Factors associated with food label use: focus on healthy aspects of orthorexia and orthorexia nervosa.

PURPOSE: This study aimed to investigate the potential relationships between the use of different section of food label, and healthy and pathological aspects of orthorexia among adults. METHODS: This cross-sectional study was conducted using an online survey (n = 1326). Inclusion criteria were being 19-64 years and graduated from at least primary school. Pregnant and lactating women were excluded. Data were collected using questionnaire including socio-demographic variables, lifestyle factors, body weight and height, frequency of reading different sections of food label ("always", "when buying a food for the first time", "when comparing similar packaged foods", "rarely", "never"), food label literacy, and Teruel Orthorexia Scale. Participants were categorized as nutrition facts panel-users, ingredients list-users or claim-users if they read at least one item from the relevant parts. RESULTS: The proportions of nutrition facts, ingredients list, and claims sections users were 72.3%, 76.3%, and 79.9%, respectively. Both healthy and pathological aspects of orthorexia were associated with reading food labels. The healthy orthorexia had the strongest association with using the ingredients list (OR 1.76, 95% CI 1.41-2.20), whereas the orthorexia nervosa showed the highest association with using nutrition facts panel (OR 1.48, 95% CI 1.20-1.81). While women, physically active participants and those with higher food label literacy were more likely to use all sections of food labels; older age, having children, and chronic disease increased the likelihood of using claims and ingredients list (p < 0.05). Besides, following a diet was associated with higher use of nutrition facts and ingredients list (p < 0.05). CONCLUSIONS: The study demonstrates that food label users have higher orthorexia tendencies compared to non-users. Of the food label sections, healthy orthorexia showed the strongest association with use of the list of ingredients, while pathological orthorexia showed the strongest association with use of the nutrition facts panel. LEVEL OF EVIDENCE: Level V, cross-sectional study.

Hepatic cholesterol synthesis and lipoprotein levels impaired by dietary fructose and saturated fatty acids in mice: Insight on PCSK9 and CD36.

OBJECTIVES: The aim of this study was to investigate the uncertain effects of high saturated fatty acids (SFAs) or fructose intake on cholesterol and lipoproteins with an insight of proprotein convertase subtilisin/kexin type 9 (PCSK9)- and cluster of differentiation 36 (CD36)-induced mechanisms. METHODS: Forty male C57 BL/6 mice (8 wks of age) were divided into four groups and fed ad libitum with standard chow or three isocaloric diets containing high SFAs (SFA group), monounsaturated fatty acids (MUFA group, vehicle), or fructose for 15 wks. Subsequently, mice were sacrificed and blood, liver, and heart were collected for further analysis. RESULTS: Consequently, fructose or SFA intake resulted in higher plasma and liver total cholesterol (TC) levels, plasma low-density lipoprotein cholesterol (LDL-C), non-high-density lipoprotein cholesterol (HDL-C), apolipoprotein (Apo)-B levels, TC/HDL-C, and LDL-C/HDL-C ratios, and lower plasma levels of HDL-C and Apo-A1 (P < 0.05). Levels of 3-hydroxy-3-methylglutaryl-CoA reductase and acetyl-CoA acetyltransferase 1 enzymes in liver and CD36 levels in plasma were elevated by high SFAs and fructose intake (P < 0.05), whereas plasma PCSK9 levels were not significantly changed. Fructose and SFA intake increased PCSK9 and CD36 levels in the heart, along with increased CD36 levels in the liver (P < 0.05). Furthermore, plasma LDL-C was found to be positively correlated with liver PCSK9 (r = 0.85, P = 0.02), and CD36 (r = 0.70, P = 0.02) in the SFA and fructose groups. CONCLUSION: High intakes of dietary SFAs and fructose might induce dysregulations in the cholesterol synthesis and blood lipoprotein levels via proposed nutrient-sensitive biomarkers PCSK9 and CD36 in liver and extrahepatic tissues involved in cholesterol homeostasis.

[Is There an Effect of Dietary Fructose on Development and Prognosis of Chronic Diseases?] / Diyetle Alinan Fruktozun Kronik Hastaliklarin Gelismesinde ve Prognozunda Etkisi Var midir?

Dietary sources of fructose are not only honey, fruit, sucrose, but also high fructose corn syrup in various foods and beverages. Total amount of daily fructose intake is rising by especially increasing use of high fructose corn syrup in the food industry. Fructose can lead to obesity by contributing to high-energy intake and lipogenesis in the body. Depending on the source of fructose, dose and duration, it was involved in de-novo lipid synthesis. Fructose may increase the risk of insulin resistance, non-alcoholic fatty liver and kidney diseases by affecting blood glucose and insulin levels. On the other hand, fructose may initiate inflammatory processes in the organism. In addition to these, fat or salt consisting typical western type diet with high fructose consumption, can increase the potential effect of fructose on chronic diseases. As a result, although it is not fully supported by clinical studies, it is thought that high amounts of fructose intake may increase the risk of chronic disease shown by experimental studies. Also it should be noted that beside high fructose, typical western-style high-fat and high-salt diet may increase the risk of chronic diseases such as obesity, cardiovascular diseases and worsen metabolic syndrome parameters. Furthermore, synthetic fructose, is able to cause some adverse metabolic effects when taken in large amounts; consumption of high amounts of fructose by fruit or honey these negative effects can be either not seen or less observed based on the amount.

Maternal dietary free or bound fructose diversely influence developmental programming of lipogenesis.

BACKGROUND: Maternal dietary choices throughout preconception, pregnancy, and lactation irreversibly affect the development of fetal tissues and organs, known as fetal programming. Recommendations tend to emphasize reducing added sugars. However, the impact of maternal dietary free or bound fructose in added sugars on developmental programming of lipogenesis is unknown. METHODS: Virgin Sprague-Dawley rats were randomly divided into five groups. Rats were given feed and plain water (control) or water containing maltodextrin (vehicle), fructose, high-fructose corn syrup (HFCS) containing 55% fructose, sucrose (20% w/v) for 12 weeks before mating and throughout the pregnancy and lactation periods. Body weight, water, and feed intake were measured throughout the study. At the end of the lactation period, blood was drawn to determine the fasting levels of glucose, insulin, triglycerides, and non-esterified fatty acids (NEFA) in blood. Triglycerides and acetyl Co-A Carboxylase-1 (ACC1) levels in livers were analyzed, and insulin resistance was calculated. RESULTS: The energy intake of dams in the HFCS group was higher than in the fructose group, while weight gain was less in the HFCS group than in the fructose group. HFCS resulted in greater insulin resistance in dams, whereas free fructose had a robust effect on the fetal programming of insulin resistance. Free fructose and HFCS in the maternal diet increased blood and liver triglycerides and NEFA content in pups. Furthermore, fructose and HFCS exposure increased phosphorylated ACC1 as compared to maltodextrin and control, indicating greater fatty acid synthesis in pups and dams. CONCLUSION: Different types of added sugar in the maternal diet have different metabolic effects on the developmental programming of lipogenesis. Consequently, high fructose intake via processed foods may increase the risk for chronic diseases, and free fructose might contribute to developmental programming of chronic diseases more than bound fructose.