Purpose Mild-to-moderate iodine deficiency was present in large parts of Germany up to the beginning 1990s and improved from then on. Current epidemiological data on spot urine iodine measurements in German children strongly suggest the re-occurrence of an impaired iodine status. We thus examined whether this re-occurrence is identifiable in more detail, through iodine analyses of 24-h urine samples of a well-characterized cohort of German children in whom samples have been systematically collected from 1985 onward. As iodized salt is a major source for iodine supply, urinary sodium excretion was additionally studied. Methods Daily iodine and sodium excretions were measured in 2600 24-h urine samples collected between 1985 and 2018 by 677 healthy children aged 6–12 years (participants of the DONALD study). These data were compared with 24-h iodine and sodium excretion estimates obtained from spot urine samples collected in the representative German Health Interview and Examination Surveys for Children and Adolescents KiGGS-baseline (2003–2006) and KiGGS-wave-2 (2014–2017). Results Between 1985 and1992, DONALD participants started with a median daily iodine excretion level of 40.1 µg/d. Then, during 1993–2003, iodine excretions mounted up to an approximate plateau (~ 84.8 µg/d). This plateau lasted until 2012. Thereafter, iodine concentrations started to decrease again resulting in a median iodine excretion of only 58.9 µg/d in 2018. Sodium excretion, however, had increased. The marked decrease in iodine status along with an abundant sodium excretion corresponded closely with nationwide KiGGS data. Conclusions As exemplified for the clearly worsening iodine status in German children, longitudinal cohort studies collecting detailed biomarker-based prospective data have the potential to reliably capture health-relevant nutritional changes and trends, applicable on a more comprehensive and even representative population level.

Background: A lower 24-h urine pH (24h-pH), i.e., a higher renal excretion of free protons, at a given acid load to the body, denotes a reduction in the kidney's capacity for net acid excretion (NAE). There is increasing evidence - not only for type 2 diabetes patients, but also for healthy individuals - that higher body fatness or waist circumference (WC) negatively impact on renal function to excrete acids (NAE). We hypothesized that adiposity-related inflammation molecules may mediate this relation between adiposity and renal acid excretion function. Methods: Twelve biomarkers of inflammation were measured in fasting blood samples from 162 adult participants (18-25y) of the DONALD study, who had undergone anthropometric measurements and collected 24-h urine samples. Both Baron and Kenny's steps (B&Ks) to test mediation and causal mediation analysis were conducted to examine the potential mediatory roles of biomarkers of inflammation in the WC-24h-pH relationship after strictly controlling for lab-measured NAE. Results: In B&Ks mediation analysis, leptin, soluble intercellular adhesion molecule-1 (sICAM-1), and adiponectin significantly associated with the outcome 24h-pH and attenuated the WC-pH relation. In agreement herewith, causal mediation analysis estimated the "natural indirect effects" of WC on 24h-pH via leptin (P=0.01) and adiponectin (P=0.03) to be significant with a trend for sICAM-1 (P=0.09). The calculated proportions mediated by leptin, adiponectin and sICAM-1 were 64%, 23%, and 12%, respectively. Conclusion: Both mediation analyses identified an inflammatory (leptin) and an anti-inflammatory (adiponectin) cytokine along with sICAM-1 as being potentially involved in mediating adiposity-related influences on renal acid excretion capacity.

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Background Varying protein intake is known to influence human height growth. However, whether a habitually higher protein intake consistently above dietary recommendations during childhood and adolescence impacts on adult stature is not known. Methods We, therefore, examined habitual protein intake based on 3-day weighed dietary records and 24-h urinary biomarker excretions in a longitudinal cohort of 189 healthy individuals between age 3 and 17 years (analyzing 11 diet recordings and 11 24-urine samples per child on average). Urinary urea nitrogen (uN) excretion was used as biomarker for protein intake. Multilinear regressions were applied to examine the prospective associations of average total and average animal protein intake during growth with the outcome adult height (AH) after adjusting for parental heights, energy intake, dietary potential renal acid load (PRAL), and pubertal, early life, and socioeconomic factors. Results Mean standard deviation scores of total (P = .001) and animal (P < .0001) protein intake as well as uN (P = .01) were prospectively and independently related to adult height in girls, but not in boys. Also for girls only, the fully adjusted regression for renal biomarkers (R 2total = 0.79) indicated an inverse relationship between AH and the urinary biomarker for dietary acidity PRAL (P = .06). Conclusion Our prospective, biomarker-confirmed findings on habitual protein intake during the pediatric period provide evidence that protein ingestion above dietary recommendation contributes to an enhanced AH in girls. This enhancement, in turn, may be weakened by an insufficient alkalizing potential through a PRAL-raising fruit- and vegetable-poor nutrition.