Fetal programming: Difference between revisions
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| '''How we are ushered into life determines how we leave.''' | | '''How we are ushered into life determines how we leave.''' | ||
: — Nathanielsz PW. (1999) Life in the Womb: The Origins of Health and Disease, Ithaca, NY, Promethean Press. [quoted in<ref name=coles/>] | : — Nathanielsz PW. (1999) Life in the Womb: The Origins of Health and Disease, Ithaca, NY, Promethean Press.<ref name=nathanielsz1999/> [also, quoted in<ref name=coles/>] | ||
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'<b>Fetal programming</b>', an important component of fetal development, refers to the real-time adaptive anatomical and physiological responses a fetus makes to the intrauterine environmental conditions it experiences while it is living, growing, and organizing itself in its mother's womb. The responses differ in character depending upon whether the environmental condition is beneficial or unfavorable to the viability of the fetus, and depending upon the precise nature of the environmental condition experienced by the fetus. The character of the responses are adaptive for fetal viability, consisting in setting (programming) structural, physiological, and metabolic features of the fetus, hence in the structural, physiological, and metabolic features of the its body after birth. | |||
refers to | |||
Thus a fetus's intrauterine environment contributes to the programming of its growth and developing self-organization. When a fetus experiences a suboptimal condition, such as failure of maternal supply of adequate nutrition, the fetus will grow and develop abnormally, resulting in a newborn infant with abnormal structural, metabolic, and physiological characteristics that can increase its susceptibility to disease in later life.<ref name=godfrey2001/> <ref name=godfrey2001 group=Note/> | |||
Despite its immature state, a fetus constitutes a [[Life|living system]], a living complex adaptive system. Because it continually grows and self-organizes, it can respond with high sensitivity to environmental conditions; its structural, physiological and metabolic states have a great degree of plasticity. It adapts in real-time to adverse environmental conditions that threaten its viability. Those adaptations might include slowing its growth rate, reducing the number of cells in its organs, altering metabolic pathways, and altering its physiological responses to normal stimuli. If those adaptations serve to maintain the life of the fetus, they will persist throughout the fetus's development and result in an abnormally functioning newborn, persisting throughout childhood, adolescence, and adulthood. If the threatening intrauterine conditions no longer continue after birth, the child or adult may no longer have the ability to adapt to the newer conditions, and as a result, become susceptible to the maladaptations that constitute disease. A fetus adapted to survive to suboptimal nutrition may, in later life, be unable to adapt to conditions of enriched nutrition, responding abnormally.<ref name=godfrey2001/> <ref name=godfrey2001 group=Note/> | |||
In effect, the fetus's adaptations 'program' the person it becomes to the responses it makes to its post-natal environment, as an infant and throughout the remainder of its lifetime. | |||
The major, but not exclusive, environmental influences on the type and degree of fetal programming derive from the fetus's maternal connection via the [[placenta]],<ref name=godfrey02-02/> <ref name=2013barker01/> hence in part from the health status of the mother, both physical and mental. | |||
==Overview== | |||
In a 2004 review, pioneer of fetal programming phenomena, [http://www.southampton.ac.uk/medicine/about/staff/djb2.page David Barker], summarized the following as 'key teaching points':<ref name=barker2004/> | In a 2004 review, pioneer of fetal programming phenomena, [http://www.southampton.ac.uk/medicine/about/staff/djb2.page David Barker], summarized the following as 'key teaching points':<ref name=barker2004/> | ||
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*Low birthweight followed by rapid weight gain during infancy has been shown to further increase risk for disease. | *Low birthweight followed by rapid weight gain during infancy has been shown to further increase risk for disease. | ||
