107:, forms the basis for much of the research conducted on fetal programming. This hypothesis states that if the fetus is exposed to low nutrition, it will adapt to that particular environment. Nutrients are diverted towards the development of the heart, brain, and other essential organs of the fetus. The body also undergoes metabolic alterations that ensure survival in spite of low nutrition but may cause problems in situations with normal or high nutrition. This leads to increased risk of
235:. Changes posed to the fetus through ethanol exposure may significantly effect growth and development; these are collectively known as fetal alcohol spectrum disorders (FASD). The exact interaction between ethanol and the developing fetus is complex and largely uncertain, however, several direct and indirect effects have been observed as the fetus matures. Predominant among these are irregularities in the fetus's endocrine, metabolic and physiological functions.
173:
own thyroid hormones from the onset of the second trimester; however, maternal thyroid hormones are important for brain development before and after the baby is able to synthesize the hormones while still in the uterus. Due to this, the baby may experience an increased risk of neurological or psychiatric diseases later in life.
75:. 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
194:
Mental state of the mother during pregnancy affects the fetus in the uterus, predominantly via hormones and genetics. The mother's mood, including maternal prenatal anxiety, depression and stress during pregnancy correlates with altered outcomes for the child. That being said, not every fetus exposed
119:
The developing fetus forms an impression of the world into which it will be born via its mother's nutritional status. Its development is thus modulated to create the best chance of survival. However, excessive or insufficient nutrition in the mother can provoke maladaptive developmental responses in
203:
Maternal depression poses one of the greatest risks for increased vulnerability to adverse outcomes for a baby that is developing in the uterus, especially in terms of susceptibility to a variety of psychological conditions. Mechanisms that may explain the connection between maternal depression and
212:
Maternally experienced psychological stress that occurs either prior to or during gestation can have intergenerational effects on offspring. Stress experienced during gestation has been linked with preterm delivery, low birth weight, and increased risk of psychopathology. The new mother may suffer
172:
Thyroid hormones play an instrumental role during the early development of the fetus's brain. Therefore, mothers suffering from thyroid-related issues and altered thyroid hormone levels may inadvertently trigger structural and functional changes in the fetal brain. The fetus is able to produce its
260:
There is evidence pointing towards pharmacological programming of the fetus during the first trimester. One type of drugs which is suspected of influencing the developing baby when used during pregnancy is anti-hypertensive drugs. Pre-eclampsia (a condition of hypertension during pregnancy), is a
150:
that make up most of the placenta, is a disease which is often associated with maladaptive long-term consequences of inappropriate fetal programming. Here, an inadequately developed and poorly functioning placenta fails to meet the fetusโ nutritional needs during gestation, either by altering its
221:
Toxins such as alcohol, tobacco and certain drugs to which the baby is exposed to during its development are thought to contribute to fetal programming, especially via alterations to the HPA axis. If the exposure occurs during a critical phase of fetal development, it could have drastic and dire
181:
Cortisol (and glucocorticoids more generally) is the most well studied hormonal mechanism that may have prenatal programming effects. Although cortisol has normative developmental effects during prenatal development, excess cortisol exposure has deleterious effects on fetal growth, the postnatal
185:
During gestation, cortisol concentrations in maternal circulation are up to ten times higher than cortisol concentrations in fetal circulation. The maternal-to-fetal cortisol gradient is maintained by the placenta, which forms a structural and enzymatic barrier to cortisol. During the first two
159:
A delicate balance of hormones during pregnancy is regarded as being highly relevant to fetal programming and may significantly influence the outcome on the offspring. Placental endocrine transfer from the mother to the developing fetus could be altered by the mental state of the mother, due to
251:
maternal tobacco smoke exposure (MTSE), can contribute towards various problems in babies of smoking mothers. About 20% of mothers smoke whilst pregnant and this is associated with increased risk of complications, such as preterm birth, decreased fetal growth leading to lower birth weight, and
186:
trimesters of gestation intrauterine cortisol is primarily produced by the maternal adrenal glands. 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.
204:
the offspring's future health are mostly unclear and form a current area of active research. Genetic inheritance that may be rendering the child more susceptible may play a role, including the effect on the intrauterine environment for the baby whilst the mother suffers from depression.
