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=== Responses of Plasticity ===
=== Responses of Plasticity ===
There are two different types of plasticity responses when dealing with human development. The first is an immediate adaptive response. This response will alter the development that is needed to survive if there have been changes in the environment  (book).<ref>{{Cite book |last=F. |first=Gilbert, Scott |url=http://worldcat.org/oclc/909806681 |title=Ecological developmental biology : integrating epigenetics, medicine, and evolution |date=2009 |publisher=Sinauer Associates |isbn=978-0-87893-299-3 |oclc=909806681}}</ref> An example of this type of response would be when oxygen is deprivation which causes a change in blood flow that would help with the expense of less critical tissues. [[Predictive adaptive response]] (PAR) is the second type of plasticity response. PAR are cues that happened in early life development that cause phenotype development to change that are normally adapted to environmental cues in later life. <ref>{{Cite book |last=F. |first=Gilbert, Scott |url=http://worldcat.org/oclc/909806681 |title=Ecological developmental biology : integrating epigenetics, medicine, and evolution |date=2009 |publisher=Sinauer Associates |isbn=978-0-87893-299-3 |oclc=909806681}}</ref> This can be a benefit only when the predict6ed and actual postnatal environment match
There are two different types of plasticity responses when dealing with human development. The first is an immediate adaptive response. This response will alter the development that is needed to survive if there have been changes in the environment .<ref>{{Cite book |last=F. |first=Gilbert, Scott |url=http://worldcat.org/oclc/909806681 |title=Ecological developmental biology : integrating epigenetics, medicine, and evolution |date=2009 |publisher=Sinauer Associates |isbn=978-0-87893-299-3 |oclc=909806681}}</ref> An example of this type of response would be when oxygen is deprivation which causes a change in blood flow that would help with the expense of less critical tissues. [[Predictive adaptive response]] (PAR) is the second type of plasticity response. PAR are cues that happened in early life development that cause phenotype development to change that are normally adapted to environmental cues in later life. <ref>{{Cite book |last=F. |first=Gilbert, Scott |url=http://worldcat.org/oclc/909806681 |title=Ecological developmental biology : integrating epigenetics, medicine, and evolution |date=2009 |publisher=Sinauer Associates |isbn=978-0-87893-299-3 |oclc=909806681}}</ref> This can be a benefit only when the predict6ed and actual postnatal environment match


== Mechanisms ==
== Mechanisms ==

Revision as of 21:22, 13 April 2023

Developmental Origins of Health and Disease (abbreviated DOHaD) is an approach to medical research factors that can lead to the development of human diseases during early life development. These factors include the role of prenatal and perinatal exposure to environmental factors, such as undernutrition, stress, environmental chemical, etc.[1][2] This approach includes an emphasis on epigenetic causes of adult chronic non-communicable diseases.[1][3][4] As well as physical human disease, the psychopathology of the fetus can also be predicted by epigenetic factors.[5]

Origin

DOHaD has evolved into its modern understanding from several precursor concepts. In the 19th century the idea of "Maternal Impressions" was popular. Maternal impression is the idea that anything the mother did before giving birth could affect her offspring.[6] Our modern understanding of DOHaD was developed by several studies by David Barker and his colleagues, which showed a strong relationship between infant mortality rates from 1921 to 1925 and ischemic heart disease rates from 1968 to 1978. This led to the fetal origins hypothesis of the origins of adult diseases, which proposed that this relationship was caused by differences in early life nutrition, with a supporting theory that birthweight is connected to the development of chronic disease.[7]

During the Dutch Hunger Winter Famine (1944-1945)[8] mothers were not able to receive the proper nutrition needed to healthily carry a baby. The babies who were born during this time developed diseases (such as heart disease, schizophrenia, and Type 2 diabetes) at increased levels. Researchers were able to determine decades after the famine that the babies born during Dutch Famine had an increase in methylation in some genes and a decrease in methylation in other genes compared to their siblings who were not born during the famine. The methylation levels explain why these individuals were predisposed to certain diseases. Data collected from the Dutch Famine and similar events, such as the one at Leningrad, provided a reliable source of information to scientists studying DOHaD.[6][9][10]

These studies in turn led to greater interest in the roles of developmental plasticity and early life environmental exposures in adult disease. The World Congress on Fetal Origins of Adult Disease held two meetings – one in 2001 and the other in 2003 – summarizing then-new research in these areas. This congress later evolved into the International Society for Developmental Origins of Health and Disease.[1]

