Early Life Fructose Exposure and Its Implications for Long-Term Cardiometabolic Health in Offspring

review was recently published in Nutrients which examined the relationship between early life exposure to fructose and cardiometabolic outcomes in offspring. Reviewers cited a number studies which associated fructose intake with various health outcomes such as insulin resistance, elevated low density lipoprotein cholesterol, elevated triglycerides, obesity, type 2 diabetes, cardiovascular disease, non-fatal myocardial infarction, and fatal coronary heart disease.

Reviewers then noted that there is limited human data on the effects of excessive fructose consumption during the early stages of life to include gestation, lactation, and infancy. Zheng et al. cited two cohort studies; the first found that intake of fructose from natural sources reduced the risk of pre-eclampsia whereas the second study found that sugar sweetened beverage intake was associated with increased risk of pre-term delivery.

Reviewers also examined the relevant literature on fructose consumption in rodent models. While results varied between experiments, reviewers noted several points. First, the offspring of dams consuming high fructose diets experienced elevated circulating plasma fructose, elevated plasma leptin, elevated plasma insulin, obesity, hypertension, insulin resistance, increased rates of fatty liver, increased free fatty acids, greater visceral adipose tissue stores, changes in stress-response axis, changes in nocturnal blood pressure, and hypertriglyceridemia. Additionally, the dams consuming high fructose diets experienced increased food intake, decreased water intake, sex-specific effects on placental growth and fetal and neonatal metabolic profiles, alterations in the secondary sex ratio and reduced fertility.

Lastly, reviewers outlined proposed mechanisms for the observed effects in both mothers and offspring. Reviewers first described the ability of fructose to be rapidly metabolized in the liver which can promote de novo lipogenesis which in turn, promotes dyslipidemia. The second suggested mechanism comes from a rodent study in which maternal consumption of fructose during lactation resulted in “decreased hypothalamic sensitivity to exogenous leptin, enhanced food intake, and decreased several anorexigenic signals…in the off spring.” The last proposed mechanism suggests that offspring consuming high-fructose diets demonstrate enhanced expression of glucose transporter 5. Reviewers noted “it is still unclear whether the impacts on the offspring are direct effects of fructose transfer through the placenta or the mother’s milk, or due to adaptive responses and altered maternal metabolism.”

Reviewers concluded, “One important point that should be taken into consideration is that early life fructose exposure may determine the susceptibility of long-term metabolic diseases in offspring. However, limited data suggest that the offspring would be protected from these well-known adverse effects during early life.”


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