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Developmental origins of health and disease

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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 diseases.[1][3][4] As well as physical human disease, the psychopathology of the fetus can also be predicted by epigenetic factors.[5]

Origin

The DOHaD approach originated in 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.[6][7][8] This 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 CDC also noticed how the nutritional habits of mothers can cause disease in their offspring. "During the Dutch Hunger Winter Famine (1944-1945)[9] mothers were not able to receive the proper nutrition needed to healthily carry a baby. The babies who were born during this time or directly after this time developed diseases such as heart disease, schizophrenia, and Type 2 diabetes. Researchers were able to determine decades after the famine that the babies born during this time 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.

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[10]) which had an extreme effect on pregnant women and their children. 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.[10] 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.

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.[6]

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.[11] The exact mechanism of action is unknown but is believe that it is epigenetic.[11]

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.[12]

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.[13]

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.[14] 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.[15]

A maternal high fat diet was used to help investigate how saturated fats cause unrestrained gestational weight gain and maternal obesity on offspring. [16]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 is 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.

Maternal intrauterine environment plays a vital role in development of the fetus and the conditions the offspring risk of certain metabolic diseases.

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.[17] However, being born in an urban area during this time was not associated with an increased risk of schizophrenia.[17][18] 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.[18]

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.[19]

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.[20] 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.[20]

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.[21] 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.[21]

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 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.
  7. ^ 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.
  8. ^ 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.
  9. ^ "What is Epigenetics?". Centers for Disease Control and Prevention. 2022-08-15. Retrieved 2023-02-06.
  10. ^ 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.
  11. ^ a b 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.
  12. ^ 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.
  13. ^ 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.
  14. ^ 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.
  15. ^ 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.
  16. ^ Kereliuk, Stephanie M.; Brawerman, Gabriel M.; Dolinsky, Vernon W. (2017-07-06). "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. ISSN 1422-0067.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  17. ^ a b Xu, Ming-Qing; Sun, Wen-Sheng; Liu, Ben-Xiu; Feng, Guo-Yin; Yu, Lan; Yang, Lawrence; He, Guang; Sham, Pak; Susser, Ezra; St Clair, David; He, Lin (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. ISSN 0586-7614. PMC 2669578. PMID 19155344.
  18. ^ a b He, Ping; Chen, Gong; Guo, Chao; Wen, Xu; Song, Xinming; Zheng, Xiaoying (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. ISSN 0924-9338.
  19. ^ Hoek, H. W.; Brown, A. S.; Susser, E. (1998-07-01). "The Dutch Famine and schizophrenia spectrum disorders". Social Psychiatry and Psychiatric Epidemiology. 33 (8): 373–379. doi:10.1007/s001270050068. ISSN 1433-9285.
  20. ^ a b Brown, Alan S.; Susser, Ezra S. (November 2008). "Prenatal nutritional deficiency and risk of adult schizophrenia". Schizophrenia Bulletin. 34 (6): 1054–1063. doi:10.1093/schbul/sbn096. ISSN 0586-7614. PMC 2632499. PMID 18682377.
  21. ^ a b Coussons-Read, Mary E. (May 3, 2013). "Effects of prenatal stress on pregnancy and human development: mechanisms and pathways". Retrieved April 6, 2023.
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