ABSTRACT
There is significant evidence that an unhealthy diet greatly increases the risk of complications during pregnancy and predisposes offspring to metabolic dysfunction and obesity. While fat intake is typically associated with the onset of obesity and its comorbidities, there is increasing evidence linking sugar, particularly high fructose corn syrup, to the global rise in obesity rates. Furthermore, the detrimental effects of added sugar intake during pregnancy on mother and child have been clearly outlined. Guidelines advising pregnant women to avoid food and beverages with high fat and sugar have led to an increase in consumption of 'diet' or 'light' options. Examination of some human birth cohort studies shows that heavy consumption (at least one beverage a day) of non-nutritive sweetener (NNS) containing beverages has been associated with increased risk of preterm birth and increased weight/BMI in male offspring independent of maternal weight, which appears to be offset by breastfeeding for 6 months. Rodent models have shown that NNS exposure during pregnancy can impact maternal metabolic health, adipose tissue function, gut microbiome profiles and taste preference. However, the mechanisms underlying these effects are multifaceted and further research, particularly in a translational setting is required to fully understand the effects of NNS on maternal and infant health during pregnancy. Therefore, this review examines maternal sweetener intakes and their influence on fertility, maternal health outcomes and offspring outcomes in human cohort studies and rodent models.
ABSTRACT
Pregnancy represents a period of immense maternal physiological adaptation, with progressive increases in lipid storage potential and insulin resistance to support fetal/placental growth. This requires significant change in the adipose tissue. Women living with obesity/overweight are more susceptible to these changes causing complications such as gestational diabetes. This is particularly worrying as up to 60% of European women are living with overweight/obesity at the onset of pregnancy. Furthermore, less than 1% meet all nutrition guidelines. There is now evidence that these deep metabolic changes can result in a predisposition to metabolic disease in both the mother and child in later life. Health and nutrition status during this period therefore represents a window to future health. This period offers a valuable opportunity for intervention to prevent the negative consequences of poor in utero environments and increases the long-term quality of life for mother and offspring. This review will examine a range of in utero factors which determine adipose tissue development, the impact of these factors on later-life obesity and metabolic health and the therapeutic value of dietary anti-inflammatory nutritional interventions during pregnancy and early life. When it comes to early life nutrition, a 'one size fits all' approach is not always appropriate. Understanding the mechanisms of adipose tissue development in response to differing nutritional strategies may be important in the context of complicated or adverse in utero environments and represents a substantial step towards a more personalised nutritional approach for the prevention of obesity, metabolic syndrome and related non-communicable diseases in future generations.
ABSTRACT
Understanding the factors which influence fertility is essential for developing appropriate nutritional recommendations for couples trying to conceive. Non-caloric sweeteners (NCS) are increasing in the food chain and despite being no/low calorie, several adverse metabolic consequences have been attributed to their consumption. Their effects on reproduction have been relatively under-researched, particularly in males. This review aims to systematically review the literature for evidence of the effect of NCS on male fertility in rodents, with sperm parameters (sperm quantity and quality) assessed as primary outcomes. Given the lack of information available in humans this review has been carried out using evidence from rodent models. Risk of bias assessment was carried out using the Syrcle risk of bias tool. Nine studies met the inclusion criteria. Forty-four percent showed a negative effect of NCS on male reproductive parameters compared with controls. The effects of NCS on fertility have been conflicting and selected studies have been heterogeneous in relation to study design. It is unclear if NCS has an impact on male reproductive function. There is a need for randomized controlled trials using a standardized protocol for analysis, to formulate a clear message in terms of male fertility.
