Recent studies suggest that coronary heart disease may originate in utero. Babies born small for their gestational age have higher risks of coronary heart disease, stroke, hypertension, and diabetes in adulthood. These findings are not limited to babies with intrauterine growth restriction defined by low birth weight but also apply to babies of average or above average weight. Some are small relative to their placental size, others are thin at birth or short relative to their head size, and some have below average infant weight gain despite average birth weight. Programming theory suggests that poor fetal and infant growth can permanently affect the structure and function of organs and tissues, increasing the risk of cardiovascular disease and diabetes. This concept is supported by animal studies showing that early life nutrition and other factors can influence long-term health. Geographical studies in England and Wales showed that differences in coronary heart disease mortality rates correlated with neonatal mortality rates in the early 20th century, indicating that poor maternal nutrition and low birth weight were linked to higher disease rates. Long-term studies in Hertfordshire, Preston, and Sheffield have shown that birth weight and infant weight are associated with adult blood pressure, glucose tolerance, and other cardiovascular risk factors. For example, men with lower birth weights had higher rates of impaired glucose tolerance and non-insulin dependent diabetes. These associations are strong and graded, with higher early weight linked to lower risk factors. Different risk factors are related to different patterns of early growth. Blood pressure is linked to birth weight, while cholesterol levels are influenced by infant feeding methods. Maternal undernutrition is suspected as a key factor in slowing fetal growth and programming coronary heart disease. Studies show that maternal undernutrition still affects fetal growth today, as evidenced by high rates of pregnancy anaemia. Research into the fetal origins of coronary heart disease is ongoing, with findings suggesting that early growth constraints can lead to long-term cardiovascular and metabolic issues. These findings are supported by animal studies and are attributed to programming rather than adult environmental factors. Future research is expected to provide more insights into the mechanisms underlying these effects.Recent studies suggest that coronary heart disease may originate in utero. Babies born small for their gestational age have higher risks of coronary heart disease, stroke, hypertension, and diabetes in adulthood. These findings are not limited to babies with intrauterine growth restriction defined by low birth weight but also apply to babies of average or above average weight. Some are small relative to their placental size, others are thin at birth or short relative to their head size, and some have below average infant weight gain despite average birth weight. Programming theory suggests that poor fetal and infant growth can permanently affect the structure and function of organs and tissues, increasing the risk of cardiovascular disease and diabetes. This concept is supported by animal studies showing that early life nutrition and other factors can influence long-term health. Geographical studies in England and Wales showed that differences in coronary heart disease mortality rates correlated with neonatal mortality rates in the early 20th century, indicating that poor maternal nutrition and low birth weight were linked to higher disease rates. Long-term studies in Hertfordshire, Preston, and Sheffield have shown that birth weight and infant weight are associated with adult blood pressure, glucose tolerance, and other cardiovascular risk factors. For example, men with lower birth weights had higher rates of impaired glucose tolerance and non-insulin dependent diabetes. These associations are strong and graded, with higher early weight linked to lower risk factors. Different risk factors are related to different patterns of early growth. Blood pressure is linked to birth weight, while cholesterol levels are influenced by infant feeding methods. Maternal undernutrition is suspected as a key factor in slowing fetal growth and programming coronary heart disease. Studies show that maternal undernutrition still affects fetal growth today, as evidenced by high rates of pregnancy anaemia. Research into the fetal origins of coronary heart disease is ongoing, with findings suggesting that early growth constraints can lead to long-term cardiovascular and metabolic issues. These findings are supported by animal studies and are attributed to programming rather than adult environmental factors. Future research is expected to provide more insights into the mechanisms underlying these effects.