While expecting her first child, Dr Clare Reynolds switched from normal fizzy drinks to diet.
It was a rational move - the lesser of two evils, she figured - yet when she checked what research had been done, she found surprisingly little.
That prompted Reynolds, a researcher at the University of Auckland-based Liggins Institute, to explore what effect - and harm - artificial sweeteners could be having on pregnancy.
"There's been a lot of media attention around sugary drinks of late, and that's been spurring on research," Reynolds said.
"But the problem with artificial sweeteners, specifically, is there's very little evidence about - and people assume that it's maybe a healthier approach, when it may not be."
Some of Reynold's group's preliminary results have indicated artificial sweeteners could be just as bad as regular sugary drinks.
Current international evidence from animal models suggests sugar-sweetened soft drinks, especially those high in fructose, may lead to metabolic dysfunction in the mother and the offspring when ingested during pregnancy and lactation.
But diet beverages, which are high in artificial sweeteners such as acelsulfame-K and aspartame, have also been linked to obesity and metabolic dysfunction, among other adverse health effects.
Specific issues included a higher risk of heart disease and chronic kidney disease in women who drank two or more artificial sweetened diet soft drinks when compared to those who consumed less than one - and a higher risk of pre-term delivery in pregnant women.
The broader health impacts of artificial sweeteners are still being confirmed.
Reynolds is now supervising a new PhD project by Liggins researcher Pania Bridge-Comer, which focuses on what effect artificial sweeteners, specifically acesulfame-K, during pregnancy have on a child's metabolic and reproductive health in later life.
It was already known that a diet supplemented with artificial sweeteners led to higher obesity in offspring, putting children at increased risk of type 2 diabetes, high blood pressure, and heart disease.
Often, metabolic issues could also worsen reproductive dysfunction. A higher incidence of obesity possibly reduces fertility.
Her study, supported by a three-year grant from the Health Research Council, will delve deeper by using a mouse model to pin-point any effects before, during and after pregnancy.
Offspring of the mice will be analysed for various hormone levels, specific genes linked to reproductive function, the number of follicles in the ovaries, and tests to determine timing of the estrus cycle.
"These methods will all allow an idea of how the reproductive function is influenced in the offspring," Bridge-Comer said.
The study also stood to add much to the Developmental Origins of Health and Disease model, which linked the maternal environment and that of the developing fetus and was used in labs around the world.
"Rates of obesity and obesity-related morbidities are rising in New Zealand and globally, so understanding the underlying mechanisms in generational cycles of obesity may prove a useful method in helping to mitigate these increasing rates," Bridge-Comer said.
Reynolds believed the consumption of artificial sweeteners by fathers also warranted investigation in the future.
"I think it would be really interesting to see if they can affect male fertility, and whether that has any knock-on effect on the next generation that might be born."