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In 2011, University of Columbia reseearchers, Zeltser and Leibel, emphasizing the role of the placenta, note:<ref name=zeltser2011/> | |||
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<font face="Gill Sans MT">Following on the seminal observations of Barker and associates ([cites:<ref name=hales2001/>]), maternal hormonal and nutrient environment has been systematically implicated in effects on the developing fetus that ultimately influence susceptibility to a wide range of metabolic, neurodevelopmental, and psychiatric diseases in adulthood ([cites:<ref name=twinn2001/> <ref name=bale2010/>]). There is a growing appreciation that perturbations in the maternal environment are conveyed to the fetus by changes in placental function ([cites:<ref name=jansson2007/>]).</font><ref name=zeltser2011/> | |||
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In a more recent review, psychoneuroendocrinologist [http://faculty.uci.edu/profile.cfm?faculty_id=5845 Sonja Entringer] describes fetal programming this way: | In a more recent review, psychoneuroendocrinologist [http://faculty.uci.edu/profile.cfm?faculty_id=5845 Sonja Entringer] describes fetal programming this way: | ||
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Focusing on pathophysiology, fetal programming also goes by the name, 'fetal origins of adult disease'. From a broader perspective than the pathophysiological, however, the fetus also responds to beneficial intrauterine environments, adapting its metabolism, physiology, and structure to health and lower susceptibility to disease in later life. For one example, in the studies of Barker mentioned above, the babies born with higher birth-weight due to more optimal maternal nutrition had significantly lower risk of developing coronary heart disease than did the lower birth-weight babies.<ref name=barker2004/> | Focusing on pathophysiology, fetal programming also goes by the name, 'fetal origins of adult disease'. From a broader perspective than the pathophysiological, however, the fetus also responds to beneficial intrauterine environments, adapting its metabolism, physiology, and structure to health and lower susceptibility to disease in later life. For one example, in the studies of Barker mentioned above, the babies born with higher birth-weight due to more optimal maternal nutrition had significantly lower risk of developing coronary heart disease than did the lower birth-weight babies.<ref name=barker2004/> | ||
Recognition of fetal programming led to recognition that the earliest stages of development, including infancy, could respond to environmental conditions in ways that influenced health status in later life, which, in turn, led to a new discipline, ''The Developmental Origins of Health and Disease''.<ref name=gillman2005/> <ref name=gillman2005 group=Note/> | Recognition of fetal programming led to recognition that the earliest stages of development, including infancy, could respond to environmental conditions in ways that influenced health status in later life, which, in turn, led to a new discipline, ''The Developmental Origins of Health and Disease''.<ref name=gillman2005/> <ref name=gillman2005 group=Note/> <ref name=barker2004/> | ||
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==Postnatal disease types sensitive to fetal programming== | |||
===Cardiovascular disease=== | |||
===Metabolic disease=== | |||
===Neurodevelopmental disease=== | |||
===Psychiatric disease=== | |||
==Adverse types of fetal environmental conditions promoting fetal programming== | |||
===Maternal nutritional abnormalities=== | |||
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| '''You are what you eat, and so are your children.'''<ref name=vanhees13/> | |||
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===Maternal psychosocial stress=== | |||
===Paternal genetic abnormalities=== | |||
===Maternal hormonal abnormalities=== | |||
==Examples of fetal programming in humans== | ==Examples of fetal programming in humans== | ||
