Reduction of salt: will iodine intake remain adequate in The Netherlands?

Salt is the main vehicle for iodine fortification in The Netherlands. A reduction in salt intake may reduce the supply of iodine. Our aim was to quantify the effect of salt reduction on the habitual iodine intake of the Dutch population and the risk of inadequate iodine intake. We used data of the Dutch National Food Consumption Survey (1997–8) and an update of the food composition database to estimate habitual salt and iodine intake. To take into account uncertainty about the use of iodised salt (industrial and discretionary) and food supplements, a simulation model was used. Habitual iodine and salt intakes were simulated for scenarios of salt reduction and compared with no salt reduction. With 12, 25 and 50 % salt reduction in industrially processed foods, the iodine intake remained adequate for a large part of the Dutch population. For the extreme scenario of a 50 % reduction in both industrially and discretionary added salt, iodine intake might become inadequate for part of the Dutch population (up to 10 %). An increment of the proportion of industrially processed foods using iodised salt or a small increase in iodine salt content will solve this. Nevertheless, 8–35 % of 1- to 3-year-old children might have iodine intakes below the corresponding estimated average requirement (EAR), depending on the salt intake scenario. This points out the need to review the EAR value for this age group or to suggest the addition of iodine to industrially manufactured complementary food

Food, nutrition & behaviour : research for healthy eating, healthy living

This brochure illustrates this range of research activities in the domain of food and nutrition, lifestyle and health. It does so by providing examples of collaboration of Wageningen UR with partners in the public and private sector

Misreporting of energy and micronutrient intake estimated by food records and 24 hour recalls, control and adjustment methods in practice

In order to assess nutritional adequacy, valid estimates of nutrient intake are required. One of the main errors in dietary assessment is misreporting. The objective was to review the extent, nature and determinants of misreporting in dietary assessment, how this affects reported intakes of micronutrients and how this is identified and measured, and to identify the best ways of dealing with misreporting when interpreting results. A systematic literature search was conducted for studies of misreporting of dietary intake in adults by 24 hour recalls or by estimated or weighed food records, published up to March 2008. Thirty-seven relevant studies were identified. Possible causes of misreporting were identified. Methods most used to identify misreporting were the Goldberg cut-off (46 % studies) and the doubly labelled water technique (24 % studies). The magnitude of misreporting of energy intake was similar in all three dietary assessment methods. The percentage of under-reporters was about 30 % and energy intake was underestimated by approximately 15 %. Seven papers presented usable data for micronutrient intake. Absolute intakes of Fe, Ca and vitamin C (the three micronutrients addressed in all papers) were on average 30 % lower in low-energy reporters (LER) than that in non-LER and, although results were not consistent, there was a tendency for micronutrient density to be higher in LER. Excluding underreporters or using energy adjustment methods for micronutrient intakes is discussed. Residual method of energy adjustment seems to be a good tool for practice to decrease an influence of misreporting when interpreting results of studies based on food records and 24 hour recall

Functional protection by acute phase proteins alpha(1)-acid glycoprotein and alpha(1)-antitrypsin against ischemia/reperfusion injury by preventing apoptosis and inflammation.

BACKGROUND: Ischemia followed by reperfusion (I/R) causes apoptosis, inflammation, and tissue damage leading to organ malfunction. Ischemic preconditioning can protect against such injury. This study investigates the contribution of the acute phase proteins alpha(1)-acid glycoprotein (AGP) and alpha(1)-antitrypsin (AAT) to the protective effect of ischemic preconditioning in the kidney. METHODS AND RESULTS: Exogenous AGP and AAT inhibited apoptosis and inflammation after 45 minutes of renal I/R in a murine model. AGP and AAT administered at reperfusion prevented apoptosis at 2 hours and 24 hours, as evaluated by the presence of internucleosomal DNA cleavage, terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling, and the determination of renal caspase-1- and caspase-3-like activity. AGP and AAT exerted anti-inflammatory effects, as reflected by reduced renal tumor necrosis factor-alpha expression and neutrophil influx after 24 hours. In general, these agents improved renal function. Similar effects were observed when AGP and AAT were administered 2 hours after reperfusion but to a lesser extent and without functional improvement. Moreover, I/R elicited an acute phase response, as reflected by elevated serum AGP and serum amyloid P (SAP) levels after 24 hours, and increased hepatic acute phase protein mRNA levels after 18 hours of renal reperfusion. CONCLUSIONS: We propose that the antiapoptotic and anti-inflammatory effects of AGP and AAT contribute to the delayed type of protection associated with ischemic preconditioning and other insults. This mechanism is potentially involved in the course of many clinical conditions associated with I/R injury. Moreover, exogenous administration of these proteins may provide new therapeutic means of treatmen