Association Between Dietary Intake of Phosphorus and Measures of Obesity in the Jackson Heart Study.

BACKGROUND: The relation between phosphorus (P) intake and obesity is equivocal, with hypotheses in both directions. OBJECTIVES: We investigated the relationship between P intake, assessed from a current database, and calculated bioavailable P intake and obesity among African-American adults. METHODS: We examined associations between original and bioavailable P (total, added, and natural) and BMI and waist circumference (WC) in a cross-sectional study of 5306 African-American adults (21-84 y) from the Jackson Heart Study. A total of 3300 participants had complete interviews, valid dietary data, and normal kidney function. Diet was assessed by food frequency questionnaire. A novel algorithm was used to estimate P bioavailability. BMI or WC was regressed on each P variable, adjusting for total energy intake and potential confounders. RESULTS: After adjusting for covariates, original P (total and added) and bioavailable P (total and added) intakes (expressed/100 mg) were associated with BMI (ß: 0.11, 0.67, 0.31, and 0.71, respectively; all P < 0.0001). Neither original nor bioavailable natural P was significantly associated (ß: -0.03 and 0.09, respectively; both P > 0.05). When added and natural P were included in the same model, added P (original and bioavailable) intakes remained strongly associated with BMI (0.70 and 0.73, respectively; both P < 0.0001). Similar results were seen for WC. Intake of original added P tended to be more strongly associated with BMI, in females (ß: 0.72; P < 0.0001) than in males (ß: 0.56; P = 0.003) (P-interaction = 0.06). CONCLUSIONS: We found that greater intake of added, not natural, which may be a proxy for intake of processed foods was associated with higher BMI and WC. These were somewhat stronger when bioavailability was considered and for women than for men. Further investigation is needed to fully understand the mechanisms driving these associations.

Higher Renal Net Acid Excretion, but Not Higher Phosphate Excretion, during Childhood and Adolescence Associates with the Circulating Renal Tubular Injury Marker Interleukin-18 in Adulthood.

High dietary phosphorus intake (P-In) and high acid loads may adversely affect kidney function. In animal models, excessive phosphorus intake causes renal injury, which, in humans, is also inducible by chronic metabolic acidosis. We thus examined whether habitually high P-In and endogenous acid production during childhood and adolescence may be early indicators of incipient renal inflammatory processes later in adulthood. P-In and acid-base status were longitudinally and exclusively determined by biomarker-based assessment in 277 healthy children, utilizing phosphate and net acid excretion (NAE) measurements in 24 h urine samples repeatedly collected between the ages of 3 and 17 years. Standard deviation scores (by sex and age) were calculated for anthropometric data and for the urinary biomarkers available within age range 3-17 years. Multivariable linear regression was used to analyze the relations of phosphate excretion and NAE with the adulthood outcome circulating interleukin-18 (IL-18), a marker of inflammation and kidney dysfunction. After adjusting for growth- and adulthood-related covariates and pro-inflammatory biomarkers to rule out confounding by non-renal inflammatory processes, regression models revealed a significant positive relationship of long-term NAE (p = 0.01), but not of long-term phosphate excretion with adult serum IL-18. Similar significant positive regression results were obtained after replacing NAE with 24 h urinary ammonium excretion as the exposition variable. Our results suggest that even moderate elevations in renal ammonia production, as caused by habitually higher acid loading during growth, may affect the intrarenal pro-inflammatory system in the long-term, known to be boosted by acidosis-induced raised ammoniagenesis.

A U-shaped association between dietary phosphorus intake and new-onset diabetes: A nationwide cohort study in China.

