Specific causes include:
Chronic high blood pressure
Severe malnutrition
Genetic mutations, Ehlers–Danlos syndrome

Symmetrical
Symmetrical IUGR is commonly known as global growth restriction, and indicates that the fetus has developed slowly throughout the duration of the pregnancy and was thus affected from a very early stage. The head circumference of such a newborn is in proportion to the rest of the body. Since most neurons are developed by the 18th week of gestation, the fetus with symmetrical IUGR is more likely to have permanent neurological sequelae. Common causes include:
Early intrauterine infections, such as cytomegalovirus, rubella or toxoplasmosis
Chromosomal abnormalities
Anemia
Maternal substance use (prenatal alcohol use can result in Fetal alcohol syndrome)

Causes
IUGR is caused by a variety of factors; these can be fetal, maternal, placental or genetic factors. Maternal
Pre-pregnancy weight and nutritional status
Poor weight gain during pregnancy
Malnutrition
Anemia
Substance use: smoking, alcohol, drugs including marijuana or cocaine
Medication: warfarin, steroids, anticonvulsants
Inter-pregnancy interval of less than 6 months
Assisted reproductive technologies
Pre-gestational diabetes
Gestational diabetes
Pulmonary disease
Cardiovascular disease
Kidney disease
Hypertension
Celiac disease increases the risk of intrauterine growth restriction by an odds ratio of approximately 2.48
Subclinical hypothyroidism
Blood clotting disorder/disease (e.g., Factor V Leiden)

Uteroplacental
Preeclampsia
Multiple gestation
Uterine malformations
Placental insufficiency

Fetal
Chromosomal abnormalities
Vertically transmitted infections: TORCH, Malaria, congenital HIV infection, Syphilis
Erythroblastosis fetalis
Congenital abnormalities

Genetic
Placental genes
Maternal genes: Endothelin-1 over-expression, Leptin under-expression
Fetal genes

Pathophysiology
If the cause of IUGR is extrinsic to the fetus (parental or uteroplacental), transfer of oxygen and nutrients to the fetus is decreased. This causes a reduction in the fetus’ stores of glycogen and lipids. This often leads to hypoglycemia at birth. Polycythemia can occur secondary to increased erythropoietin production caused by the chronic hypoxemia.
Furthermore, rapid metabolic and physiologic changes in the first few days after birth can yield susceptibility to hypocalcemia, polycythemia, immunologic compromise, and renal dysfunction. Long-term consequences
According to the theory of thrifty phenotype, intrauterine growth restriction triggers epigenetic responses in the fetus that are otherwise activated in times of chronic food shortage. If the offspring actually develops in an environment where food is readily accessible, it may be more prone to metabolic disorders, such as obesity and type II diabetes.Infants with IUGR may continue to show signs of abnormal growth throughout childhood. Infants with asymmetric IUGR (head-sparing) typically have more robust catch-up postnatal growth, as compared with infants with symmetric IUGR, who may remain small throughout life. The majority of catch-up growth occurs in the first 6 months of life, but can continue throughout the first two years. Approximately 10% of infants who are small for gestational age due to IUGR will still have short stature in late childhood.Infants with IUGR are also at elevated risk for neurodevelopmental abnormalities, including motor delay and cognitive impairments. Low IQ in adulthood may occur in up to one third of infants born small for gestational age due to IUGR. Infants who fail to display adequate catch-up growth in the first few years of life may exhibit worse outcomes.Catch-up growth can alter fat distribution in children diagnosed with IUGR as infants and increase risk of metabolic syndrome. Infants with IUGR may be susceptible to long-term dysfunction of several endocrine processes, including growth hormone signaling, the hypothalamic-pituitary-adrenal axis, and puberty.