mom holding baby's hand

Developmental origins of health and disease

Originally hypothesized by David Barker, M.D., Ph.D., FRS, more than 30 years ago, the developmental origins of health and disease field of research, also known as DOHaD, has grown exponentially. Professor Barker based his work on observations that adult heart disease mortality in England was inversely correlated with low birth weight infants fifty years earlier. In other words, if a baby had low birth weight, that baby had a higher risk of heart disease later in life. While initially met with skepticism, a surge of basic animal studies demonstrated the ways in which low birth weight, and other environmental adversities, can compromise organ development and maturation of developing mammals. 

Epidemiologic data from multiple populations, time frames, and geographic areas  - as well as data from clinical and experimental studies - indicate that our earliest environments play a powerful role in predicting risk for many chronic diseases.

While the birth weight data have been replicated several times over in multiple countries, further research has led to the discovery of a number of additional pregnancy related factors that predict disease.

Dig deeper

Read a brief description of several issues impacted by developmental origins followed by a list of research articles to dig deeper into the science.

DOHaD Overview
Birthweight and the Placenta
 - Fun Facts About the Placenta
Developmental Trade-Offs
Toxic Stress
Maternal Phenotype
Breastfeeding and Early Nutrition
Food Insecurity
Heart Disease

Ten facts about chronic disease origins

  1. Babies who are born underweight, or shorter or thinner than average, are at higher risk for chronic diseases later in life. Such babies have made developmental "trade-offs" in the womb and will have enduring epigenetic modifications throughout life.
  2. It is now certain that the sensitivity to nutritional causes of disease is highest during a person’s early development.
  3. There are associations between maternal phenotype and an offspring's chronic disease risk in adult life.
  4. While paternal phenotype has not been studied, there are clear disease risks associated with malnutrition in fathers and grandfathers. These effects are caused by epigenetic modifications of sperm.
  5. The size and shape of the placenta is a powerful predictor of offspring disease risk.
  6. Disease risk is passed across many generations. The so-called 100 year effect is so named because chronic disease risk in elderly adults can be traced, in part, back ~100 years earlier when the egg from which they were derived was nourished in the ovary of their fetal mother.
  7. Disease risk is additive across generations. This is the likely explanation for the rising rates of diabetes and obesity in the USA. Americans are in the 3rd generation of eating high calorie, overly processed foods that contain few nutrients. Most Americans suffer from high calorie malnutrition.
  8. Toxic social stress during pregnancy affects the growth of the fetus, and sets the baby up for disease in later life.
  9. People carry disease risk according to the culture in which they found themselves during their developmental years. Thus social determinants of health and disease act through epigenetic mechanisms that place populations at risk for chronic health problems.
  10. Unlike inherited gene sequences, epigenetic mechanisms can be modified and early detrimental pathways can gradually be reversed. Thus, the current epidemic of chronic disease can be reversed if communities work together to improve the environments in which we live, through improved nutrition and stress reduction.