Fructose, pregnancy and later life impacts

Abstract

Fructose is an increasingly common constituent of the Westernized diet due to cost and production efficiencies. Although an integral component of our pre-industrial revolution diet, over the past two decades human and animal studies have highlighted that excessive fructose intake appears to be associated with adverse metabolic effects. Excessive intake of fructose is the combined result of increased total energy consumption and increased portion sizes of foods, which often incorporate the fructose-containing sugars sucrose and high-fructose corn-syrup (HFCS). The adverse metabolic effects following excessive fructose consumption have become a hot topic in mainstream media and there is now rigorous scientific debate regarding periods of exposure, dosage levels, interactive effects with other sugars and fats and mechanisms underlying the actions of fructose. There is still a degree of controversy regarding the extent to which sugars such as sucrose and HFCS have contributed to the current epidemic of obesity and diabetes. Furthermore, an increasing number of infants are being exposed to sugar-sweetened food and beverages before birth and during early postnatal life, highlighting the importance of determining the long-term effects of this perinatal exposure on the developing offspring. There are limited human observational and controlled studies identifying associations of excessive sweetened food and beverage consumption with poor pregnancy outcomes. Animal research has demonstrated an increased incidence of gestational diabetes as well as altered maternal, fetal and offspring metabolic function, although the long-term effects and the mechanism underlying these perturbations are ill defined. This review aims to understand the role of early life fructose exposure in modifying postnatal risk of disease in the offspring, focusing on fructose intake during pregnancy and in early postnatal life.

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

“…Thus far, only a limited number of human studies have shown an association between excessive sweetened food and beverage consumption and poor pregnancy outcome [24]. Animal studies have shown that fructose alone alters fetal and offspring metabolism [24]. However, several animal studies have often used fructose as a part of diet along with sucrose, fat, and salt.…”

Impact of maternal obesity on offspring adipose tissue: lessons for the clinic

“…This increased nutrient supply appears to be due to the combined effects of the tendency of overweight/obese women to consume diets that contain greater amounts of noncore foods [13] and the fact that these women also tend to be more insulin resistant than their lean counterparts (FIGURE 1) [2]. A number of dietary factors have been implicated in metabolic programming, including higher intakes of total energy, saturated and omega-6 fats, refined/high-glycemic index (GI) carbohydrates, fructose and sucrose, and reduced intakes of key micronutrients [13][14][15][16]. Thus far, however, which of these nutritional factors are the key drivers of metabolic programming remains unclear.…”