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Fetal origins hypothesis

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Developmental origins of health and disease hypothesis

The developmental origins of health and disease hypothesis (also known as the fetal origins hypothesis) proposes that the period of gestation has significant impacts on the developmental health and wellbeing outcomes for an individual ranging from infancy to adulthood. The effects of fetal origin are marked by three characteristics: latency, wherein effects may not be apparent until much later in life; persistency, whereby conditions resulting from a fetal effect continue to exist for a given individual; and genetic programming, which describes the 'switching on' of a specific gene due to prenatal environment.[1] Research in the areas of economics, epidemiology, and epigenetics offer support for the hypothesis.[2]

Background

The fetus was once believed to be a "perfect parasite,"[3] immune to harmful environmental toxins passed from the mother via the placenta. Stemming from this belief, pregnant women of the early to mid 20th century freely drank alcohol, ingested medications, smoked cigarettes, and were largely ignorant of any nutritional needs for a developing fetus. This easy going attitude about pregnancy was challenged, however, by findings relating substances ingested by a mother to tragic outcomes for a fetus. The birth defects crisis due to the medication thalidomide in the 1960s, where thousands of children were born with defects ranging from brain damage to truncated and missing arms and legs is an example of how a seemingly miracle medication (supposed to prevent morning sickness) instead had disastrous consequences. [4] Similarly, in 1971, a drug known as DES, diethylstilbestrol, when taken by pregnant women, was found to be causing an incredibly rare vaginal cancer known as clear-cell aadenocarcinoma in young girls when the cancer was traditionally only found to affect those of post-menopausal age.[2] This finding, in particular, demonstrates that events occurring during gestation are capable of impacting future health into adulthood. As perhaps the most well-known fetal risk, It wasn't until 1973 that fetal alcohol syndrome was first formally diagnosed, and not until 1989 that the United States government began requiring warning labels directed at pregnant women to be in place on all alcoholic beverages for sale.[2] While the risks associated with certain medications have been well documented during pregnancy, the fetal origins hypothesis goes beyond medical substances to expand upon the effects of maternal stress, obesity, influenza, nutrition, and pollution on a developing fetus.[2]

Barker's Hypothesis

The epidemiologist Dr. David Barker was the earliest proponent of the theory of fetal origins of adult disease, prompting the theory to be denoted as "Barker's hypothesis". In 1986, Dr. Barker published findings proposing a direct link between prenatal nutrition and late-onset coronary heart disease.[5] He had noticed that the poorest areas of England were the same areas with the highest rates of heart disease, unearthing the predictive relationship between low birth weight and adult disease. His findings were met with criticism, mainly because at the time heart disease was considered to be predominantly determined by lifestyle and genetic factors. Since Barker's initial findings, the results have been replicated in diverse populations of Europe, Asia, North American, Africa, and Australia.[2] In explanation of such findings, Barker suggests that fetuses learn to adapt to the environment they expect to enter into once outside of the womb. Essentially, all transmissions entering the placenta act as "postcards" giving the fetus clues as to the outside world, preparing its physiology appropriately.[2]

Thrifty Phenotype

The thrifty phenotype hypothesis proposes that a low availability of nutrients during the prenatal stage followed by an improvement in nutritional availability in early childhood causes an increase risk of metabolic disorders, including Type II Diabetes, as a result of permanent changes in the metabolic processing of glucose-insulin determined in utero.[6]. This predominantly affects poor communities, where maternal malnutrition may be rampant, in turn causing fetuses to be biologically programmed to expect sparse nutritional environments. But, once in the world, the readily accessible processed foods consumed are unable to be processed efficiently by individuals who had their metabolic systems pre-set to expect scarcity. This difference between expected nutritional deficits and actual food surplus results in obesity and eventually Type II Diabetes.[7] Janet Rich-Edwards, an epedemiologist at Harvard Medical School, initially set out to disprove the fetal origins theory with her database of over 100,000 nurses. Instead, she found that the results hold: a strong relationship exists between low birth weight and later coronary heart disease and stroke.[8]

Research Findings

Economic support

Epidemiological support

Epidemiological research, or the study of the health and disease patterns of certain populations, allow for controls not possible in other research avenues. When a significant situation, disaster, or event occurs across a given population, it can be assumed that the entire population is affected, thus generalizing findings across all demographics in a given group. Certain historical events provide epidemiological support for the developmental origins of health and disease, including the Dutch Hunger Winter, the influenza pandemic of 1918, and the practice of Ramadan.