The Dutch hunger winter study

Between 1944-1945, in the western regions of the Netherlands and in Amsterdam, a famine broke out due to a railway strike and German control limiting supplies. The people of these countries were receiving extremely limited calories (around 400-800 a day[11]) which had an extreme effect on pregnant women and their children. Researchers began studying a cohort of middle-aged individuals who's mothers had been pregnant with them during the famine. The Dutch Hunger Winter study provided significant data to support the DOHaD. Results concluded that the women with low caloric and nutritional intake during pregnancy had children that had greater rates of obesity as opposed to those who were not exposed to famine.[11] This is conclusive with the DOHaD theory. The study goes on to investigate at what points in development did the DOHaD stand true. It is thought that exposure to famine in early gestational periods have a greater effect on the fetus, however, these theories are still under investigation.

Developmental plasticity

Thrifty phenotype hypothesis

The Thrifty Phenotype Hypothesis was proposed by C. Nicholas Hales and David Barker in a study published in 1992.[12] This hypothesis suggested that poor growth during the fetal and infant stages can cause a development of type 2 diabetes later in life. Hales and Barker suggested that this poor growth was due to maternal malnutrition which leads to low birth weight. As previously stated, low infant birth weight usually leads to an increased risk of obesity which if not acted on can lead to type 2 diabetes.[13]

The paper suggests that due to maternal malnutrition, infants can have lower birth weights. Since this is occurring during the plastic stage of development, this can cause the fetus to be "programmed" to conserve energy and store fat thus leading to lower metabolism. If there is a surplus of food during adulthood their body simply stores this abundance as more fat. This can then lead to not only diabetes but other metabolic diseases too.[14]

Responses of Plasticity

There are two different types of plasticity responses when dealing with human development. The first is an immediate adaptive response. This response will alter the development that is needed to survive if there have been changes in the environment .[15] An example of this type of response would be when oxygen is deprivation which causes a change in blood flow that would help with the expense of less critical tissues. Predictive adaptive response (PAR) is the second type of plasticity response. PAR are cues that happened in early life development that cause phenotype development to change that are normally adapted to environmental cues in later life. [16] This can be a benefit only when the predict6ed and actual postnatal environment match

Mechanisms

Epigenetic alterations of gene expression are closely related with developmental origins of health and disease hypothesis. DNA methylation, histone modifications and non-coding RNAs are altered by the environment in the womb and therefore go on to produce higher rates of adult disease later in life.[17]

DNA mdethylation

The process of DNA methylation is the most studied epigenetic response as it relates to the developmental origins of health and disease. The methylation of chief regulatory cytosines changes the DNA's hydrophobicity and begins to inhibit interactions with transcription factors responsible for the expression of the gene. Certain metabolic disorders, cancer and neurodegenerative disorders can be attributed to DNA methylation events.[17]

Histone modification

Non-coding RNAs

Examples

Cardiovascular disease

In his study done by David Barker, found a strong connection between poor prenatal environment and increased possibility of cardiovascular diseases in adults. He found a direct correlation between infant mortality in 1921-25 and mortality rates in 1968-78 because of heart diseases in England. In areas where pregnant mothers had to face poor nutritional state, their newborn children were at a high risk of death. If they survived the early ages of life, they had developed a higher risk of cardiovascular diseases.[7]

Studies on rats found that maternal nutrient restriction resulted in damage to the cardiac renin-angiotensin system (which regulates blood pressure and volume). Additionally, these studies have shown a decrease in the number of nephrons produced by the offspring of these mothers. These differences have been found to affect males and females differently, at least in the early stages.[6] The exact mechanism of action is unknown but is believe that it is epigenetic.[6]

Metabolic diseases

A study done at UC Irvine looked at the impact that maternal stress has on fetal development and overall fetal health. The researchers determined that the mothers' stress and adverse pregnancy outcomes (APOs) related to the length of gestation and growth of the fetus along with impacts on the endocrine and immune systems of the fetus.[18]

Early life influences, both prenatal and postnatal, have important effects on children later in life. It was determined that breastfed infants have significantly lower risks of obesity later in life than infants that were formula-fed.[19]

Nutrition and growth during the early years of life can be related to the growth of diseases in humans later in their lives. For example, a study done in Jamaica showed that the blood pressure of children was associated with the mother's hemoglobin levels and body fat during pregnancy.[20] Another example of this is shown in an article from the New England Journal of Medicine which takes place during the Dutch famine. This study concluded that those who were in utero at the time of the famine were at a greater risk of obesity, hypertension, and heart disease than those who were born before or after the famine.[21]

A maternal high fat diet was used to help investigate how saturated fats cause unrestrained gestational weight gain and maternal obesity on offspring.[22] When there is high fat feeding during pregnancy, there are effects on the maternal metabolism and body composition. Some of the effects are insulin resistance, increased circulating lipids, increased adiposity, and hyperinsulinemia (high insulin in blood). When fat intake was increased it starts to adjust consumption of other macronutrients in the diet, which will reduce the carbohydrate and protein consumption to match the increase of fatty acid.

