Recent studies suggest that coronary heart disease (CHD) may originate in utero, with babies who are small at birth or in infancy having a higher risk of CHD, stroke, hypertension, and diabetes in adulthood. This effect is observed in babies born small for their gestational age, not just those born prematurely. The impact is seen in both babies with intrauterine growth retardation and those with average or above-average weight, though some are small relative to their placentas, thin at birth, or short in relation to their head size. The concept of "programming" explains how processes associated with low fetal and infant growth can program cardiovascular disease and diabetes. Poor nutrition and other influences during critical periods of early life can permanently affect the structure and physiology of organs and tissues. Studies in Hertfordshire, England, found that men who weighed 18 pounds or less at one year of age had nearly three times higher death rates from CHD compared to those who weighed 27 pounds or more. Similar trends were observed in women. Geographical studies also provided clues that impaired early development of blood vessels, the liver, and the endocrine pancreas might contribute to CHD. For example, high neonatal mortality in a population often indicates a high incidence of low birth weight and poor maternal nutrition. Individual studies in Hertfordshire and Preston have shown that birth weight and infant weight are associated with adult risk factors for CHD, such as blood pressure, glucose tolerance, and abdominal fat storage. Different risk factors are related to different patterns of early growth, suggesting that critical periods for programming vary. For instance, blood pressure is related to birth weight, while cholesterol concentrations are influenced by infant feeding methods. Maternal undernutrition is a significant influence on fetal growth and CHD. Studies in Salisbury found that children with large placentas relative to birth weight have higher blood pressure, similar to older individuals. Research into glucose tolerance suggests that impaired early development can lead to adult diabetes by reducing the number of pancreatic beta cells. Future research aims to understand the influences on fetal growth, how the fetus responds, and the long-term cardiovascular, metabolic, and endocrine consequences of early growth.Recent studies suggest that coronary heart disease (CHD) may originate in utero, with babies who are small at birth or in infancy having a higher risk of CHD, stroke, hypertension, and diabetes in adulthood. This effect is observed in babies born small for their gestational age, not just those born prematurely. The impact is seen in both babies with intrauterine growth retardation and those with average or above-average weight, though some are small relative to their placentas, thin at birth, or short in relation to their head size. The concept of "programming" explains how processes associated with low fetal and infant growth can program cardiovascular disease and diabetes. Poor nutrition and other influences during critical periods of early life can permanently affect the structure and physiology of organs and tissues. Studies in Hertfordshire, England, found that men who weighed 18 pounds or less at one year of age had nearly three times higher death rates from CHD compared to those who weighed 27 pounds or more. Similar trends were observed in women. Geographical studies also provided clues that impaired early development of blood vessels, the liver, and the endocrine pancreas might contribute to CHD. For example, high neonatal mortality in a population often indicates a high incidence of low birth weight and poor maternal nutrition. Individual studies in Hertfordshire and Preston have shown that birth weight and infant weight are associated with adult risk factors for CHD, such as blood pressure, glucose tolerance, and abdominal fat storage. Different risk factors are related to different patterns of early growth, suggesting that critical periods for programming vary. For instance, blood pressure is related to birth weight, while cholesterol concentrations are influenced by infant feeding methods. Maternal undernutrition is a significant influence on fetal growth and CHD. Studies in Salisbury found that children with large placentas relative to birth weight have higher blood pressure, similar to older individuals. Research into glucose tolerance suggests that impaired early development can lead to adult diabetes by reducing the number of pancreatic beta cells. Future research aims to understand the influences on fetal growth, how the fetus responds, and the long-term cardiovascular, metabolic, and endocrine consequences of early growth.