Dian Shepperson Mills' 'Commentary' in BioNews 493 (2/2/2009) 'Why fertility patients should consider what they eat before resorting to more invasive treatment' directs us to observational studies on the links between diet and (in)fertility as well as pregnancy outcomes. Since the original observations were made in the 1980s there has been an increasing understanding of the importance of optimal male and female nutrition as an adjunct to fertility treatments, not an alternative.
A large number of factors affecting fertility in women can be affected by, if not attributed to, lifestyle issues. Obesity in women has been clearly linked to ovulatory disorders, poorer pregnancy outcomes, and an increased likelihood of miscarriage. In an IVF setting, obese patients generally demonstrate a resistance to ovarian stimulation and require larger doses of gonadotrophins to effect the same response as patients in the healthy weight range (1). Many studies have demonstrated that even moderate weight loss can be sufficient to stimulate the resumption of spontaneous ovulation. However, ovulatory disorders are not purely the domain of the obese. Some studies have demonstrated that disorders of ovulation can also be linked to increased consumption of energy from trans-fats (when compared with carbohydrates or unsaturated fats). A mere extra two per cent of daily energy derived from dietary trans-fats (instead of unsaturated fats) may be enough to double an individual's risk of infertility from ovulatory disorder (2). On the flipside, the likelihood of ovulatory disorders occurring appears to be reduced by multivitamin intake - perhaps due to the protective effects of antioxidants (3).
Antioxidants also play in important role in oocyte (egg cell) quality. The normal mature oocyte is suspended in metaphase II (MII) [a stage in gamete development] where it stays until fertilisation occurs and metaphase is resumed. An excess of reactive oxygen species (ROS) due to insufficient antioxidant activity can adversely affect the supporting granulosa and luteal cells and result in reduced gonadotrophin action, DNA damage and may prevent the resumption of metaphase (4).
Men wishing to father children would also do well to watch their nutrient intake. Excess ROS production in men has been linked to lipid peroxidation of the sperm membranes and DNA fragmentation. Membrane damage is associated with a reduced ability of the sperm to bind to the oocyte, whilst DNA fragmentation is strongly associated with poor embryo development and poor pregnancy outcomes (5).
In addition, optimal nutrition during gametogenesis, pregnancy and after birth is now recognised as a determinant of future childhood and adult health status and susceptibility to disease (6,7,8). More intriguing still is the suggestion that environmental factors (grandpaternal nutritional status during mid childhood) can be linked to the mortality risk ratio (in their grandsons) two generations later (9). One mechanism by which this may occur is through changes in gene expression without changes in DNA sequence. Such 'epigenetic' changes may result from environmental factors such as folate status and in some situations possibly the IVF process itself (10). The UK committee on Toxicology concluded in 2008 (11) that 'There is reasonable evidence that epigenetic changes associated with environmental exposures during development can result in adverse effects'. We should clearly include 'environmental exposure' to nutritional deficiencies in this context. Nutritional intervention periconceptually, throughout pregnancy and in early childhood should be a priority for health care systems around the world. In Australia there is a particular need for this in relation to the burden of chronic disease in the indigenous Aboriginal community (12).
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