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I completed my PhD at the University of Adelaide, Australia, before undertaking postdoctoral training: first at the National Institute for Medical Research in London; and later at the Victor Chang Cardiac Research Institute in Sydney, Australia. I started my own research group at the University of Oxford in 2015, and was awarded a Senior Basic Science Research Fellowship from the British Heart Foundation in 2017. This fellowship was renewed for a further 5 years in 2023. In 2020 I was awarded the title of Associate Professor. My research group is based in the Department of Physiology, Anatomy and Genetics.


Congenital heart disease (CHD), where a baby’s heart does not form properly in the womb, is the most common type of birth defect, affecting 1% of all babies. Even with the advent of modern surgical correction techniques, it is the major cause of infant mortality and morbidity, often requiring lifelong medical treatment. However, we do not always know why it happens. One-third of cases result from a genetic fault, but in the other two-thirds of cases the cause is less clear. Some of the latter result from the embryo being exposed to an abnormal environment in the womb in early pregnancy. My research focusses on these environmental causes of CHD.

In my most recent work in Oxford, I identified an entirely new risk factor for CHD in mice. I showed that if the mother is severely iron deficient and anaemic during early pregnancy, this can cause her offspring to develop a severe heart defect. I am using the knowledge and techniques developed in these studies as a springboard to investigate how other environmental factors cause CHD. I am investigating three new environmental factors, exposure to which has previously been shown to greatly increase the risk of offspring CHD in humans: (i) maternal diabetes; (ii) Valproic acid, a commonly used anti-epileptic and bipolar medication; and (iii) maternal hyperthermia, arising from either viral infection or exposure to extreme weather.

To confirm that my results also apply to human populations, I am collaborating with epidemiologists at the University of Oxford, looking in particular at the effects of maternal anaemia and iron-deficiency. These are a major global health problem, especially in developing nations. However, they are relatively easy to correct clinically. Therefore, if our studies are successful, we may be able to reduce the global incidence of CHD by dietary iron supplementation, in a similar way to the way that dietary folic acid supplementation is used today to reduce the incidence of another type of birth defect – spina bifida.

Selected Recent Publications

Kalisch-Smith JI, Ved N, Szumska D, Munro J, Troup M, Harris SE, Rodriguez-Caro H, Jacquemot A, Miller JJ, Stuart EM, Wolna M, Hardman E, Prin F, Lana-Elola E, Aoidi R, Fisher EMC, Tybulewicz VLJ, Mohun TJ, Lakhal-Littleton S, De Val S, Giannoulatou E, Sparrow DB. (2021). Maternal iron deficiency perturbs embryonic cardiovascular development in mice. Nat Commun 12, 3447.

Shi H, Enriquez A, Rapadas M, Martin EMMA. Wang R, Moreau J, Lim CK, Szot JO, Ip E, Hughes J, Sugomoto K, Humphreys D, McInerney-Leo AM, Leo PJ, Maghzal GJ, Halliday J, Smith J, Colley A, Mark PR, Collins F, Sillence DO, Winlaw DS, Ho J, Guillemin GJ, Brown MA, Kikuchi K, Thomas PQ, Stocker R, Giannoulatou E, Chapman G, Duncan EL, Sparrow DB, Dunwoodie SL. (2017). NAD Deficiency, Congenital Malformations and Niacin Supplementation. New Engl J Med 377, 544-552.

Sparrow DB*, Chapman G, Smith AJ, Mattar MZ, Major JA, O’Reilly VC, Saga Y, Zackai EH, Dormans JA, Alman BA, McGregor L, Kageyama R, Kusumi K, Dunwoodie SL*. (2012). A mechanism for gene-environment interaction in the etiology of congenital scoliosis. Cell 149, 295-306. Co-corresponding authors.