BACKGROUND AND AIMS: The association between dietary phosphorus intake and the risk of diabetes remains uncertain. We aimed to investigate the relation of dietary phosphorus intake with new-onset diabetes among Chinese adults. METHODS AND RESULTS: A total of 16,272 participants who were free of diabetes at baseline from the China Health and Nutrition Survey were included. Dietary intake was measured by 3 consecutive 24-h dietary recalls combined with a household food inventory. Participants with self-reported physician-diagnosed diabetes, or fasting glucose ≥7.0 mmol/L or glycated hemoglobin ≥6.5% during the follow-up were defined as having new-onset diabetes. During a median follow-up of 9.0years, 1101 participants developed new-onset diabetes. Overall, the association between dietary phosphorus intake with new-onset diabetes followed a U-shape (P for nonlinearity<0.001). The risk of new-onset diabetes significantly decreased with the increment of dietary phosphorus intake (per SD increment: HR, 0.64; 95%CI, 0.48-0.84) in participants with phosphorus intake <921.6 mg/day, and increased with the increment of dietary phosphorus intake (per SD increment: HR, 1.33; 95%CI, 1.16-1.53) in participants with phosphorus intake ≥921.6 mg/day. Consistently, when dietary phosphorus intake was assessed as quintiles, compared with those in the 3rd quintile (905.0-<975.4 mg/day), significantly higher risks of new-onset diabetes were found in participants in the 1st-2nd quintiles (<905.0 mg/day: HR, 1.59; 95%CI, 1.30-1.94), and 4th-5th quintiles (≥975.4 mg/day: HR, 1.46; 95%CI, 1.19-1.78). CONCLUSIONS: There was a U-shaped association between dietary phosphorus intake and new-onset diabetes in general Chinese adults, with an inflection point at 921.6 mg/day and a minimal risk at 905.0-975.4 mg/day of dietary phosphorus intake.

High phosphorus intake and gut-related parameters - results of a randomized placebo-controlled human intervention study.

BACKGROUND: In recent years, high phosphate intakes were discussed critically. In the small intestine, a part of the ingested phosphate and calcium precipitates to amorphous calcium phosphate (ACP), which in turn can precipitate other intestinal substances, thus leading to a beneficial modulation of the intestinal environment. Therefore, we analysed faecal samples obtained from a human intervention study regarding gut-related parameters. METHODS: Sixty-two healthy subjects (men, n = 30; women, n = 32) completed the double-blind, placebo-controlled and parallel designed study (mean age: 29 ± 7 years; mean BMI: 24 ± 3 kg/m2). Supplements were monosodium phosphate and calcium carbonate. During the first 2 weeks, all groups consumed a placebo sherbet powder, and afterwards a sherbet powder for 8 weeks according to the intervention group: P1000/Ca0 (1000 mg/d phosphorus), P1000/Ca500 (1000 mg/d phosphorus and 500 mg/d calcium) and P1000/Ca1000 (1000 mg/d phosphorus and 1000 mg/d calcium). After the placebo period and after 8 weeks of intervention faecal collections took place. We determined in faeces: short-chain fatty acids (SCFA) and fat as well as the composition of the microbiome (subgroup) and cyto- and genotoxicity of faecal water (FW). By questionnaire evaluation we examined tolerability of the used phosphorus supplement. RESULTS: Faecal fat concentrations did not change significantly due to the interventions. Concentrations of faecal total SCFA and acetate were significantly higher after 8 weeks of P1000/Ca500 supplementation compared to the P1000/Ca0 supplementation. In men, faecal total SCFA and acetate concentrations were significantly higher after 8 weeks in the P1000/Ca1000 group compared to the P1000/Ca0 one. None of the interventions markedly affected cyto- and genotoxic activity of FW. Men of the P1000/Ca1000 intervention had a significantly different gut microbial community compared to the men of the P1000/Ca0 and P1000/Ca500 ones. The genus Clostridium XVIII was significantly more abundant in men of the P1000/Ca1000 intervention group compared to the other groups. Supplementations did not cause increased intestinal distress. CONCLUSIONS: The used high phosphorus diet did not influence cyto- and genotoxicity of FW and the concentrations of faecal fat independent of calcium intake. Our study provides first hints for a potential phosphorus-induced modulation of the gut community and the faecal total SCFA content. TRIAL REGISTRATION: The trial is registered at ClinicalTrials.gov as NCT02095392 .

Phosphorus Additives and Albuminuria in Early Stages of CKD: A Randomized Controlled Trial.

BACKGROUND: Little is known about the effects of phosphorus additives on patients with kidney disease. STUDY DESIGN: Randomized, double-blind, crossover trial. SETTING & PARTICIPANTS: 31 adults with early stages of presumed chronic kidney disease (estimated glomerular filtration rate ≥ 45mL/min/1.73m2; urine albumin-creatinine ratio sex-specific cutoff points: men ≥ 17mg/g, women ≥ 25mg/g). INTERVENTION: Higher versus lower phosphorus intake for 3 weeks. Higher phosphorus intake was achieved by the addition of commercially available diet beverages and breakfast bars to diet. OUTCOMES: Change in 24-hour urine albumin excretion and plasma fibroblast growth factor 23 level. MEASUREMENTS: Two 24-hour urine collections and a single fasting blood draw at the end of each period. RESULTS: Mean baseline values for phosphorus intake, 24-hour urine phosphorus excretion, and estimated glomerular filtration rate were 1,113±549 (SD) mg/d, 688±300mg/d, and 74.6±22.0mL/min/1.73m2. Median urine albumin excretion of 82.7 (IQR, 39.6-174.1) mg/d. Although phosphorus intake from study products increased by 993mg/d (P<0.001) during the higher compared to lower phosphorus additive period, background phosphorus intake decreased by 151mg/d (P=0.004). Higher phosphorus additive consumption increased 24-hour urine phosphorus excretion by 505 (95% CI, 381 to 629) mg/d (P<0.001), but did not significantly increase albuminuria (higher vs lower: 14.3%; 95% CI, -2.5% to 34.0%; P=0.1) or fibroblast growth factor 23 level (higher vs lower: 3.4%; 95% CI, -5.9% to 13.6%; P=0.4). LIMITATIONS: Small sample size, short duration of intervention, changes in background diet during the intervention. CONCLUSIONS: A 3-week consumption of higher phosphorus food additives did not significantly increase albuminuria. Further studies are needed to confirm these results.

The New Nordic Diet: phosphorus content and absorption.

PURPOSE: High phosphorus content in the diet may have adverse effect on cardiovascular health. We investigated whether the New Nordic Diet (NND), based mainly on local, organic and less processed food and large amounts of fruit, vegetables, wholegrain and fish, versus an Average Danish Diet (ADD) would reduce the phosphorus load due to less phosphorus-containing food additives, animal protein and more plant-based proteins. METHODS: Phosphorus and creatinine were measured in plasma and urine at baseline, week 12 and week 26 in 132 centrally obese subjects with normal renal function as part of a post hoc analysis of data acquired from a 26-week controlled trial. We used the fractional phosphorus excretion as a measurement of phosphorus absorption. RESULTS: Mean baseline fractional phosphorus excretion was 20.9 ± 6.6 % in the NND group (n = 82) and 20.8 ± 5.5 % in the ADD group (n = 50) and was decreased by 2.8 ± 5.1 and 3.1 ± 5.4 %, respectively, (p = 0.6) at week 26. At week 26, the mean change in plasma phosphorus was 0.04 ± 0.12 mmol/L in the NND group and -0.03 ± 0.13 mmol/L in the ADD group (p = 0.001). Mean baseline phosphorus intake was 1950 ± 16 mg/10 MJ in the NND group and 1968 ± 22 mg/10 MJ in the ADD group and decreased less in the NND compared to the ADD (67 ± 36 mg/10 MJ and -266 ± 45 mg/day, respectively, p < 0.298). CONCLUSION: Contrary to expectations, the NND had a high phosphorus intake and did not decrease the fractional phosphorus excretion compared with ADD. Further modifications of the diet are needed in order to make this food concept beneficial regarding phosphorus absorption.

Estimate of dietary phosphorus intake using 24-h urine collection.

Increases in serum phosphorus levels and dietary phosphorus intake induces vascular calcification, arterial sclerosis and cardiovascular diseases. Limiting phosphorus intake is advisable, however, no assessment methods are capable of estimating dietary phosphorus intake. We hypothesized that urinary phosphorus excretion can be translated into estimation of dietary phosphorus intake, and we evaluated whether a 24-h urine collection method could estimate dietary phosphorus intake. Thirty two healthy subjects were recruited for this study. Subjects collected urine samples over 24 h and weighed dietary records. We calculated dietary protein intake and phosphorus intake from dietary records and urine collection, and investigated associations between the two methods in estimating protein and phosphorus intake. Significant positive correlations were observed between dietary records and UC for protein and phosphorus intake. The average intakes determined from dietary records were significantly higher than from urine collection for both protein and phosphorus. There was a significant positive correlation between both the phosphorus and protein difference in dietary records and urine collection. The phosphorus-protein ratio in urine collection was significantly higher than in dietary records. Our data indicated that the 24-h urine collection method can estimate the amount of dietary phosphorus intake, and the results were superior to estimation by weighed dietary record.

Intakes of selected nutrients, bone mineralisation and density of adolescent female swimmers over a three-year period.

The aim of this study was to conduct three-year monitoring of bone mineralization (BMC) and bone mineral density (BMD) of adolescent girls engaged in swimming at the time of attaining the peak bone mass and of their counterparts leading a rather sedentary life, considering the intakes of calcium, phosphorus and protein, as well as the proportions among those nutrients. Two groups of girls aged 11-13 years were studied 3 times at yearly intervals: untrained controls (n = 20) and those engaged in competitive swimming (n = 20). Bone density was determined by dual-energy X-ray absorptiometry (DXA) in the lumbar spine (L2 - L4). Nutrient intakes (energy, protein, calcium, phosphorus) were assessed from 24-h recalls. The group of swimmers had significantly lower BMI values than the control group. No systematic, significant between-group differences were found in nutrient intake or in bone mineralization variables. Calcium intake was below the recommended norm in all subjects but mean values of bone mineralization variables (BMC, BMD) steadily increased in both groups. The BMD z-scores proved negative throughout the three-year period of early adolescence in both groups of girls and that decrease was significant in swimmers. This could have been due to insufficient calcium intake as well as to inadequate calcium-to-phosphate and protein-to-calcium ratios and, when continued, might result in a decreased bone mass in adulthood.

Stepwise Reduction of Dietary Phosphorus in Diets for Piglets and Fattening Pigs of Different Genetic Origin Housed under Various Station Environments-A Ringtest.

The reduction of emissions of nutrients from livestock is one of the main topics in areas with intensive animal husbandry. In order to minimize the loss of nutrients into the environment, it is common practice to feed animals as close as possible to metabolic demands. For phosphorus (P), there are various studies for swine and poultry, which showed that a reduction of dietary P levels is possible, if a sufficient level of phytase is added to the diet. The supplementation of a sufficient dosage of phytase to plant-based diets leads to an increase in digestible phosphorus (dP) upon the hydrolisation of phytate (InsP6) to P and lower inositol-phosphates. However, most of these studies were conducted under standardized experimental conditions. In terms of transfer to practical conditions with varying housing, management and genetics, there are concerns that have led to speculation by farmers and veterinarians whether the reduction of dietary P could negatively affect bone health and therefore animal welfare. In order to test whether a reduction of dietary P according to the recommendations for dP of the German Society of Nutrition Physiology (GfE) affects bone mineralization and growth performance, a ringtest was conducted where piglets and fattening pigs were fed at four experimental stations with three centrally produced diets from the same batches. The diets contained three different levels of P and were designed to reflect practical diets. The P level decreased from diet one to three, respectively. Diets one and two were calculated to contain P levels, which are typically fed under practical conditions in Germany. The third diet was optimized to fulfill the requirements of dP by the GfE. The animals were fed in two phases as post-weaning piglets (8-15 kg and 15-28 kg BW) followed by a three-phase fattening regime (28-60 kg, 60-90 kg and 90-120 kg BW). Individual body weight and feed consumption (pen basis or individually, depending on the experimental station) were recorded for every feeding phase. At the end of the experiment, animals were slaughtered. At one experimental station, additional blood serum, metatarsi of the left leg and kidney tissue were sampled to analyze serum P concentration, expression of P transporters in the kidney and bone traits. In two experimental stations, femur and vertebra were sampled, and bone ash was determined. Overall, animal performance and all other traits analyzed did not differ between the treatment with the highest and the treatment with the lowest dietary P concentration. The results demonstrate that it is possible to decrease dietary P according to the recommendations for dP of the GfE, without impairing the animals' performance or mineral homeostasis and health. A reduction of total P by reducing mineral P to the levels of the present study require the supplementation of phytase to achieve sufficient concentrations of dP.

Industrial Use of Phosphate Food Additives: A Mechanism Linking Ultra-Processed Food Intake to Cardiorenal Disease Risk?

The consumption of ultra-processed food (UPF) keeps rising, and at the same time, an increasing number of epidemiological studies are linking high rates of consumption of UPF with serious health outcomes, such as cardiovascular disease, in the general population. Many potential mechanisms, either in isolation or in combination, can explain the negative effects of UPF. In this review, we have addressed the potential role of inorganic phosphate additives, commonly added to a wide variety of foods, as factors contributing to the negative effects of UPF on cardiorenal disease. Inorganic phosphates are rapidly and efficiently absorbed, and elevated serum phosphate can lead to negative cardiorenal effects, either directly through tissue/vessel calcification or indirectly through the release of mineral-regulating hormones, parathyroid hormone, and fibroblast growth factor-23. An association between serum phosphate and cardiovascular and bone disease among patients with chronic kidney disease is well-accepted by nephrologists. Epidemiological studies have demonstrated an association between serum phosphate and dietary phosphate intake and mortality, even in the general American population. The magnitude of the role of inorganic phosphate additives in these associations remains to be determined, and the initial step should be to determine precise estimates of population exposure to inorganic phosphate additives in the food supply.

Acute Effects of an Inorganic Phosphorus Additive on Mineral Metabolism and Cardiometabolic Risk Factors in Healthy Subjects.

CONTEXT: Hyperphosphatemia and high levels of fibroblast growth factor 23 (FGF23) are risk factors for cardiovascular events in patients with chronic kidney diseases. However, the impact of an inorganic phosphorus additive in healthy people is largely unknown. OBJECTIVE: We aimed to investigate the acute effect of excessive dietary phosphorus administered as sodium dihydrogen phosphate on the postprandial levels of Pi and FGF23 and the response to food. METHODS: This study was a double-blind placebo-controlled crossover study with 29 healthy male and female participants from the general community who were administered a single dose of either 700 mg phosphorus (NaH2PO4) or a sodium-adjusted placebo in combination with a test meal. Postprandial plasma levels of Pi and FGF23 were measured. RESULTS: Compared with placebo, oral phosphorus increased the plasma Pi level, which remained elevated during the ensuing 8 hours (at 480 minutes: 1.31 vs 1.16 mmol/l; P < 0.001), increased urinary Pi (iAUC0-480 789 vs 95 mmol/mmol; P < 0.001), reduced tubular Pi reabsorption (iAUC0-480 -31.5 vs -6.2; P < 0.001), decreased urinary calcium (iAUC0-240 30.6 vs 53.0 mmol/mmol; P = 0.009), and stimulated the release of parathyroid hormone (iAUC0-480 2212 vs 768 ng/l; P < 0.001). However, the FGF23 levels did not change. Postprandial levels of glucose, insulin, and lipids were not substantially affected by phosphorus vs placebo. CONCLUSION: An oral phosphorus load can induce elevated postprandial levels of circulating Pi for hours in healthy subjects, despite rapid homeostatic counterreactions. FGF23 levels and the postprandial response to food were not affected.

Effect of Dietary Phosphorous Restriction on Fibroblast Growth 2 Factor-23 and sKlotho Levels in Patients with Stages 1-2 Chronic Kidney Disease.

Hyperphosphatemia has emerged as an independent risk factor for cardiovascular disease (CVD) and excess mortality in chronic kidney disease (CKD). The study evaluates the effect of dietary phosphorus (Ph) restriction (DPhR) at an early stage as a therapeutic strategy for delaying CKD progression and preventing CVD. Methods: This was a one-year interventional study conducted on 79 stage 1 and 2 CKD patients. The dietary phosphorus intake (DPhI), fibroblast growth factor-23 (FGF-23), sKlotho and serum phosphorous (SP) levels were analyzed. Patients were categorized into two groups based on their DPhI, recommended DPhI (RPhI) with <1000 mg/day of dietary phosphorous (dietary counselling) and high DPhI (HPhI) with >1000 mg/day (dietary intervention). For comparisons of differences between the two groups, independent t-test; for correlation analysis, Pearson correlation; for identifying the significant associated risk factors for CKD, binary logistic regression analysis and for comparing the means across the three visits, repeated measures ANOVA were used for statistical analysis. Results: The mean age and glomerular filtration rate (GFR) of CKD patients were 38 ± 12 years and 82.95 ± 16.93 mL/min/1.73 m2. FGF-23, SP, dietary protein and DPhI were significantly higher and sKlotho was significantly lower in HPhI group than RPhI group. In HPhI group; GFR, sKlotho, SP and FGF-23 correlated significantly with DPhI. Risk factors with a statistical bearing on the progression of CKD were animal-based diet, family history of CKD and hypertension. In HPhI group; GFR, DPhI, SP and FGF-23 levels significantly improved within the intervention period whereas a significant increase in sKlotho levels was observed in both the groups. Conclusion: Restricting DPhI emerged as a favorable therapeutic strategy for CKD patients for improving renal function and controlling hyperphosphatemia. The results of the present study may serve as the basis for future interventional studies with dietary phosphate restriction in the initial stages of CKD that would preserve renal function. Highlights: Early restriction of dietary phosphorus prevents decline in eGFR, elevation in FGF23 and increases Klotho levels.

Bioavailability of phosphorus and kidney function in the Jackson Heart Study.

BACKGROUND: High phosphorus (P) exposure may have negative effects on kidney function. Nutrient databases provide total P, but bioavailability varies by source. OBJECTIVES: We aimed to assess natural, added, and bioavailable P intake, and to relate these to estimated glomerular filtration rate (eGFR) in the Jackson Heart Study (JHS). METHODS: A total of 3962 African-American participants of the JHS, aged 21-84 y, with urine albumin:creatinine ratio < 30 mg/g, and eGFR ≥ 60 mL · min-1 · 1.73 m-2, and without self-reported kidney disease, were included. Diet was assessed by FFQ. We assigned P in foods as naturally occurring or added, and weighted intake by P bioavailability, based on published literature. Relations between P variables and eGFR were assessed using multivariable regression. RESULTS: Mean ± SE intakes were 1178 ± 6.7 mg and 1168 ± 5.0 mg for total P, 296 ± 2.8 mg and 291 ± 2.1 mg for bioavailable added P, and 444 ± 2.9 mg and 443 ± 2.2 mg for bioavailable natural P, in participants with eGFR = 60-89 and ≥90 mL · min-1 · 1.73 m-2, respectively. Major sources of total P included fish, milk, beef, eggs, cheese, and poultry; and of added P, fish, beef, processed meat, soft drinks, and poultry. After adjustment for confounders, P intakes, including total (ß ± SE: -0.32 ± 0.15; P = 0.03), added (ß ± SE: -0.73 ± 0.27; P = 0.01), bioavailable total (ß ± SE: -0.62 ± 0.23; P = 0.01), and bioavailable added (ß ± SE: -0.77 ± 0.29; P = 0.01), were significantly associated with lower eGFR. However, neither total nor bioavailable P from natural sources were associated with eGFR. CONCLUSIONS: Added, but not natural, P was negatively associated with kidney function, raising concern about P additives in the food supply. Further studies are needed to improve estimation of dietary P exposure and to clarify the role of added P as a risk factor for kidney disease.

Trends in Total, Added, and Natural Phosphorus Intake in Adult Americans, NHANES 1988-1994 to NHANES 2015-2016.

Dietary phosphorus intake in the USA has been consistently greater than the Recommended Daily Allowance (RDA) with several studies reporting associations between intake and health risks as well as all-cause mortality within healthy subjects and patients with chronic kidney disease (CKD). The current study utilized a novel approach to calculate added phosphorus content in foods to determine sources (National Health and Nutrition Examination Survey, NHANES 2001-2016, n = 39,796) and trends in consumption (NHANES 1988-1994, 2001-2016, n = 55,744) of total, naturally occurring, and added phosphorus. Among adults (19+ years), the mean intake of total and natural phosphorus (mg/day) in 1988-1994 as compared with 2015-2016 increased (total: 1292 ± SE 11 vs. 1398 ± SE 17; natural: 1113 ± SE 10 vs. 1243 ± SE 16 mg/day); in contrast, added phosphorus intake decreased during this time (178 ± SE 2.9 vs. 155 ± SE 4.1 mg/day). Added phosphorus as a percent of total ranged from about 14.6% in 1988-1994 to about 11.6% in 2015-2016. The top five sources of total and naturally occurring phosphorus, representing approximately 20% of intake, were cheese, pizza, chicken (whole pieces), reduced-fat milk, and eggs/omelets. The top five sources of added phosphorus were cheese, soft drinks, cakes/pies, rolls/buns, and cookies/brownies, representing 45% of added phosphorus in the diet. Consumption of added phosphorus has decreased over the past few decades, possibly due to increased demand for foods with less additives/ingredients but may also be due to inaccurate phosphorus values in nutrition databases. Further studies are needed to validate the added phosphorus calculations utilized in this study and nutrition databases should consider providing added phosphorus content.

mRNA Profiles of Porcine Parathyroid Glands Following Variable Phosphorus Supplies throughout Fetal and Postnatal Life.

Knowledge of gene expression profiles reflecting functional features and specific responsiveness of parathyroid glands (PTGs) contributes to understanding mineral homeostasis and parathyroid function in healthy and diseased conditions. The study aims to reveal effector molecules driving the maintenance of phosphorus (P) homeostasis and parathyroid hormone (PTH) responsiveness to variable P supply throughout fetal and postnatal life. In this study, a long-term dietary intervention was performed by keeping pig offspring on distinct mineral P levels throughout fetal and postnatal life. Respective adaptation processes of P homeostasis were assessed in mRNA profiles of PTGs and serum minerals. RNA sequencing data and resulting molecular pathways of PTGs showed that the PTH abundance is very strictly controlled via e.g., PIN1, CaSR, MAfB, PLC and PKA signaling to regulate PTH expression, stability, and secretion. Additionally, the observed dietary effects on collagen expression indicate shifts in the ratio between connective tissue and parenchyma, thereby affecting cell-cell contacts as another line of PTH regulation. Taken together, the mRNA profiles of porcine PTGs reflect physiological responses in-vivo following variable dietary P supplies during fetal and postnatal life. The results serve to evaluate a long-term nutrition strategy with implications for improving the mineral balance in individuals with pathological disorders.

Dietary Phosphorus as a Marker of Mineral Metabolism and Progression of Diabetic Kidney Disease.

