Small for gestational age (SGA) infants account for approximately 10% of live births in developed countries and are those born below the 10th percentile for their age, as a result of in utero growth restriction [
1]. Factors causing growth restriction include maternal disease, stress, smoking, malnutrition and placental insufficiency. While maternal malnutrition is the primary cause of growth restriction in low-income countries, placental insufficiency is the most common cause in high-income countries [
2]. Placental insufficiency causes reduced blood, nutrient and oxygen supply to the developing fetus, consequently restricting fetal growth. Another common pregnancy complication resulting in growth restriction is Gestational Diabetes Mellitus (GDM), however the metabolic dysfunction that occurs in GDM can also produce average or large for gestational age infants [
3]. In utero growth plays a critical role in programming lifelong health and disease, therefore insults during this time that lead to altered growth could result in sex-specific increased risk of cardiovascular and metabolic diseases [
4,
5]. These diseases, however, often require further insult (such as pregnancy, which places additional stress on the maternal adaptations to pregnancy) to reveal the dysfunction. This can also impact the next generation [
6]. In order to minimise this programmed disease risk, the infant’s weight gain would ideally match their genetic growth trajectory. However 10 to 30% of SGA infants do not shift their weight trajectory upwards and continue to experience poor growth throughout childhood [
7]. Conversely, the infant may experience very rapid weight gain, which is also associated with increased risk of obesity and metabolic diseases in later life [
8,
9]. Human milk is the ideal nutrition for the infant, shown to promote optimum growth and thought to uniquely match the infant’s requirements [
10]. The human milk macronutrient concentrations in healthy women breastfeeding healthy term infants are 35–50 g/L fat, 9–12 g/L protein, and 60–100 g/L lactose, with a minimum volume of 478 mL/day required [
11,
12]. Animal studies have reported that infant growth restriction results in compromised maternal quantity and quality of milk [
13]. This is in contrast to the few human studies that have reported no change in milk composition in cases of growth restriction [
14‐
16]. These studies, however, used inappropriate sampling methods for fat analysis, collecting samples from one time point in the first 28 days post-partum, and did not consider the daily or monthly variation of fat [
11,
17]. Further, they did not measure infant milk intake and therefore could not determine the macronutrient dosage the infant received. We present the first case study in which both the quantity and quality of human milk was compromised in a lactating mother who experienced placental insufficiency and GDM, and gave birth to an SGA infant.