In 1986, David Barker and Clive Osmond reported on their studies of the relationships among infant mortality, childhood nutrition, and adult ischemic heart disease in England and Wales. By geographical regions, past infant mortality rates, highest where poverty was greatest, associated positively with present occurrences of ischemic heart disease, whereas increasing heart disease presently associated with increasing prosperity. From their analysis the investigators suggested that “<i>poor nutrition in early life increases susceptibility to the effects of an affluent diet</i>”.<ref name=barker1986/> | In 1986, David Barker and Clive Osmond reported on their studies of the relationships among infant mortality, childhood nutrition, and adult ischemic heart disease in England and Wales. By geographical regions, past infant mortality rates, highest where poverty was greatest, associated positively with present occurrences of ischemic heart disease, whereas increasing heart disease presently associated with increasing prosperity. From their analysis the investigators suggested that “<i>poor nutrition in early life increases susceptibility to the effects of an affluent diet</i>”.<ref name=barker1986/> | ||
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==References cited in text== | ==References cited in text== | ||
{{reflist3 test|refs= | {{reflist3 test|refs= | ||
<ref name=2013barker01> | |||
Barker DJ, Thornburg KL. (2013)[http://dx.doi.org/10.1016/j.placenta.2013.07.063 Placental programming of chronic diseases, cancer and lifespan: A review]. ''Placenta'' 34:841-5. | |||
</ref> | |||
<ref name=barker1986> | <ref name=barker1986> | ||
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<ref name=barouki2012> | <ref name=barouki2012> | ||
Barouki R, Gluckman PD, Grandjean P, et al. (2012) [http://dx.doi.org/10.1186/1476-069X-11-42 Developmental origins of noncommunicable disease: implications for research and public health]. ''Environ Health'' 11:42. | Barouki R, Gluckman PD, Grandjean P, et al. (2012) [http://dx.doi.org/10.1186/1476-069X-11-42 Developmental origins of noncommunicable disease: implications for research and public health]. ''Environ Health'' 11:42. | ||
</ref> | |||
<ref name=coles> | |||
Coles CD. [http://www.psychiatry.emory.edu/PROGRAMS/GADrug/Feature%20Articles/Fetal%20Programming_Coles_rev.pdf What is “Fetal Programming”?] | Clicking title opens PDF file. | |||
</ref> | </ref> | ||
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<ref name=gillman2005> | <ref name=gillman2005> | ||
Gillman MW. (2005) [http://dx.doi.org/10.1056/NEJMe058187 Developmental Origins of Health and Disease]. ‘’N Engl J Med.’’ October 27; 353(17): 1848–1850. | Gillman MW. (2005) [http://dx.doi.org/10.1056/NEJMe058187 Developmental Origins of Health and Disease]. ‘’N Engl J Med.’’ October 27; 353(17): 1848–1850. | Read excerpt in [http://en.citizendium.org/wiki/Fetal_programming#Notes Notes] section. | ||
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<ref name=godfrey2001> | |||
Godfrey KM, Barker DJP. (2001) [http://dx.doi.org/10.1079/PHN2001145 Fetal programming and adult health]. ''Public Health Nutrition'' 4(2B):611-624. | Read Abstract in [http://en.citizendium.org/wiki/Fetal_programming#Notes Notes] section. | |||
</ref> | |||
<ref name= | <ref name=godfrey02-02> | ||
Godfrey KM | Godfrey KM. (2002) [http://doi.dx.org/10.1053/plac.2002.0773 The Role of the Placenta in Fetal Programming—A Review]. ''Placenta'' 23, Supplement A, Trophoblast Research, 16, S20–S27. | available online [http://www.idealibrary.com here]. | ||
</ref> | |||
<ref name=nathanielsz1999> | |||
Nathanielsz PW. (1999) ''Life in the Womb: The Origin of Health and Disease''. Promethean Press. | |||
</ref> | </ref> | ||
<ref name=raikkonen2013> | <ref name=raikkonen2013> | ||
Katri Raikkonen, Eero Kajantie, Anu-Katriina Pesonen, Kati Heinonen, Hanna Alastalo, Jukka T. Leskinen, Kai Nyman, Markus Henriksson, Jari Lahti, Marius Lahti, Riikka Pyhälä, Soile Tuovinen, Clive Osmond, David J. P. Barker,Johan G. Eriksson. (2013) [http://dx.doi.org/10.1371/journal.pone.0054707 Early Life Origins Cognitive Decline: Findings in Elderly Men in the Helsinki Birth Cohort Study]. ''PLoS ONE'' 8(1): e54707. | Katri Raikkonen, Eero Kajantie, Anu-Katriina Pesonen, Kati Heinonen, Hanna Alastalo, Jukka T. Leskinen, Kai Nyman, Markus Henriksson, Jari Lahti, Marius Lahti, Riikka Pyhälä, Soile Tuovinen, Clive Osmond, David J. P. Barker,Johan G. Eriksson. (2013) [http://dx.doi.org/10.1371/journal.pone.0054707 Early Life Origins Cognitive Decline: Findings in Elderly Men in the Helsinki Birth Cohort Study]. ''PLoS ONE'' 8(1): e54707. | ||