230:
Prenatal and/or early postnatal exposure to alcohol (ethanol) has been found to have a negative effect on child's neuroendocrine and behavioral factors. Alcohol passes through the placenta on being ingested by the mother during her pregnancy, and makes its way to the baby
53:
changes which alter disease risk of not only the child but also that of the next generation - i.e. after a famine, grandchildren of women who were pregnant during the famine, are born smaller than the normal size, despite nutritional deficiencies having been
135:, which is present in the blood of individuals that are overweight or obese. There is a theory that this hormone has a negative impact on the regulatory systems of the fetus, and renders it impossible to maintain normal blood pressure levels.
131:
prior to pregnancy and weight gain during pregnancy are both linked to high blood pressure in the offspring during adulthood. Mouse models suggest that this is due to high levels of the fetal hormone
281:
Fleming TP, Velazquez MA, Eckert JJ, Lucas ES, Watkins AJ (February 2012). "Nutrition of females during the peri-conceptional period and effects on foetal programming and health of offspring".
151:
selection for nutrients which can cross into fetal blood or restricting total volume thereof. Consequences of this for the fetus in adult life include cardiovascular and metabolic conditions.
120:
the fetus, which in turn manifest in the form of post-natal diseases. It is possible that this has such a profound effect on the fetusโ adult life that it can even outweigh lifestyle factors.
213:
from after-effects too, such as postpartum depression, and subsequently may find parenting more difficult as compared to those who did not experience as much stress during their pregnancies.
1257:
Bayliss H, Churchill D, Beevers M, Beevers DG (January 2002). "Anti-hypertensive drugs in pregnancy and fetal growth: evidence for "pharmacological programming" in the first trimester?".
261:
serious problem for the majority of pregnant mothers and can predispose the mother to a variety of complications, including increased risk of mortality and problems during parturition.
684:
Kapoor A, Petropoulos S, Matthews SG (March 2008). "Fetal programming of hypothalamic-pituitary-adrenal (HPA) axis function and behavior by synthetic glucocorticoids".
195:
to these factors is affected in the same way and to the same degree, and genetic and environmental factors are believed to have a significant degree of influence.
827:
Travers S, Martinerie L, Boileau P, Xue QY, Lombรจs M, Pussard E (April 2018). "Comparative profiling of adrenal steroids in maternal and umbilical cord blood".
1087:"An experimental test of the fetal programming hypothesis: Can we reduce child ontogenetic vulnerability to psychopathology by decreasing maternal depression?"
780:"Maternal Cortisol Concentrations During Pregnancy and Sex-Specific Associations With Neonatal Amygdala Connectivity and Emerging Internalizing Behaviors"
37:, is the theory that environmental cues experienced during fetal development play a seminal role in determining health trajectories across the lifespan.
182:
function of physiological systems such as the hypothalamic-pituitary-adrenal axis and brain structure or connectivity (e.g., amygdala).
1139:"Fetal alcohol programming of hypothalamic proopiomelanocortin system by epigenetic mechanisms and later life vulnerability to stress"
247:
are well-known, and these may be even more apparent during pregnancy. Exposure to tobacco smoke during pregnancy, commonly known as
58:
These changes in the maternal environmental can be due to nutritional alteration, hormonal fluctuations or exposure to toxins.
729:"Maternal cortisol over the course of pregnancy and subsequent child amygdala and hippocampus volumes and affective problems"
1303:
100:
1197:"Prenatal alcohol exposure: foetal programming, the hypothalamic-pituitary-adrenal axis and sex differences in outcome"
72:
1323:
1328:
88:
1033:"Maternal smoking as a model for environmental epigenetic changes affecting birthweight and fetal programming"
1308:
80:
973:"Development and function of the human fetal adrenal cortex: a key component in the feto-placental unit"
778:
Graham AM, Rasmussen JM, Entringer S, Ben Ward E, Rudolph MD, Gilmore JH, et al. (January 2019).
509:"Stress, the Placenta, and Fetal Programming of Behavior: Genes' First Encounter With the Environment"
1333:
1338:
600:
Moisiadis VG, Matthews SG (July 2014). "Glucocorticoids and fetal programming part 2: Mechanisms".
1282:
1234:
852:
709:
625:
582:
433:
108:
872:"11ฮฒ-hydroxysteroid dehydrogenases: intracellular gate-keepers of tissue glucocorticoid action"
71:
In 1944โ45, the German blockade of the
Netherlands led to a lack of food supplies, causing the
1274:
1226:
1168:
1116:
1062:
1002:
950:
919:
Stirrat LI, Sengers BG, Norman JE, Homer NZ, Andrew R, Lewis RM, Reynolds RM (February 2018).
901:
844:
809:
760:
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666:
617:
574:
530:
482:
425:
384:
347:
298:
104:
76:
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836:
799:
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693:
656:
645:"Fetal Origins of Mental Health: The Developmental Origins of Health and Disease Hypothesis"
609:
564:
520:
472:
464:
415:
374:
337:
329:
290:
40:
Three main forms of programming that occur due to changes in the maternal environment are:
128:
318:"Antenatal maternal stress and long-term effects on child neurodevelopment: how and why?"
342:
317:
1221:
1196:
1163:
1138:
1111:
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1057:
1032:
997:
972:
945:
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871:
804:
779:
755:
728:
477:
452:
404:"Maternal obesity and the developmental programming of hypertension: a role for leptin"
161:
697:
294:
27:
Theory that suggests environment factors during fetal development affect disease risks
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333:
143:
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713:
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1238:
856:
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661:
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525:
508:
17:
468:
840:
147:
50:
887:
733:
Proceedings of the
National Academy of Sciences of the United States of America
1102:
921:"Transfer and Metabolism of Cortisol by the Isolated Perfused Human Placenta"
1048:
745:
1278:
1230:
1172:
1120:
1066:
1006:
954:
905:
848:
813:
764:
727:
Buss C, Davis EP, Shahbaba B, Pruessner JC, Head K, Sandman CA (May 2012).
705:
670:
621:
613:
578:
534:
486:
429:
388:
379:
366:
351:
302:
1270:
936:
988:
1154:
420:
403:
244:
84:
1304:
MRC Lifecourse
Epidemiology Unit page at the University of Southampton
966:
964:
569:
552:
1309:
Fetal
Programming page on the Centre for Fetal Programming's website.
132:
322:
Journal of Child
Psychology and Psychiatry, and Allied Disciplines
371:
International
Journal of Obesity and Related Metabolic Disorders
103:
began a research study on this topic. The Barker
Hypothesis, or
1195:
Weinberg J, Sliwowska JH, Lan N, Hellemans KG (April 2008).
1085:
Davis EP, Hankin BL, Swales DA, Hoffman MC (August 2018).
829:
The
Journal of Steroid Biochemistry and Molecular Biology
44:
Changes in development that lead to greater disease risk;
925:
The
Journal of Clinical Endocrinology and Metabolism
453:"Placental adaptive responses and fetal programming"
367:"Programming of obesity and cardiovascular disease"
551:Andersen SL, Olsen J, Laurberg P (December 2015).
402:Taylor PD, Samuelsson AM, Poston L (March 2014).
365:Remacle C, Bieswal F, Reusens B (November 2004).
1190:
1188:
1186:
1184:
1182:
1031:Suter MA, Anders AM, Aagaard KM (January 2013).
553:"Foetal programming by maternal thyroid disease"
1252:
1250:
1248:
1137:Bekdash R, Zhang C, Sarkar D (September 2014).
1132:
1130:
546:
544:
164:transfer that takes place across the placenta.
1143:Alcoholism: Clinical and Experimental Research
502:
500:
498:
496:
276:
274:
1080:
1078:
1076:
1026:
1024:
1022:
1020:
1018:
1016:
8:
146:, involving oxygen deprivation and death of
870:Chapman K, Holmes M, Seckl J (July 2013).
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1110:
1056:
996:
944:
895:
803:
754:
744:
660:
568:
524:
476:
419:
378:
341:
316:Talge NM, Neal C, Glover V (March 2007).
47:Genetic changes which alter disease risk;
190:Psychological stress and psychopathology
270:
643:O'Donnell KJ, Meaney MJ (April 2017).
7:
971:Ishimoto H, Jaffe RB (June 2011).
649:The American Journal of Psychiatry
513:The American Journal of Psychiatry
25:
698:10.1016/j.brainresrev.2007.06.013
295:10.1016/j.anireprosci.2012.01.015
252:impaired fetal lung development.
1213:10.1111/j.1365-2826.2008.01669.x
334:10.1111/j.1469-7610.2006.01714.x
1091:Development and Psychopathology
796:10.1016/j.biopsych.2018.06.023
662:10.1176/appi.ajp.2016.16020138
526:10.1176/appi.ajp.2016.16050502
1:
1201:Journal of Neuroendocrinology
602:Nature Reviews. Endocrinology
243:The negative consequences of
1037:Molecular Human Reproduction
469:10.1113/jphysiol.2006.104968
222:consequences for the fetus.
