Consuming Alcohol During Pregnancy Causes Significant Damage to the Fetus

The ingestion of alcohol during pregnancy can significantly damage the developing foetal brain and result in a number of disorders grouped under the term foetal alcohol spectrum disorders (FASD), it is characterised by stunted growth, a number of physical and physiological abnormalities and often, mental retardation (Leman, 2012). This damage can vary due to the pattern of consumption, the dose and the duration of exposure to ethanol (Brocardo, Gil-Mohapel, & Christie, 2011). Omega-3 fatty acids are polyunsaturated fatty acids (PUFAs) that are found in high concentrations in neuronal membranes and that have antioxidant properties (Simopoulos, 2009). The most common of the PUFAs in the brain is docosahexaenoic acid (DHA) which improves membrane fluidity and enhances synaptic transmission (Gomez-Pinilla, 2008). Prenatal ethanol exposure (PNEE) decreases brain concentrations of DHA which can lead to oxidative stress and deficits of synaptic plasticity, research has suggested that omega-3 supplementation can correct these imbalances (Patten, Brocardo, & Christie, 2013; Patten, Sickmann, Dyer, Innis, & Christie, 2013).

Omega-3 fatty acid supplementation may be a viable treatment option for preventing oxidative stress in infants diagnosed with FASD (Patten, Brocardo, et al., 2013). Children with FASD are often mentally retarded which may be related to the loss of oxygen in the foetal brain during development, the foetus’s breathing can stop temporarily due to ethanol consumption (Fox et al., 1978). Ethanol exposure can lead to the generation of reactive oxygen species (ROS) and produce an imbalance in the intracellular redox state, leading to an overall increase in oxidative stress (Brocardo et al., 2011). Oxidative stress results in ...

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... such as rescuing the deficits in synaptic plasticity and reducing oxidative stress associated with FASD. Omega-3 supplementation given from birth until adulthood may prevent oxidative stress in infants with PNEE by overcoming long-lasting deficits in GSH levels. Progressive oxidative stress is linked to deficits in synaptic plasticity which is also prevalent in FASD. An omega-3 intervention can improve LTP through reducing oxidative stress which helps animals with PNEE to overcome deficits in synaptic plasticity. However, further studies are warranted in order to explain the differences between effects of PNEE on the male and female brains. To conclude, omega-3 fatty acids may be a useful therapeutic strategy for the treatment of some of the symptoms associated with FASD such as the reduction of oxidative stress and to eliminate the deficits of synaptic plasticity.