</ref> | |||
<ref name=zeltser2011> | |||
Zeltser LM, Leibel RL. (2011) [http://dx.doi.org/10.1073/pnas.1112239108 Roles of the placenta in fetal brain development]. PNAS 108:15667-15668. | |||
</ref> | |||
<ref name=hales2001> | |||
Hales CN, Barker DJ (2001) The thrifty phenotype hypothesis. Br Med Bull 60:5–20. | |||
</ref> | |||
<ref name=twinn2001> | |||
Fernandez-Twinn DS, Ozanne SE (2010) Early life nutrition and metabolic programming. Ann N Y Acad Sci 1212:78–96. | |||
</ref> | |||
<ref name=bale2010> | |||
Bale TL, et al. (2010) Early life programming and neurodevelopmental disorders. Biol Psychiatry 68:314–319. | |||
</ref> | |||
<ref name=jansson2007> | |||
Jansson T, Powell TL (2007) Role of the placenta in fetal programming: Underlying mechanisms and potential interventional approaches. Clin Sci (Lond) 113:1–13. | |||
</ref> | |||
<ref name=vanhees13> | |||
Vanhees K, Vonhogen IG, van Schooten FJ, Godschalk RW. (2013) [[http://dx.doi.org/10.1007/s00018-013-1427-9 You are what you eat, and so are your children: the impact of micronutrients on the epigenetic programming of offspring]. ''Cell Mol Life Sci''. 2013 Jul 27. [Epub ahead of print]. | |||
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Latest revision as of 07:00, 16 August 2024
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How we are ushered into life determines how we leave. |
'Fetal programming', an important component of fetal development, refers to the real-time adaptive anatomical and physiological responses a fetus makes to the intrauterine environmental conditions it experiences while it is living, growing, and organizing itself in its mother's womb. The responses differ in character depending upon whether the environmental condition is beneficial or unfavorable to the viability of the fetus, and depending upon the precise nature of the environmental condition experienced by the fetus. The character of the responses are adaptive for fetal viability, consisting in setting (programming) structural, physiological, and metabolic features of the fetus, hence in the structural, physiological, and metabolic features of the its body after birth.
Thus a fetus's intrauterine environment contributes to the programming of its growth and developing self-organization. When a fetus experiences a suboptimal condition, such as failure of maternal supply of adequate nutrition, the fetus will grow and develop abnormally, resulting in a newborn infant with abnormal structural, metabolic, and physiological characteristics that can increase its susceptibility to disease in later life.[3] [Note 1]
Despite its immature state, a fetus constitutes a living system, a living complex adaptive system. Because it continually grows and self-organizes, it can respond with high sensitivity to environmental conditions; its structural, physiological and metabolic states have a great degree of plasticity. It adapts in real-time to adverse environmental conditions that threaten its viability. Those adaptations might include slowing its growth rate, reducing the number of cells in its organs, altering metabolic pathways, and altering its physiological responses to normal stimuli. If those adaptations serve to maintain the life of the fetus, they will persist throughout the fetus's development and result in an abnormally functioning newborn, persisting throughout childhood, adolescence, and adulthood. If the threatening intrauterine conditions no longer continue after birth, the child or adult may no longer have the ability to adapt to the newer conditions, and as a result, become susceptible to the maladaptations that constitute disease. A fetus adapted to survive to suboptimal nutrition may, in later life, be unable to adapt to conditions of enriched nutrition, responding abnormally.[3] [Note 1]
In effect, the fetus's adaptations 'program' the person it becomes to the responses it makes to its post-natal environment, as an infant and throughout the remainder of its lifetime.
