McMaster University

Medical Sciences
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Deborah Sloboda

Deborah Sloboda

Associate Professor

Research Interests

The Sloboda Lab interests are founded in the early life origins of health and disease. We are interested in understanding the impact of early life adversity on the mother, and the developing fetus and how fetal adaptations to adversity influence the risk of chronic disease later in life. Our experimental studies investigate the effects of early life nutritional or endocrine stress on maternal, fetal and placental development.

Current research themes:

  1. The maternal microbiome. Late pregnancy is characterized by maternal inflammation, insulin and leptin resistance and it has been proposed that these changes involve the maternal microbiome. In these studies we investigate how shifts in the pregnant gut microbiome affect maternal adaptation to pregnancy and how these microbial shifts impact placental and fetal development. These studies are part of our long-term goal of determining the underlying early life precipitating factors that confer an increased risk of obesity and metabolic disease in offspring of obese mothers.
  2. Maternal nutritional impacts on offspring reproduction. The perinatal nutritional environment independently and critically impacts offspring risk of obesity and susceptibility to metabolic compromise, and altered reproductive function can now be added to this list. We have shown that fetal adaptations to perinatal adversity significantly advances puberty and impairs ovarian function in offspring. We have shown that maternal nutritient restriction induces in offspring an early ovarian aging phenotype, characterized by a loss of ovarian follicular reserve. We have now identified key upstream mediators of this early follicular loss and believe that this compromise is partly mediated by ovarian oxidative stress and controlled by melatonin. Recently, this work has expanded to investigate the role of peripheral circadian rhythms and clock genes in mediating ovarian follicle loss.
  3. Early life origins of obesity and metabolic compromise. There is now no doubt that events occurring before birth influence weight gain, deposition of body fat and metabolic function during childhood and beyond. The increase in childhood obesity in recent decades has been more rapid than can be explained purely by genetic susceptibility or diet. Both poor maternal nutrition and prenatal stress have long-term effects on offspring growth and development and increase risk of disease in adulthood. Our lab is currently investigating the long-term impacts of maternal nutrition on offspring obesity risk and metabolic function. We are also interested in understanding if effects are seen in subsequent generations, ie trans-generational transmission of chronic disease risk.


McMaster University Health Sciences Centre

telephone: 905-525-9140 ext. 22250

web: Sloboda Lab

Program Area

Metabolism & Nutrition

Research Focus

Perinatal programming, Reproduction, Metabolism, Early life origins, Maternal microbiome, Obesity

Selected Publications

  • Sloboda DM, Li M, Patel R, Clayton Z, Yap C, Vickers MH. (2014) Early life exposure to fructose and offspring phenotype: implications for long-term metabolic homeostasis. Journal of Obesity. 2014:203474.
  • Regnault TRH, Gentill S, Sarr O, Toop CR and Sloboda DM. (2013) Fructose, pregnancy and later life impacts. Clinical and Experimental Pharmacology and Physiology 40(11) p824-37.
  • Li M, Reynolds C, Sloboda DM, Gray C, Vickers MH (2013). Effects of taurine supplementation on hepatic markers of inflammation and lipid metabolism in offspring and mothers in the setting of maternal obesity. PLoS ONE 8(10):e76961
  • Braun T, Challis JRG, Newnham, Sloboda DM (2013). Early life glucocorticoid exposure: The hypothalamic pituitary adrenal axis, placental function and long-term disease risk. Endocrine Reviews 34(6) p885-916.
  • Vickers MH and Sloboda DM. (2012) Strategies for reversing the effects of metabolic disorders induced as a consequence of developmental programming. Frontiers in Integrative Physiology 3 p 242.