomere". Genome.gov. Retrieved 2023-10-27.
- ^ "What is a telomere?". @yourgenome · Science website. Retrieved 2023-10-27.
- ^ a b Send, Tabea Sarah; Gilles, Maria; Codd, Veryan; Wolf, Isabell; Bardtke, Svenja; Streit, Fabian; Strohmaier, Jana; Frank, Josef; Schendel, Darja; Sütterlin, Mark W; Denniff, Matthew; Laucht, Manfred; Samani, Nilesh J; Deuschle, Michael; Rietschel, Marcella (2017-11). "Telomere Length in Newborns is Related to Maternal Stress During Pregnancy". Neuropsychopharmacology. 42 (12): 2407–2413. doi:10.1038/npp.2017.73. ISSN 0893-133X.
{{cite journal}}: Check date values in:|date=(help) - ^ Shammas, Masood A (2011-01). "Telomeres, lifestyle, cancer, and aging:". Current Opinion in Clinical Nutrition and Metabolic Care. 14 (1): 28–34. doi:10.1097/MCO.0b013e32834121b1. ISSN 1363-1950.
{{cite journal}}: Check date values in:|date=(help) - ^ van den Heuvel, Marion I. (2022-03). "From the Womb into the World: Protecting the Fetal Brain from Maternal Stress During Pregnancy". Policy Insights from the Behavioral and Brain Sciences. 9 (1): 96–103. doi:10.1177/23727322211068024. ISSN 2372-7322.
{{cite journal}}: Check date values in:|date=(help) - ^ Waterhouse, Lynn (2013), "Genetic Risk Factors Link Autism to Many Other Disorders", Rethinking Autism, Elsevier, pp. 157–222, retrieved 2023-11-26
- ^ Polotskaia, Anna; Grizenko, Natalie; Bellingham, Johanne; Ter-Stepanian, Mariam; Joober, Ridha (2007). "Children and Parent-Based Assessment of ADHD Symptoms and Comorbid Disorders in Children Diagnosed With ADHD". PsycEXTRA Dataset. Retrieved 2023-11-26.
- ^ Suwaluk, Arbthip; Chutabhakdikul, Nuanchan (2022-11). "Long-term effects of prenatal stress on the development of prefrontal cortex in the adolescent offspring". Journal of Chemical Neuroanatomy. 125: 102169. doi:10.1016/j.jchemneu.2022.102169. ISSN 1873-6300. PMID 36241049.
{{cite journal}}: Check date values in:|date=(help) - ^ Arnsten, Amy F.T. (2009-05). "ADHD and the Prefrontal Cortex". The Journal of Pediatrics. 154 (5): I–S43. doi:10.1016/j.jpeds.2009.01.018. PMC 2894421. PMID 20596295.
{{cite journal}}: Check date values in:|date=(help)CS1 maint: PMC format (link) - ^ Marečková, Klára; Klasnja, Anja; Bencurova, Petra; Andrýsková, Lenka; Brázdil, Milan; Paus, Tomáš (2019-03-01). "Prenatal Stress, Mood, and Gray Matter Volume in Young Adulthood". Cerebral Cortex. 29 (3): 1244–1250. doi:10.1093/cercor/bhy030. ISSN 1047-3211. PMC 6373666. PMID 29425268.
{{cite journal}}: CS1 maint: PMC format (link) - ^ "Grey matter". Cleveland Clinic. Retrieved 2023-11-28.