The major, but not exclusive, environmental influences on the type and degree of fetal programming derive from the fetus's maternal connection via the placenta,[4] [5] hence in part from the health status of the mother, both physical and mental.
Overview
In a 2004 review, pioneer of fetal programming phenomena, David Barker, summarized the following as 'key teaching points':[6]
|
In 2011, University of Columbia reseearchers, Zeltser and Leibel, emphasizing the role of the placenta, note:[7]
Following on the seminal observations of Barker and associates ([cites:[8]]), maternal hormonal and nutrient environment has been systematically implicated in effects on the developing fetus that ultimately influence susceptibility to a wide range of metabolic, neurodevelopmental, and psychiatric diseases in adulthood ([cites:[9] [10]]). There is a growing appreciation that perturbations in the maternal environment are conveyed to the fetus by changes in placental function ([cites:[11]]).[7] |
In a more recent review, psychoneuroendocrinologist Sonja Entringer describes fetal programming this way:
Substantial evidence in humans and animals suggests that conditions during intrauterine life play a major role in shaping not only all aspects of fetal development and birth outcomes but also subsequent newborn, child, and adult health outcomes and susceptibility for many of the complex, common disorders that confer the major burden of disease in society (i.e., the concept of fetal, or developmental, origins of health and disease risk) [cites: [12] [13]].[14] |
Focusing on pathophysiology, fetal programming also goes by the name, 'fetal origins of adult disease'. From a broader perspective than the pathophysiological, however, the fetus also responds to beneficial intrauterine environments, adapting its metabolism, physiology, and structure to health and lower susceptibility to disease in later life. For one example, in the studies of Barker mentioned above, the babies born with higher birth-weight due to more optimal maternal nutrition had significantly lower risk of developing coronary heart disease than did the lower birth-weight babies.[6]
Recognition of fetal programming led to recognition that the earliest stages of development, including infancy, could respond to environmental conditions in ways that influenced health status in later life, which, in turn, led to a new discipline, The Developmental Origins of Health and Disease.[15] [Note 3] [6]
Postnatal disease types sensitive to fetal programmingCardiovascular diseaseMetabolic diseaseNeurodevelopmental diseasePsychiatric diseaseAdverse types of fetal environmental conditions promoting fetal programmingMaternal nutritional abnormalities
Maternal psychosocial stressPaternal genetic abnormalitiesMaternal hormonal abnormalitiesExamples of fetal programming in humansIn 1986, David Barker and Clive Osmond reported on their studies of the relationships among infant mortality, childhood nutrition, and adult ischemic heart disease in England and Wales. By geographical regions, past infant mortality rates, highest where poverty was greatest, associated positively with present occurrences of ischemic heart disease, whereas increasing heart disease presently associated with increasing prosperity. From their analysis the investigators suggested that “poor nutrition in early life increases susceptibility to the effects of an affluent diet”.[17] Fetal programming applies also to age-related cognitive decline. A long term follow-up study in men by Katri Raikkonen and colleagues showed that lower cognitive ability at mean age 67.9 years associated with lower birth-weight, birth-length, and birth-head-circumference.[18] Similarly, cognitive decline after age 20 years associated with those lower measures of intrauterine physical growth. The investigator found that in "predicting resilience to age related cognitive decline, the period before birth seems to be more critical" compared to the period of infancy. Examples of fetal programming in non-human animalsIn sheep, suboptimal maternal nutrition coincident with early fetal kidney development results in enhanced renal lipid deposition following juvenile obesity and could accelerate the onset of the adverse metabolic, rather than cardiovascular, symptoms accompanying the metabolic syndrome.[19] Fetal programming response to maternal stress
Reverse fetal programming: fetal programming of motherHolding ref: http://www.sciencedaily.com/releases/2012/06/120606155802.htm References cited in text
Notes
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