The Hunger Winter

Pollution

Pollution may affect the health of the mother, or cross over the placenta and enter the developing fetus. Beate Ritz, a professor at UCLA, found significantly higher rates of heart malformations and valve defects in the children born to women living in highly polluted areas of Los Angeles.

Maternal Stress

Maternal stress has been linked to a number of negative outcomes for the developing fetus. Pregnant women who firsthand experienced the devastation of the World Trade Center attack on September 11, 2001 were studied to observe the effects of PTSD (post-traumatic stress disorder) on the child's future health. Of the women studied, those who developed PTSD following the attacks had lower basal cortisol levels than a control group. Their children, also, had lower basal cortisol levels than those not exposed to extreme prenatal stressors. The finding was strongest for the women who were in their third trimester during 9/11. 9/11 is also correlated with lower birth weights of children born to women with Arabic sounding names following the attacks; this could possibly be due to fear of retaliation or stereotyping associations with the attackers.[9] Based on the findings that there was a trimester distinction in strength, conclusions can be drawn that the development of a vulnerability to stress was due at least in part to environment in utero.[2] Stress has also been linked to preterm birth, as shown by research studies conducted following the Tarapaca, Chile earthquake in 2005, as well as the Northridge, California earthquake in 1994.[10] Similar findings have been replicated for stressful life experiences and fetal outcomes in the Hurricane Katrina population of 2005. Women in New Orleans at the time who reported enduring multiple severe disaster experiences also had a significantly higher chance of delivering early or low birth weight children.[11] Experiencing loss during pregnancy also influences postnatal outcomes. Women who experienced the death of a close family member, friend, or spouse, or were pregnant during a wartime conflict, were more likely to have children prematurely, and the children of these women were significantly more likely than the general population to suffer from schizophrenia in adulthood.[9][12]Besides birth weight, mental health, and reduced cortisol levels, effects of stress during pregnancy have also been linked to impaired cognitive development in children as seen in the maternal population exposed to a severe snowstorm in Canada.[13] Women who experienced the most stressful storm related events had children with detriments in cognitive, language, behavioral, and attention outcomes.[13] Shockingly, the poorer performance by these children has persisted until the age of ten. [13] Even job related stress has been found to be associated with low birth weight and preterm birth. Working long hours, having temporarily employment, or reporting physically demanding job tasks showed "significant and strong" associations with poorer later birth outcomes.[14]

Epigenetics support

Epigenetics refers to the study of the behavior of genes, and how gene expression can be altered by the environment without changes made in DNA. This is believed to be particularly possible during prenatal development, and both stress and diet have been known to causes changes to a fetus.[15] Findings linking maternal exposure to pollution with poor health outcomes for children are possibly linked to the altering of gene expression.[2] Additionally, studies focusing on maternal weight show gene altering may be occurring. Women who are overweight at the time of pregnancy have children that are more likely to be overweight themselves. This could be due to the genetic heritability of genes related to obesity. But, siblings born to these same women after they had weight reduction surgery were no more likely to be overweight than the rest of the general population. The metabolic nature of the children was completely different, despite being born to the same mother, supporting the idea that the gestational environment strongly influences future outcomes. [2]

"The long-vaunted distinction between nature and nurture is therefore “outdated and unhelpful”, says Janet Currie of Princeton University’s Centre for Health and Child Wellbeing. Poor nurture during pregnancy can worsen the hand that nature has dealt."[16]

Cancer, diabetes, mental illness, cognitive decline, osteoporosis, arthritis, obesity have all been linked with fetal origins. [2]

Criticism of theory

Criticism of the developmental origins of health and disease can be aimed at the limitations of the research. Confounds abound due to the intertwined nature of environment before and after birth, as well as the correlational factors associated with poverty outcomes. Additionally, the use of historical and longitudinal data raises the question of reliability. [17] Also, some critics maintain that despite the compelling relationship documented between low birth weight and later disease, it is too soon to begin to mandate interventions aimed at increasing birth weight. Such interventions could instead have increased negative effects,[18] until the specific mechanisms and processes are more deeply understood by which birth and early childhood weight determine development. As stated in "Killing Me Softly: The Fetal Origins Hypothesis", "Such pre-emptive targeting would constitute a radical departure from current policies that steer nearly all healthcare resources to the sick, i.e. the “pound of cure” approach. That said, the existing evidence is not sufficient to allow us to rank the cost-effectiveness of interventions targeted at women against more traditional interventions targeted at children, adolescents, or adults. For example, broadening the target population to women who might get pregnant would reduce the set of policies which are cost effective."[1]