During the Dutch famine Doctors found that under nutrition during gestation period related to reduced glucose tolerance and raised insulin concentrations between the ages 50 and 58. There was 120 minute glucose and insulin concentrations that were known to be higher in people that was exposed to the famine at any stage during fetal development than those who were not exposed.[13] The effect could be explained due to the lower birth rates of babies that were born during the famine and the low weight gain of their mothers. People that were born before the famine had a larger increase in glucose and insulin concentration. That was due to them experiencing starvation during the early stage of their life which might have impacted their postnatal growth pattern.

Autism Spectrum Disorder

Autism Spectrum Disorder (ASD) is a condition that typically manifests during the first three years of a person's life. It is a developmental disorder that impairs the brain's ability to develop the typical social and communication skills that are necessary for everyday life. People with ASD may experience difficulties with social interactions, verbal and nonverbal communication, and repetitive or restricted behaviors. The degree to which ASD affects an individual can vary widely, with some people experiencing mild symptoms while others may face more significant challenges.

The precise cause of ASD is still unknown, but it is believed that a combination of factors may contribute to its development. Research suggests that genetics may play a role, as ASD can run in families. In addition, certain medications taken during pregnancy may increase the risk of a child developing ASD. While some theories have been proposed, they have yet to be proven. For instance, some scientists believe that damage to a specific region of the brain, the amygdala, may be linked to ASD, while others are examining the possibility that a viral infection may trigger the disorder.

There has been some controversy regarding whether vaccines can cause ASD, but numerous studies have shown that there is no evidence of a link between vaccines and ASD. Major medical and government organizations have also confirmed this finding. The increase in ASD diagnoses in recent years may be attributed to better awareness and more comprehensive definitions of the disorder. Treatment for ASD involves a highly structured schedule of constructive activities that build on the child's interests and various techniques. It is important to avoid unproven treatments and seek advice from ASD specialists.[23]

Schizophrenia

Large-scale famines offer insights into the effects prenatal malnutrition has on developing fetuses. A team led by Dr. Ping He investigated this possible connection between prenatal malnutrition and schizophrenia by analyzing medical records of people born between 1960-1961. This study found that there was a two-fold risk for someone who was born in a rural area during this period of famine to later develop schizophrenia than someone who was born either before or after.[24] However, being born in an urban area during this time was not associated with an increased risk of schizophrenia.[24][25] This is probably due to factors that exacerbated the impact of the famine in rural areas such as grain procurement and lack of large-scale grain storage.[25]

Similar results have been found in studying the effects of the Dutch famine from 1944-1945. A study by Dr. Hoek compared the levels of schizophrenia born between August 15 - December 31, 1945 to those born after than famine had ended. This study found that those born during the time period were around 2 and a half times more likely to have schizophrenia than those born after the famine had ended.[26]

Famines may lead to an enhanced risk of schizophrenia because it deprives the developing fetus of key micronutrients. Some of the leading candidates are folate, essential fatty acids, retinoids, vitamin D, and iron.[27] Another leading theory that explains the connection between famine and schizophrenia is protein-calorie malnutrition. Protein-calorie malnutrition has been associated with increased dopamine and serotonin release and malfunctions in the hippocampus such as reduced dendritic branching and a lower cell count, which are also found in people with schizophrenia.[27]

Maternal stress

The effect stress has on expecting women may not only affect them, but their child as well. Studies have shown a link between child mental health and behavioral problems to maternal stress during pregnancy. Stress in the body leads to an increase in the cortisol levels. Maternal stress, therefore, exposes the fetus to high cortisol levels. These levels have been linked to neurological and behavioral regulation issues in the child later in life.[28] Severe stress has its impact on birth when it appears early in the pregnancy. From the Carmichael and Shaw study stated that during the time of conception if there is a high volume of stress there is an increased chance for a woman to deliver an offspring that may have heart defects.[28]

Throughout the course of recent year the UC Irvine Development Health and Disease program analyzed the connection between Behavioral, Biological, and Social processes in human pregnancy. The study focused more on the impact of stress during fetal development, birth outcomes, and health outcomes.[29]

Animal experiments where the animals (monkey or rat) was exposed to stressors during pregnancy such as immobilization, loud noises, etc demonstrated changes in their offspring. The animals that were prenatally stressed had delays in motor development, and adaptive behavior. Study on the Rhesus monkey demonstrated how postnatal effects can affect mothers that are exposed to stress during early pregnancy. Offspring that were prenatally stressed have higher basal blood glucocorticoid levels with reduced glucocorticoid receptors.