841:10.1016/j.jsbmb.2017.11.012
373:. 28 Suppl 3 (S3): S46-53.
283:Animal Reproduction Science
1355:
888:10.1152/physrev.00020.2012
1259:Hypertension in Pregnancy
1103:10.1017/S0954579418000470
457:The Journal of Physiology
89:non-communicable diseases
507:Hoffman MC (July 2016).
746:10.1073/pnas.1201295109
73:Dutch famine of 1944โ45
686:Brain Research Reviews
614:10.1038/nrendo.2014.74
557:Clinical Endocrinology
451:Myatt L (April 2006).
380:10.1038/sj.ijo.0802800
139:Insufficient nutrition
81:cardiovascular disease
1271:10.1081/prg-120013785
1049:10.1093/molehr/gas050
937:10.1210/jc.2017-02140
876:Physiological Reviews
784:Biological Psychiatry
989:10.1210/er.2010-0001
208:Psychological stress
67:Dutch famine 1944โ45
35:prenatal programming
148:trophoblastic cells
124:Excessive nutrition
1155:10.1111/acer.12497
421:10.1111/apha.12223
155:Hormonal influence
115:Nutritional status
109:metabolic syndrome
18:Foetal programming
977:Endocrine Reviews
570:10.1111/cen.12744
408:Acta Physiologica
105:Thrifty phenotype
95:Barker hypothesis
31:Fetal programming
16:(Redirected from
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968:
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33:, also known as
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1329:Human pregnancy
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1030:
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970:
969:
962:
918:
917:
913:
882:(3): 1139โ206.
869:
868:
864:
826:
825:
821:
777:
776:
772:
739:(20): E1312-9.
726:
725:
721:
683:
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678:
642:
641:
637:
599:
598:
594:
550:
549:
542:
506:
505:
494:
463:(Pt 1): 25โ30.
450:
449:
445:
401:
400:
396:
364:
363:
359:
328:(3โ4): 245โ61.
315:
314:
310:
280:
279:
272:
267:
258:
241:
228:
219:
210:
201:
192:
179:
170:
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129:Body mass index
126:
117:
97:
69:
64:
28:
23:
22:
15:
12:
11:
5:
1352:
1350:
1342:
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1336:
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1324:Women's health
1316:
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1312:
1311:
1306:
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1298:External links
1296:
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1244:
1178:
1149:(9): 2323โ30.
1126:
1097:(3): 787โ806.
1072:
1012:
960:
931:(2): 640โ648.
911:
862:
819:
790:(2): 172โ181.
770:
719:
676:
655:(4): 319โ328.
635:
592:
540:
492:
443:
394:
357:
308:
289:(3โ4): 193โ7.
269:
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224:
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162:glucocorticoid
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99:In the 1980s,
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1265:(2): 161โ74.
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1223:
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1207:(4): 470โ88.
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983:(3): 317โ55.
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734:
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692:(2): 586โ95.
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663:
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654:
650:
646:
639:
636:
631:
627:
623:
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608:(7): 403โ11.
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563:(6): 751โ8.
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519:(7): 655โ7.
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101:David Barker
98:
87:, and other
70:
57:
39:
34:
30:
29:
1334:Epigenetics
835:: 127โ134.
1339:Embryology
1318:Categories
1043:(1): 1โ6.
265:References
199:Depression
54:fulfilled.
51:Epigenetic
160:affected
1287:30016072
1279:12175444
1231:18266938
1173:25069392
1121:30068416
1067:23139402
1007:21051591
955:29161409
906:23899562
849:29191401
814:30122286
765:22529357
714:30865698
706:17716742
671:27838934
630:11475810
622:24863383
587:32873121
579:25682985
535:27363547
487:16469781
438:22295003
430:24433239
389:15543219
352:17355398
343:11016282
303:22341375
249:in utero
233:in utero
177:Cortisol
77:diabetes
1239:4574957
1222:8942074
1164:4177357
1112:7040571
1058:3521486
998:3365797
946:5800837
897:3962546
857:3705475
805:6632079
756:3356611
478:1779654
245:smoking
239:Smoking
226:Alcohol
168:Thyroid
85:obesity
62:History
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