It’s widely known that a baby is a precious gift that is a combination of its mother’s genes and its father’s genes. You hear it all the time from doting relatives and friends when a new baby is born: ‘He has his father’s eyes’, ‘She has her mother’s chin’, ‘He’s the spitting image of his daddy at the same age’. The parents’ physical features are passed down to the child. As the child grows some other similarities may become apparent also – the like or dislike of certain foods, the natural abilities or talents with particular sports, an interest in specific academic pursuits. Many of these things can be attributed to genetics.
We see this ‘passing down’ of traits as something fairly rigid and outside our control. The kid will either have dad’s eyes or he won’t – nothing to be done about it. But did you know that a mother’s health can have a far wider reaching impact on her unborn child than just that of physical traits or lifestyle predispositions?
We all know that, for example, smoking during pregnancy can be very bad for the unborn baby. It is very clear cause and effect. Now, research suggests that what the mother does and doesn’t do during pregnancy can have a far more complex effect on the baby – on a genetic level. A mother’s health can change a child’s genetic predisposition to disease.
Though there are many examples of how a mother’s health, nutrition, gestational wellbeing and birthing process can influence the health of her child, studies on specific genetic expressions have begun to shed light on epigenetic effects of intrauterine life. Intrauterine exposure to poor maternal nutrition or maternal obesity has consistently been demonstrated to contribute to a particular epigenotype that has a higher risk of obesity and metabolic syndrome. So mothers who have poor nutrition and/or are obese are, in effect, writing these same health problems into the genes of their unborn children.
Studies have shown that despite a genetic predisposition to type 2 diabetes, body mass index (BMI), body fat index (BFI), family history, age, sex, HDL cholesterol, triglyceride levels, and other risk factors outperform our ability to predict diabetic onset. Studies using familial clustering of type 2 diabetes found that the risk for onset of this disease is not entirely due to genetic factors. Epigenetic processes can produce inherited risk over one or several generations. So basically your risk for ending up with type 2 diabetes is not simply genetic (you either get it or you don’t) but can be influenced by things outside of genetics (epigenetics). For instance, pregnancy related factors, nutrition, toxins and infectious agents can also play a role in the activation of genes that may influence the risk of diabetes.
Mechanisms like histone acetylation, DNA-methylation, RNA coding patterns and the regulation of gene expressions in response to environmental cues can be passed on generations later. But the one factor that has the most epigenetic impact remains obesity. Studies focused on epigenetic markers found altered methylation and histone acetylation levels in genes involved in metabolic processes. For one, there is a huge influence of maternal obesity (including gestational and postnatal diet, maternal insulin resistance and metabolic syndrome) on changes in the biochemical structure of the baby’s DNA that alter gene expression involved in the risk for developing metabolic syndrome in adulthood. Put simply, the mother’s obesity can literally change how her child’s genes are expressed.
The exact reason behind this is unclear, though leptin and adiponectin may play significant roles. Leptin is a hormone secreted by fat tissues that traveles from the mother’s blood to the fetus and works on the development of the central nervous system. After birth, leptin regulates appetite and energy expenditure. Maternal hyperglycemia have been shown to be related to increased leptin levels in offspring. Similarly, adiponectin should maintain insulin sensitivity but has been found to be significantly lower in children from mothers with high-fat diets. Meanwhile, a mother’s insulin resistance can cause pregnancy complications due to impaired glucose transport, including an increased risk for metabolic disturbances, cardiovascular disease and even telomere length.
In a nutshell, science is still hard at work figuring out exactly how a mother’s health has such a huge impact on the child’s genes. But one thing that is becoming increasingly more evident as each new study is released, is that the health of the mother is more important than we ever realised to the health and development of the child.
Now, if this has all left you searching for a medical dictionary to understand all the complicated words above while freaking out that you might be giving your unborn baby some genetic disease without even knowing it, please don’t stress. The intention of this article is not to further add to the fear and anxiety of pregnancy. It is simply to inform. It is to let you know that if you take care of yourself first you will be giving your baby the best, healthiest possible start in life. Eat well, exercise, avoid stress. Put yourself first because at it’s simplest, this article is about one thing: healthy mom = healthy bub.
Talmud PJ, Hingorani AD, Cooper JA, Marmot MG, Brunner EJ, Kumari M, Kivimäki M, Humphries SE. Utility of genetic and non-genetic risk factors in prediction of type 2 diabetes: Whitehall II prospective cohort study. BMJ. 2010;340:b4838
Skinner MK. Environmental epigenetic transgenerational inheritance and somatic epigenetic mitotic stability. Epigenetics. 2011;6:838-842
Burgio, Ernesto, Angela Lopomo, and Lucia Migliore. “Obesity and diabetes: from genetics to epigenetics.” Molecular biology reports 42.4 (2015): 799-818.
Kaar JL, Crume T, Brinton JT, Bischoff KJ, McDuffie R, Dabelea D. Maternal obesity, gestational weight gain, and offspring adiposity: the exploring perinatal outcomes among children study. J Pediatr. 2014;165(3):509-515.
Smith, Caitlin J., and Kelli K. Ryckman. “Epigenetic and developmental influences on the risk of obesity, diabetes, and metabolic syndrome.” Diabetes, metabolic syndrome and obesity: targets and therapy 8 (2015): 295.
Briffa JF, McAinch AJ, Romano T, Wlodek ME, Hryciw DH. Leptin in pregnancy and development: a contributor to adulthood disease? Am J Physiol Endocrinol Metab. 2015;308(5):E335-E350.
Hou M, Chu Z, Liu T, et al. A high-fat maternal diet decreases adiponectin receptor-1 expression in offspring. J Matern Fetal Neonatal Med. 2015;28(2):216-221.
Doblado M, Moley KH. Glucose metabolism in pregnancy and embryogenesis. Curr Opin Endocrinol Diabetes Obes. 2007;14(6):488-493.
West NA, Crume TL, Maligie MA, Dabelea D. Cardiovascular risk factors in children exposed to maternal diabetes in utero. Diabetologia. 2011;54(3):504-507.
Xu J, Ye J, Wu Y, et al. Reduced fetal telomere length in gestational diabetes. PloS One. 2014;9(1):e86161.