Early Life Exposure to Fructose and Offspring Phenotype: Implications for Long Term Metabolic Homeostasis

Abstract

The consumption of artificially sweetened processed foods, particularly high in fructose or high fructose corn syrup, has increased significantly in the past few decades. As such, interest into the long term outcomes of consuming high levels of fructose has increased significantly, particularly when the exposure is early in life. Epidemiological and experimental evidence has linked fructose consumption to the metabolic syndrome and associated comorbidities—implicating fructose as a potential factor in the obesity epidemic. Yet, despite the widespread consumption of fructose-containing foods and beverages and the rising incidence of maternal obesity, little attention has been paid to the possible adverse effects of maternal fructose consumption on the developing fetus and long term effects on offspring. In this paper we review studies investigating the effects of fructose intake on metabolic outcomes in both mother and offspring using human and experimental studies.

Mexico City normal weight children exposed to high concentrations of ambient PM2.5 show high blood leptin and endothelin-1, vitamin D deficiency, and food reward hormone dysregulation versus low pollution controls. Relevance for obesity and Alzheimer disease

“…The problem is certainly a deep concern in Mexicans and Mexican-Americans for whom socioeconomic disadvantage, race/ethnic disparities and genetics play a key role in overweight and obesity status (Bonvecchio et al, 2009;Piernas et al, 2014;Fowler et al, 2013;Rossen, 2014;Bauer et al, 2014). Compounding the problem in Mexican children is their current high fructose consumption: Mexico is the world's biggest per capita consumer of soft drinks and the change from cane sugar to high fructose corn syrup will aggravate obesity, chronic metabolic disease, cognitive decline and increase the risk of Alzheimer's disease (Lakhan and Kirchgessner, 2013;Lustig, 2013;Regnault et al, 2013;Sloboda et al, 2014).…”

“…Effective January 2014, a significant increment in the cost of soft drinks by the 8% federal tax, resulted in the substitution of sugar cane by high-fructose corn syrup (HFCS) by the soft drink industry in Mexico. An increase in HFCS will severely aggravate the obesity, chronic metabolic disease, cognitive decline and risk of Alzheimer's disease in exposed children (Lakhan and Kirchgessner, 2013;Lustig, 2013;Regnault et al, 2013;Sloboda et al, 2014). The complexity of the systemic inflammation, neuroinflammation and the early hallmarks of AD in Mexico City teens is worsen by data supporting that adipokines mediate inflammation and insulin resistance (Kwon and Pessin,2013) and deficient brain insulin signaling pathways are critical etiological factors in Alzheimer's disease De la Monte, 2014).…”

Maternal Fructose Intake Affects Transcriptome Changes and Programmed Hypertension in Offspring in Later Life

“…Several intervention strategies, including taurine, arginine, resveratrol, grape-derived polyphenols, sardine protein, vitamin E, and α-lipoic acid, have been used to prevent the adverse metabolic effects of excess fructose consumption in adults [44]. However, none of these strategies has been examined as a candidate reprogramming strategy for preventing maternal HF consumption-induced programmed hypertension.…”

Early-life nutritional effects on the female reproductive system

“…In addition to the increased availability and consumption of low-cost, hypercaloric food contributing to the obesity epidemic, high fructose consumption, through both beverages and food, has been identified as another important conducive factor in the progression of obesity (Sloboda et al 2014). The long-term female reproductive outcomes of early-life exposure to maternal high fructose intake currently remain unclear.…”