Fetal programming: Difference between revisions

Revision as of 06:33, 22 April 2024

Revision as of 16:04, 24 July 2024

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== History ==

=== Dutch famine 1944–45 ===

In 1944–45, the German blockade of the Netherlands led to a lack of food supplies, causing the [[Dutch famine of 1944–45]]. The famine caused severe malnutrition among the population, including women in various stages of pregnancy. The Dutch Famine Birth Cohort Study examined the impact of lack of nutrition on children born during or after this famine. It showed that over the course of their life, these children were at greater risk of [[Diabetes mellitus|diabetes]], [[cardiovascular disease]], [[obesity]], and other [[non-communicable disease]]s.{{cncitation needed|date=April 2023}}

=== Barker hypothesis ===

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=== Cortisol ===

Cortisol (and glucocorticoids more generally) is the most well studied hormonal mechanism that may have prenatal programming effects.<ref>{{cite journal | vauthors = Moisiadis VG, Matthews SG | title = Glucocorticoids and fetal programming part 2: Mechanisms | journal = Nature Reviews. Endocrinology | volume = 10 | issue = 7 | pages = 403–11 | date = July 2014 | pmid = 24863383 | doi = 10.1038/nrendo.2014.74 | s2cid = 11475810 }}</ref> Although cortisol has normative developmental effects during prenatal development, excess cortisol exposure has deleterious effects on fetal growth,<ref>{{cite journal | vauthors = O'Donnell KJ, Meaney MJ | title = Fetal Origins of Mental Health: The Developmental Origins of Health and Disease Hypothesis | journal = The American Journal of Psychiatry | volume = 174 | issue = 4 | pages = 319–328 | date = April 2017 | pmid = 27838934 | doi = 10.1176/appi.ajp.2016.16020138 | doi-access = free }}</ref> the postnatal function of physiological systems such as the hypothalamic-pituitary-adrenal axis <ref>{{cite journal | vauthors = Kapoor A, Petropoulos S, Matthews SG | title = Fetal programming of hypothalamic-pituitary-adrenal (HPA) axis function and behavior by synthetic glucocorticoids | journal = Brain Research Reviews | volume = 57 | issue = 2 | pages = 586–95 | date = March 2008 | pmid = 17716742 | doi = 10.1016/j.brainresrev.2007.06.013 | s2cid = 30865698 }}</ref> and brain structure or connectivity (ege.g., amygdala).<ref>{{cite journal | vauthors = Buss C, Davis EP, Shahbaba B, Pruessner JC, Head K, Sandman CA | title = Maternal cortisol over the course of pregnancy and subsequent child amygdala and hippocampus volumes and affective problems | journal = Proceedings of the National Academy of Sciences of the United States of America | volume = 109 | issue = 20 | pages = E1312-9 | date = May 2012 | pmid = 22529357 | pmc = 3356611 | doi = 10.1073/pnas.1201295109 | doi-access = free }}</ref><ref>{{cite journal | vauthors = Graham AM, Rasmussen JM, Entringer S, Ben Ward E, Rudolph MD, Gilmore JH, Styner M, Wadhwa PD, Fair DA, Buss C | display-authors = 6 | title = Maternal Cortisol Concentrations During Pregnancy and Sex-Specific Associations With Neonatal Amygdala Connectivity and Emerging Internalizing Behaviors | journal = Biological Psychiatry | volume = 85 | issue = 2 | pages = 172–181 | date = January 2019 | pmid = 30122286 | pmc = 6632079 | doi = 10.1016/j.biopsych.2018.06.023 }}</ref>

During gestation, cortisol concentrations in maternal circulation are up to ten times higher than cortisol concentrations in fetal circulation.<ref>{{cite journal | vauthors = Travers S, Martinerie L, Boileau P, Xue QY, Lombès M, Pussard E | title = Comparative profiling of adrenal steroids in maternal and umbilical cord blood | journal = The Journal of Steroid Biochemistry and Molecular Biology | volume = 178 | pages = 127–134 | date = April 2018 | pmid = 29191401 | doi = 10.1016/j.jsbmb.2017.11.012 | s2cid = 3705475 }}</ref> The maternal-to-fetal cortisol gradient is maintained by the placenta, which forms a structural and enzymatic barrier to cortisol.<ref>{{cite journal | vauthors = Chapman K, Holmes M, Seckl J | title = 11β-hydroxysteroid dehydrogenases: intracellular gate-keepers of tissue glucocorticoid action | journal = Physiological Reviews | volume = 93 | issue = 3 | pages = 1139–206 | date = July 2013 | pmid = 23899562 | pmc = 3962546 | doi = 10.1152/physrev.00020.2012 }}</ref><ref>{{cite journal | vauthors = Stirrat LI, Sengers BG, Norman JE, Homer NZ, Andrew R, Lewis RM, Reynolds RM | title = Transfer and Metabolism of Cortisol by the Isolated Perfused Human Placenta | journal = The Journal of Clinical Endocrinology and Metabolism | volume = 103 | issue = 2 | pages = 640–648 | date = February 2018 | pmid = 29161409 | pmc = 5800837 | doi = 10.1210/jc.2017-02140 }}</ref> During the first two trimesters of gestation intrauterine cortisol is primarily produced by the maternal adrenal glands.<ref name="Development and function of the hum">{{cite journal | vauthors = Ishimoto H, Jaffe RB | title = Development and function of the human fetal adrenal cortex: a key component in the feto-placental unit | journal = Endocrine Reviews | volume = 32 | issue = 3 | pages = 317–55 | date = June 2011 | pmid = 21051591 | pmc = 3365797 | doi = 10.1210/er.2010-0001 }}</ref> However, during the third trimester the fetal adrenal glands begin to endogenously produce cortisol and become responsible for most intrauterine cortisol by the time the fetus reaches term.<ref name="Development and function of the hum"/>