References

  1. ^ a b c Wadhwa PD, Buss C, Entringer S, Swanson JM (September 2009). "Developmental origins of health and disease: brief history of the approach and current focus on epigenetic mechanisms". Seminars in Reproductive Medicine. 27 (5): 358–368. doi:10.1055/s-0029-1237424. PMC 2862635. PMID 19711246.
  2. ^ Gillman MW (October 2005). "Developmental origins of health and disease". The New England Journal of Medicine. 353 (17): 1848–1850. doi:10.1056/NEJMe058187. PMC 1488726. PMID 16251542.
  3. ^ Godfrey KM, Lillycrop KA, Burdge GC, Gluckman PD, Hanson MA (May 2007). "Epigenetic mechanisms and the mismatch concept of the developmental origins of health and disease". Pediatric Research. 61 (5 Pt 2): 5R – 10R. doi:10.1203/pdr.0b013e318045bedb. PMID 17413851.
  4. ^ Heindel JJ, Balbus J, Birnbaum L, Brune-Drisse MN, Grandjean P, Gray K, et al. (October 2015). "Developmental Origins of Health and Disease: Integrating Environmental Influences". Endocrinology. 156 (10): 3416–3421. doi:10.1210/EN.2015-1394. PMC 4588819. PMID 26241070.
  5. ^ O'Donnell KJ, Meaney MJ (April 2017). "Fetal Origins of Mental Health: The Developmental Origins of Health and Disease Hypothesis". The American Journal of Psychiatry. 174 (4): 319–328. doi:10.1176/appi.ajp.2016.16020138. PMID 27838934.
  6. ^ a b c d Rosenfeld CS, ed. (2016). The Epigenome and Developmental Origins of Health and Disease. doi:10.1016/c2013-0-23131-7. ISBN 978-0-12-801383-0.
  7. ^ a b Arima Y, Fukuoka H (July 2020). "Developmental origins of health and disease theory in cardiology". Journal of Cardiology. 76 (1): 14–17. doi:10.1016/j.jjcc.2020.02.003. PMID 32115330. S2CID 211726894.
  8. ^ "What is Epigenetics?". Centers for Disease Control and Prevention. 2022-08-15. Retrieved 2023-02-06.
  9. ^ Almond D, Currie J (2011-08-01). "Killing Me Softly: The Fetal Origins Hypothesis". The Journal of Economic Perspectives. 25 (3): 153–172. doi:10.1257/jep.25.3.153. PMC 4140221. PMID 25152565.
  10. ^ Henriksen T, Clausen T (February 2002). "The fetal origins hypothesis: placental insufficiency and inheritance versus maternal malnutrition in well-nourished populations". Acta Obstetricia et Gynecologica Scandinavica. 81 (2): 112–114. doi:10.1034/j.1600-0412.2002.810204.x. PMID 11942899. S2CID 25255975.
  11. ^ a b Schulz LC (September 2010). "The Dutch Hunger Winter and the developmental origins of health and disease". Proceedings of the National Academy of Sciences of the United States of America. 107 (39): 16757–16758. doi:10.1073/pnas.1012911107. PMC 2947916. PMID 20855592.
  12. ^ Hales CN, Barker DJ (July 1992). "Type 2 (non-insulin-dependent) diabetes mellitus: the thrifty phenotype hypothesis". Diabetologia. 35 (7): 595–601. doi:10.1007/BF00400248. PMID 1644236. S2CID 35676219.
  13. ^ a b Roseboom T, de Rooij S, Painter R (August 2006). "The Dutch famine and its long-term consequences for adult health". Early Human Development. Special Abstract Issue. 82 (8): 485–491. doi:10.1016/j.earlhumdev.2006.07.001. PMID 16876341.
  14. ^ Hales CN, Barker DJ (2001-11-01). "The thrifty phenotype hypothesis". British Medical Bulletin. 60 (1): 5–20. doi:10.1093/bmb/60.1.5. PMID 11809615.
  15. ^ F., Gilbert, Scott (2009). Ecological developmental biology : integrating epigenetics, medicine, and evolution. Sinauer Associates. ISBN 978-0-87893-299-3. OCLC 909806681.{{cite book}}: CS1 maint: multiple names: authors list (link)
