Reducing early preterm birth for 25 cents a day

Preterm birth (before 37 weeks of gestation) is the most common direct cause of death and disability in children.1 Early preterm birth (EPTB) (less than 34 weeks) is the main cause of neonatal death and severe disability.2 Most women who experience early preterm birth are at low risk.1 In those women who have already experienced one early preterm birth, we can involve tertiary hospital clinics and implement strategies such as cervical screening and either vaginal progesterone therapy or cervical suturing.3 However, these measures require levels of clinical expertise that are not available at a global level. Even within Australia, some rural women do not have access to trained ultrasonographers who can perform reliable transvaginal scanning necessary to detect cervical shortening. In many countries in the world, any sort of ultrasound scan in pregnancy is not feasible, let alone access to secondary interventions following on from discovery of a short cervix, such as progesterone therapy or cervical suturing. Tertiary hospital clinics are simply a dream. The severe consequences of early preterm birth and high cost and need for clinical expertise in existing strategies of prevention have led to calls for a public health approach to reduce the rate of early preterm birth.3 Implementation of omega 3 long chain polyunsaturated fatty acids (omega3 LCPUFA) supplements in pregnancy is now a feasible and costeffective public health strategy.4–6 The omega3 LCPUFA story is remarkable and involves multidisciplinary researchers from around the world. The discovery is a gold standard in progressing from benchtop to bedside in medical research. The journey started with basic science studies evaluating the mechanisms of initiation of labour, progressed through observational and epidemiological studies of populations, advanced into randomised trials testing a specific hypothesis and culminated in a Cochrane Review. Understanding the omega3 LCPUFA story begins with knowledge of factors leading to the initiation of cervical ripening and labour.3,7–11 Omega3 LCPUFA enters the maternofetoplacental unit from the maternal circulation. Tissue concentrations are heavily influenced by diet.3,7,9 Increases in omega3 LCPUFA levels in cervical tissues directly counter local production of proinflammatory 2series prostaglandins such as PGE2 and PGF2α within those same tissues, resulting in a delicate balance in hormonal drivers that inhibit cervical ripening and those that augment these processes. The balance plays a critical role in the duration of gestation.9 Omega3 LCPUFA is a direct dietary antagonist of the production of 2series prostaglandins in the cervix. Arachidonic acid directly competes with omega3 LCPUFA for incorporation into cells. Diets that are high in omega3 LCPUFA result in preferential incorporation of the 3series prostaglandins into cellular phospholipids and the displacement of arachidonic acid and this results in lower outputs of 2series prostaglandins.3,10 If endogenous levels of 2series prostaglandins within the cervix are too high, or local availability of omega3 LCPUFA to act as an antagonist is too low, the cervix may prematurely ripen, basal uterine contractions increase in strength, and the outcome may be preterm birth.7–11 A population strategy to reduce preterm birth would therefore need to target either: