An objective noninvasive biomarker for fruit and vegetable (FV) consumption would help to more reliably characterize the relationship between FV intake and health status in observational studies. Because increases in urinary hippuric acid (HA) were observed after consumption of several FV varieties, we aimed to investigate whether 24-h urinary HA may represent a potential biomarker for FV consumption in children and adolescents. The association of FV and juice (FVJ) intake calculated from 3-d weighed dietary records with 24-h urinary HA excretion was analyzed in 240 healthy children and adolescents and compared with associations of the established biomarkers urinary nitrogen (uN) and urinary potassium (uK) with protein and potassium intake, respectively. Spearman correlation coefficients (r) and cross-classifications were calculated for all diet-biomarker associations. Potential confounders for the HA-FVJ association were examined in linear regression models. In children, correlations of HA with FVJ (r = 0.62), uN with protein (r = 0.64), and potassium intake with uK (r = 0.65) were comparable. In adolescents, the HA-FVJ association was weaker (r = 0.41) compared with the biomarkers uN (r = 0.60) and uK (r = 0.58) (all P < 0.0001). Cross-classification into the same/adjacent quartile by dietary and urinary data were >85% for all analyzed comparisons except for a 75% classification agreement between HA and FVJ in adolescents. Unadjusted and adjusted linear regression models indicated significant (P < 0.0001) HA-FVJ associations in both age groups. FVJ explained more of the variability in HA excretion in children (R(2) = 0.38) than in adolescents (R(2) = 0.22). Our findings in children showing HA-FVJ associations comparable to those for well-established biomarkers with their respective dietary intakes suggest that HA may represent a useful biomarker for FVJ.

Low salt intake and high fruit and vegetable intake (FVI) have been shown to reduce blood pressure (BP) in adults. Longitudinal data on the independent effect of both FVI and salt intake on BP in healthy normotensive children are not available yet. In the present study, we aimed to characterise the concomitant influence of salt intake and FVI on BP development throughout childhood and adolescence. We examined 435 healthy subjects, for whom at least three repeated measurements of BP had been taken and who had provided 24 h urine samples and 3 d weighed dietary records between 4 and 18 years of age. BP was measured using a mercury sphygmomanometer (Mercuro 300, WelchAllyn) and salt intake was determined based on 24 h Na excretion. The intra-individual change in salt intake was almost significantly associated with the change in systolic BP (SBP, P¼0·06) and marginally (P¼ 0·09) with that in diastolic BP (DBP) in puberty, but not in pre-puberty. A 1 g/d increase in salt intake was associated with a 0·2 mmHg increase in SBP. In pre-puberty, but not in puberty, differences in FVI between children predicted between-person variations in SBP and DBP (P¼ 0·03). Corresponding findings were obtained for 24 h K excretion (a urinary indicator for FVI). A 100 g/d lower FVI was related to a 0·4 mmHg higher BP value. In conclusion, in healthy children and adolescents with BP in the low-normal range, both salt intake and FVI may already start to influence BP, although at a small magnitude. The potential importance of establishing healthy eating habits in childhood for later BP development emphasises the role of higher FVI and lower salt intake in the prevention of hypertension in the long run.Key words: Blood pressure: Salt: fruit and vegetable: Children: Potassium CVD and cerebrovascular diseases are two leading causes of death (1) and hypertension is a main risk factor for the occurrence of CHD and stroke (2) . The evidence for a causal relationship between chronic high salt intake and high blood pressure (BP) in adults is strong (3,4) . Apart from salt intake, the potential of a higher fruit and vegetable intake (FVI) to decrease BP has been documented in well-conducted intervention studies (5,6) . In one well-controlled trial, the Dietary Approaches to Stop Hypertension (DASH) Study, it has been shown that a reduction of salt intake together with the consumption of a FV-rich diet leads to the greatest reduction of BP (7) .Concern exists about the rising prevalence of hypertension in childhood and adolescence (8) and the existing tracking pattern of BP (9) . Therefore, it is important that modifiable risk factors be identified and preventive nutritional measures be started early in childhood. A meta-analysis of ten controlled trials (10) with a median duration of 4 weeks has provided evidence that dietary salt intake during growth plays a role in the regulation of BP in children. Longitudinal or intervention studies on the influence of FVI on BP are rare, especially in normotensive children. So far, a small longitudina...

Diets high in sulfur-rich protein and low in fruits and vegetables affect human acid-base balance adversely. Corresponding subclinical forms of metabolic acidosis have been linked to hypertension in adults. We longitudinally examined relations of dietary acid load with blood pressure in 257 healthy prepuberty children with 3 or more parallel 3-day weighed dietary records, 24-h urine, and blood pressure measurements. Urinary net acid excretion and the potential renal acid load (PRAL), determined as the difference of major urinary nonbicarbonate anions and mineral cations, were used to predict dietary acid load. PRAL was also calculated from dietary data. In repeated-measures regression analyses, adjusted for body size and dietary fiber, an intraindividual increase of 10 mEq above the 'usual' net acid excretion or urine PRAL were each significantly related to a 0.6-0.7 mm Hg increased systolic blood pressure. Differences in urine PRAL among the children also significantly predicted between-person differences in systolic blood pressure. A higher individual net acid excretion or urine PRAL and intraindividual increase in urine PRAL were significantly related to higher diastolic blood pressure. Blood pressure associations were nonsignificant for dietary PRAL and urinary sodium. Thus, in healthy children, renal biomarker analyses reveal an association of proton load with higher blood pressure. Especially for systolic blood pressure, a more alkalizing nutrition may be beneficial for blood pressure development within a given individual. Experimental confirmation of a causal acid load-blood pressure link is required.

A variety of genetic, mechano-response-related, endocrine-metabolic, and nutritional determinants impact bone health. Among the nutritional influences, protein intake and dietary acid load are two of the factors most controversially discussed. Although in the past high protein intake was often assumed to exert a primarily detrimental impact on bone mass and skeletal health, the majority of recent studies indicates the opposite and suggests a bone-anabolic influence. Studies examining the influence of alkalizing diets or alkalizing supplement provision on skeletal outcomes are less consistent, which raises doubts about the role of acid-base status in bone health. The present review critically evaluates relevant key issues such as acid-base terminology, influencing factors of intestinal calcium absorption, calcium balance, the endocrine-metabolic milieu related to metabolic acidosis, and some methodological aspects of dietary exposure and bone outcome examinations. It becomes apparent that for an adequate identification and characterization of either dietary acid load's or protein's impact on bone, the combined assessment of both nutritional influences is necessary.

Nonalcoholic fatty liver disease (NAFLD), frequently already present in young subjects, has been linked to reduced growth hormone levels and signaling. Similar hormonal changes occur during metabolic acidosis (MA), which may thus contribute to an increased NAFLD risk. Because subclinical MA can be diet induced, we aimed to examine whether a higher diet-dependent acid load during adolescence is prospectively associated with several currently used NAFLD surrogates in young adulthood. Dietary acidity during adolescence (boys:10-15 y, girls: 9-14 y) was calculated as potential renal acid load (PRAL) from at least three 3-d weighed dietary records according to a published algorithm considering dietary protein and minerals in 145 healthy participants. Routine measurements derived from blood analysis and anthropometric data in participants' young adulthood (18-25 y) were used to determine the NAFLD surrogates alanine-aminotransferase (ALT), hepatic steatosis index (HSI), and fatty liver index (FLI). Sex-stratified linear regression models, adjusted for dietary fiber, saturated fat, protein, and adolescent BMI SD scores, were run with PRAL as the independent variable. Dietary PRAL during puberty was positively associated with ALT (P = 0.02), HSI (P = 0.002), and FLI (P = 0.005) in adult females but not males. Females with an adolescent dietary acid load in the highest tertile had 3.5, 4.4, and 4.5 higher values of ALT, HSI, and FLI as adults, respectively, compared to females with the lowest PRAL. The present findings suggest that higher dietary acidity in adolescence may be prospectively associated with hepatic lipid accumulation in females. Whether this relationship is due to the higher proton load or rather represents an unhealthy dietary pattern requires further investigation.