Overweight, obesity, and their comorbidities remain global health challenges. When established early in life, overweight is often sustained into adulthood and contributes to the early onset of non-communicable diseases. Parental pre-conception overweight and obesity is a risk factor for overweight and obesity in childhood and beyond. This increased risk likely is based on an interplay of genetic alterations and environmental exposures already at the beginning of life, although mechanisms are still poorly defined. In this narrative review, potential routes of transmission of pre-conceptional overweight/obesity from mothers and fathers to their offspring as well as prevention strategies are discussed. Observational evidence suggests that metabolic changes due to parental overweight/obesity affect epigenetic markers in oocytes and sperms alike and may influence epigenetic programming and reprogramming processes during embryogenesis. While weight reduction in overweight/obese men and women, who plan to become pregnant, seems advisable to improve undesirable outcomes in offspring, caution might be warranted. Limited evidence suggests that weight loss in men and women in close proximity to conception might increase undesirable offspring outcomes at birth due to nutritional deficits and/or metabolic disturbances in the parent also affecting gamete quality. A change in the dietary pattern might be more advisable. The data reviewed here suggest that pre-conception intervention strategies should shift from women to couples, and future studies should address possible interactions between maternal and paternal contribution to longitudinal childhood outcomes. Randomized controlled trials focusing on effects of pre-conceptional diet quality on long-term offspring health are warranted.
Background: Fructose consumption increases risk factors for cardiometabolic disease. It is assumed that the effects of free sugars on risk factors are less potent because they contain less fructose. We compared the effects of consuming fructose, glucose or their combination, high fructose corn syrup (HFCS), on cardiometabolic risk factors. Methods: Adults (18-40 years; BMI 18-35 kg/m 2 ) participated in a parallel, double-blinded dietary intervention during which beverages sweetened with aspartame, glucose (25% of energy requirements (ereq)), fructose or HFCS (25% and 17.5% ereq) were consumed for two weeks. Groups were matched for sex, baseline BMI and plasma lipid/lipoprotein concentrations. 24-h serial blood samples were collected at baseline and at the end of intervention. Primary outcomes were 24-h triglyceride AUC, LDL-cholesterol (C), and apolipoprotein (apo)B. Interactions between fructose and glucose were assessed post hoc. Findings: 145 subjects (26.0 ± 5.8 years; body mass index 25.0 ± 3.7 kg/m 2 ) completed the study. As expected, the increase of 24-h triglycerides compared with aspartame was highest during fructose consumption (25%: 6.66 mmol/Lx24h 95% CI [1.90 to 11.63], P = 0.0013 versus aspartame), intermediate during HFCS consumption (25%: 4.68 mmol/Lx24h 95% CI [−0.18 to 9.55], P = 0.066 versus aspartame) and lowest during glucose consumption. In contrast, the increase of LDL-C was highest during HFCS consumption (25%: 0.46 mmol/L 95% CI [0.16 to 0.77], P = 0.0002 versus aspartame) and intermediate during fructose consumption (25%: 0.33 mmol/L 95% CI [0.03 to 0.63], P = 0.023 versus aspartame), as was the increase of apoB (HFCS-25%: 0.108 g/L 95%CI [0.032 to 0.184], P = 0.001; fructose 25%: 0.072 g/L 95%CI [−0.004 to 0.148], P = 0.074 versus aspartame). The post hoc analyses showed significant interactive effects of fructose*glucose on LDL-C and apoB (both P < 0.01), but not on 24-h triglyceride (P = 0.340). Conclusion: A significant interaction between fructose and glucose contributed to increases of lipoprotein risk factors when the two monosaccharides were co-ingested as HFCS. Thus, the effects of HFCS on lipoprotein risks factors are not solely mediated by the fructose content and it cannot be assumed that glucose is a benign component of HFCS. Our findings suggest that HFCS may be as harmful as isocaloric amounts of pure fructose and provide further support for the urgency to implement strategies to limit free sugar consumption.
Context Studies in rodents and humans suggest that high fructose corn syrup (HFCS)-sweetened diets promote greater metabolic dysfunction than sucrose-sweetened diets. Objective To compare the effects of consuming sucrose-sweetened beverage (-SB), HFCS-SB, or a control beverage sweetened with aspartame on metabolic outcomes in humans. Design A parallel, double-blinded, NIH-funded study. Setting Experimental procedures were conducted during 3.5 days of inpatient residence with controlled feeding at a research clinic before (baseline) and after a 12-day outpatient intervention period. Participants 75 adults (18-40 years) were assigned to beverage groups matched for sex, BMI (18-35kg/m 2), fasting triglyceride, lipoprotein and insulin concentrations. Intervention 3 servings/day of sucrose- or HFCS-SB providing 25% of energy requirement or aspartame-SB, consumed for 16 days. Main Outcome Measures %Hepatic lipid, Matsuda insulin sensitivity index (ISI), and Predicted M ISI. Results Sucrose-SB increased %hepatic lipid (absolute change: 0.6±0.2%) compared with aspartame-SB (-0.2±0.2%, P<0.05) and compared with baseline (P<0.001). HFCS-SB increased %hepatic lipid compared with baseline (0.4±0.2%, P<0.05). Compared with aspartame-SB, Matsuda ISI decreased after consumption of HFCS- (P<0.01) and sucrose-SB (P<0.01), and Predicted M ISI decreased after consumption of HFCS-SB (P<0.05). Sucrose- and HFCS-SB increased plasma concentrations of lipids, lipoproteins, and uric acid compared with aspartame-SB. No outcomes were differentially affected by sucrose- compared with HFCS-SB. Beverage group effects remained significant when analyses were adjusted for changes in body weight. Conclusions Consumption of both sucrose- and HFCS-SB induced detrimental changes in hepatic lipid, insulin sensitivity, and circulating lipids, lipoproteins and uric acid in 2 weeks.
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