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Evidence of whether nutrition students are free from food-related issues or at higher risk for eating disorders is inconsistent. This study aimed to assess disordered eating behaviors and food addiction among nutrition and non-nutrition major college students. Students (n = 967, ages 18–25, female 72.7%, white 74.8%) enrolled at a public university completed online demographic characteristics surveys and validated questionnaires measuring specific disordered eating behaviors. Academic major category differences were compared. Additionally, high risk participants were assessed by weight status and academic year. Overall, 10% of respondents were a high level of concern for developing eating disorders. About 10.3% of respondents met criteria for food addiction. In addition, 4.5% of respondents had co-occurrence of eating disorder risk and food addiction risk out of total respondents. There were no significant differences in level of concern for developing an eating disorder, eating subscales, or food addiction among academic majors. The percentage of high risk participants was lower in the underweight/normal weight group than in the overweight/obese group in health-related non-nutrition major students but not in nutrition students. Early screening, increasing awareness, and promoting healthy eating habits could be potential strategies to help treat and prevent the development of disorders or associated health conditions in nutrition as well as non-nutrition students.

It has been postulated that fructose-induced triglyceride synthesis is augmented when accompanied by glucose. Chronic elevations could lead to excess fat accumulation in the liver and ectopic fat deposition in muscles, which in turn could contribute to the induction of abnormalities in glucose homeostasis, insulin resistance, and the subsequent development of type 2 diabetes. Our objective was to evaluate the effect of the addition of commonly consumed fructose- and (or) glucose-containing sugars in the usual diet on liver fat content and intramuscular adipose tissue. For 10 weeks, 64 individuals (mean age, 42.16 ± 11.66 years) consumed low-fat milk sweetened with either high-fructose corn syrup (HFCS) or sucrose; the added sugar matched consumption levels of fructose in the 25th, 50th, and 90th percentiles of the population. The fat content of the liver was measured with unenhanced computed tomography imaging, and the fat content of muscle was assessed with magnetic resonance imaging. When the 6 HFCS and sucrose groups were averaged, there was no change over the course of 10 weeks in the fat content of the liver (13.32% ± 10.49% vs. 13.21% ± 10.75%; p > 0.05), vastus lateralis muscle (3.07 ± 0.74 g per 100 mL vs. 3.15 ± 0.84 g per 100 mL; p > 0.05), or gluteus maximus muscle (4.08 ± 1.50 g per 100 mL vs. 4.24 ± 1.42 g per 100 mL; p > 0.05). Group assignment did not affect the result (interaction > 0.05). These data suggest that when fructose is consumed as part of a typical diet in normally consumed sweeteners, such as sucrose or HFCS, ectopic fat storage in the liver or muscles is not promoted.

The American Heart Association (AHA) and World Health Organization (WHO) have recommended restricting calories from added sugars at lower levels than the Institute of Medicine (IOM) recommendations, which are incorporated in the Dietary Guidelines for Americans 2010 (DGAs 2010). Sucrose (SUC) and high fructose corn syrup (HFCS) have been singled out for particular concern, because of their fructose content, which has been specifically implicated for its atherogenic potential and possible role in elevating blood pressure through uric acid-mediated endothelial dysfunction. This study explored the effects when these sugars are consumed at typical population levels up to the 90th percentile population consumption level for fructose. Three hundred fifty five overweight or obese individuals aged 20–60 years old were placed on a eucaloric diet for 10 weeks, which incorporated SUC- or HFCS-sweetened, low-fat milk at 8%, 18% or 30% of calories. There was a slight change in body weight in the entire cohort (169.1 ± 30.6 vs. 171.6 ± 31.8 lbs, p < 0.01), a decrease in HDL (52.9 ± 12.2 vs. 52.0 ± 13.9 mg/dL, p < 0.05) and an increase in triglycerides (104.1 ± 51.8 vs. 114.1 ± 64.7 mg/dL, p < 0.001). However, total cholesterol (183.5 ± 42.8 vs. 184.4 mg/dL, p > 0.05), LDL (110.3 ± 32.0 vs. 110.5 ± 38.9 mg/dL, p > 0.05), SBP (109.4 ± 10.9 vs. 108.3 ± 10.9 mmHg, p > 0.05) and DBP (72.1 ± 8.0 vs. 71.3 ± 8.0 mmHg, p > 0.05) were all unchanged. In no instance did the amount or type of sugar consumed affect the response to the intervention (interaction p > 0.05). These data suggest that: (1) when consumed as part of a normal diet, common fructose-containing sugars do not raise blood pressure, even when consumed at the 90th percentile population consumption level for fructose (five times the upper level recommended by the AHA and three times the upper level recommended by WHO); (2) changes in the lipid profile are mixed, but modest.