Implications for intervention

The implications of the developmental origins of health and disease hypothesis are akin to changing the focus of public health intervention from childhood to in utero. Because the demonstrated effects range from dramatic to subtle in the wide spread areas of educational achievement, emotional stability, career trajectory, life expectancy, disease prognosis, and psychological disorders, interventions addressing the gestational period could potentially have significant impact on individual and societal levels. Proposed and in effect interventions include the following:

  • Address poverty and nutritional needs of pregnant women[7]
  • Pre-natal iodine supplements[16]
  • The federal food stamp program
  • The Supplemental Feeding Program for Women, Infants, and Children (WIC)

Future research

See also

References

  1. ^ a b Almond, Douglas; Currie, Janet (2011). "Killing Me Softly: The Fetal Origins Hypothesis". The Journal of Economic Perspectives. 25 (3): 153–172. {{cite journal}}: |access-date= requires |url= (help)
  2. ^ a b c d e f g h i j Paul, Annie Murphy (2011). Origins : how the nine months before birth shape the rest of our lives (1st Free Press trade pbk. ed. ed.). New York: Free Press. ISBN 978-0743296632. {{cite book}}: |edition= has extra text (help)
  3. ^ al.], Zena Stein ... [et (1975). Famine and human development : the Dutch hunger winter of 1944-1945. New York: Oxford University Press. ISBN 978-0195018110.
  4. ^ Fintel, Bara; Samaras, Athena T.; Carias, Edson. "THE THALIDOMIDE TRAGEDY: LESSONS FOR DRUG SAFETY AND REGULATION". Helix. Northwestern University. Retrieved 12 November 2015.
  5. ^ Barker, David; Osmond, C. (1986). "Infant mortality, childhood nutrition, and ischaemic heart disease in England and Wales". Lancet: 1077–1081. {{cite journal}}: |access-date= requires |url= (help)
  6. ^ Hales, C Nicholas; Barker, David J P (2001). "The thrifty phenotype hypothesis: Type 2 diabetes". British Medical Bulletin. 60 (1): 5-20.
  7. ^ a b "Thrifty Phenotype Hypothesis: Curing Poverty Leads To Obesity And Diabetes". Science2.0. Retrieved 12 November 2015.
  8. ^ Hall, Stephen S. "Small and Thin: The controversy over the fetal origins of adult health". The New Yorker. Retrieved 12 November 2015.
  9. ^ a b Velasquez-Manoff, Moises. "Should You Bring Your Unborn Baby to Work?". The Atlantic. The Atlantic Magazine. Retrieved 12 November 2015.
  10. ^ Madrigal, Alexis. "Big Earthquakes Cause Premature Births". Wired. Retrieved 12 November 2015.
  11. ^ Lundy, Karen Saucier; Janes, Sharyn (2010). Community Health Nursing (2nd ed.). Jones & Bartlett Learning.
  12. ^ "Pregnancy Stress, Schizophrenia Linked?". WebMD. Retrieved 12 November 2015.
  13. ^ a b c "DNA signature in Ice Storm babies: Prenatal maternal stress exposure to natural disasters predicts epigenetic profile of offspring". ScienceDaily.com. Retrieved 13 November 2015.
  14. ^ Collingwood, Jane. "Work Stress Linked to Low Birthweight and Preterm Birth". Psych Central. Retrieved 13 November 2015.
  15. ^ "Epigenetics". Begin Before Birth: What happens in the womb can last a lifetime. Retrieved 12 November 2015.
  16. ^ a b "Unequal beginnings". The Economist. 4 April 2015. Retrieved 12 November 2015.
  17. ^ Delisle, Hélène. "Programming of chronic disease by impaired fetal nutrition" (PDF). World Health Organization. Retrieved 12 November 2015.
  18. ^ Eriksson, Johan G. (12 May 2005). "The fetal origins hypothesis—10 years on". The BMJ (330): 1096.
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