  16. ^ F., Gilbert, Scott (2009). Ecological developmental biology : integrating epigenetics, medicine, and evolution. Sinauer Associates. ISBN 978-0-87893-299-3. OCLC 909806681.{{cite book}}: CS1 maint: multiple names: authors list (link)
  17. ^ a b Goyal D, Limesand SW, Goyal R (July 2019). "Epigenetic responses and the developmental origins of health and disease". The Journal of Endocrinology. 242 (1): T105 – T119. doi:10.1530/JOE-19-0009. PMID 31091503. S2CID 155101302.
  18. ^ Entringer S, Buss C, Wadhwa PD (December 2010). "Prenatal stress and developmental programming of human health and disease risk: concepts and integration of empirical findings". Current Opinion in Endocrinology, Diabetes, and Obesity. 17 (6): 507–516. doi:10.1097/MED.0b013e3283405921. PMC 3124255. PMID 20962631.
  19. ^ Arenz S, Rückerl R, Koletzko B, von Kries R (October 2004). "Breast-feeding and childhood obesity--a systematic review". International Journal of Obesity and Related Metabolic Disorders. 28 (10): 1247–1256. doi:10.1038/sj.ijo.0802758. PMID 15314625. S2CID 25205202.
  20. ^ Godfrey KM, Forrester T, Barker DJ, Jackson AA, Landman JP, Hall JS, et al. (May 1994). "Maternal nutritional status in pregnancy and blood pressure in childhood". British Journal of Obstetrics and Gynaecology. 101 (5): 398–403. doi:10.1111/j.1471-0528.1994.tb11911.x. PMID 8018610. S2CID 3102246.
  21. ^ Ravelli GP, Stein ZA, Susser MW (August 1976). "Obesity in young men after famine exposure in utero and early infancy". The New England Journal of Medicine. 295 (7): 349–353. doi:10.1056/NEJM197608122950701. PMID 934222.
  22. ^ Kereliuk SM, Brawerman GM, Dolinsky VW (July 2017). "Maternal Macronutrient Consumption and the Developmental Origins of Metabolic Disease in the Offspring". International Journal of Molecular Sciences. 18 (7): 1451. doi:10.3390/ijms18071451. PMID 28684678.
  23. ^ "Autism spectrum disorder Information | Mount Sinai - New York". Mount Sinai Health System. Retrieved 2023-04-13.
  24. ^ a b Xu MQ, Sun WS, Liu BX, Feng GY, Yu L, Yang L, et al. (May 2009). "Prenatal malnutrition and adult schizophrenia: further evidence from the 1959-1961 Chinese famine". Schizophrenia Bulletin. 35 (3): 568–576. doi:10.1093/schbul/sbn168. PMC 2669578. PMID 19155344.
  25. ^ a b He P, Chen G, Guo C, Wen X, Song X, Zheng X (June 2018). "Long-term effect of prenatal exposure to malnutrition on risk of schizophrenia in adulthood: Evidence from the Chinese famine of 1959-1961". European Psychiatry. 51: 42–47. doi:10.1016/j.eurpsy.2018.01.003. PMID 29514118. S2CID 3804975.
  26. ^ Hoek HW, Brown AS, Susser E (August 1998). "The Dutch famine and schizophrenia spectrum disorders". Social Psychiatry and Psychiatric Epidemiology. 33 (8): 373–379. doi:10.1007/s001270050068. PMID 9708024. S2CID 30257704.
  27. ^ a b Brown AS, Susser ES (November 2008). "Prenatal nutritional deficiency and risk of adult schizophrenia". Schizophrenia Bulletin. 34 (6): 1054–1063. doi:10.1093/schbul/sbn096. PMC 2632499. PMID 18682377.
  28. ^ a b Coussons-Read ME (June 2013). "Effects of prenatal stress on pregnancy and human development: mechanisms and pathways". Obstetric Medicine. 6 (2): 52–57. doi:10.1177/1753495X12473751. PMC 5052760. PMID 27757157.
  29. ^ Entringer S, Buss C, Wadhwa PD (December 2010). "Prenatal stress and developmental programming of human health and disease risk: concepts and integration of empirical findings". Current Opinion in Endocrinology, Diabetes, and Obesity. 17 (6): 507–516. doi:10.1097/MED.0b013e3283405921. PMC 3124255. PMID 20962631.
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