Phosphorus is an essential nutrient that is critically important in the control of cell and tissue function and body homeostasis. Phosphorus excess may result in severe adverse medical consequences. The most apparent is an impact on cardiovascular (CV) disease, mainly through the ability of phosphate to change the phenotype of vascular smooth muscle cells and its contribution to pathologic vascular, valvular and other soft tissue calcification. Chronic kidney disease (CKD) is the most prevalent chronic disease manifesting with the persistent derangement of phosphate homeostasis. Diabetes and resulting diabetic kidney disease (DKD) remain the leading causes of CKD and end-stage kidney disease (ESRD) worldwide. Mineral and bone disorders of CKD (CKD-MBD), profound derangement of mineral metabolism, develop in the course of the disease and adversely impact on bone health and the CV system. In this review we aimed to discuss the data concerning CKD-MBD in patients with diabetes and to analyze the possible link between hyperphosphatemia, certain biomarkers of CKD-MBD and high dietary phosphate intake on prognosis in patients with diabetes and DKD. We also attempted to clarify if hyperphosphatemia and high phosphorus intake may impact the onset and progression of DKD. Careful analysis of the available literature brings us to the conclusion that, as for today, no clear recommendations based on the firm clinical data can be provided in terms of phosphorus intake aiming to prevent the incidence or progression of diabetic kidney disease.

Association between ultrapocessed food and chronic kidney disease.

The modern diet is closely linked to the consumption of processed foods, causing an increase in the intake of salt, simple sugars, phosphorus and added potassium. This excess intake is associated with an increased risk of obesity, diabetes, hypertension and chronic kidney disease (CKD). CKD, which according to data from the ENRICA study affects 15% of the population, magnifies its impact due to the higher prevalence of diabetes and hypertension and due to limitations in the management of sodium and phosphorus. The intake of these products far exceeds the established recommendations, assuming 72% of total sodium, 25%-35% of phosphorus, 12%-18% of potassium and exceeding 10% of the caloric intake in simple sugars. Measures are necessary to reduce their contribution through nutritional advice, labeling review, education campaigns on healthy habits, fees and institutional actions that involve food safety agencies, industry, distribution and scientific societies.

Mineral Intake and Clinical Symptoms in Adult Patients with Hypophosphatasia.

BACKGROUND: Hypophosphatasia (HPP) is a rare inherited metabolic disorder characterized by deficient activity of the tissue-nonspecific alkaline phosphatase entailing impaired turnover of phosphorus metabolites. Dietary mineral intake is suspected to influence clinical symptoms of HPP, but scientific evidence is missing. METHODS: Cross-sectional matched-pairs study collecting comprehensive data on nutrient intake in 20 HPP patients and 20 unaffected, age- and gender-matched controls. Dietary information and clinical symptoms were documented in detail over 7 consecutive days using structured diaries. RESULTS: Baseline data and type of energy-supplying nutrients were balanced between both groups. Median nutritional intake of phosphorus and calcium were significantly lower in HPP patients versus controls, which is partially attributable to lower energy consumption in HPP patients. Differences regarding phosphorus and calcium (Ca/P) ratio and uptake of magnesium, zinc, and vitamin B6 were not statistically significant. Both high (≥ 1375 mg/d) and low intakes (< 1100 mg/d) of phosphorus were significantly associated with an increased frequency of neuropsychiatric symptoms (P = 0.02). Similarly, very high and very low intake of calcium was significantly associated with musculoskeletal (P < 0.01), gastrointestinal (P = 0.02), and neuropsychiatric (P < 0.001) symptoms. An increased Ca/P ratio was associated with increased tiredness/fatigue (P < 0.01), whereas a decreased Ca/P was associated with gastrointestinal issues (P = 0.01). CONCLUSION: Phosphorus and calcium intake seem reduced in HPP patients along with reduced total energy consumption. Particularly high as well as very low absolute or unbalanced phosphorus and calcium intake are associated with an increased frequency of clinical symptoms.

Habitual Intakes, Food Sources and Excretions of Phosphorus and Calcium in Three German Study Collectives.

Phosphorus intake in Europe is far above recommendations. We present baseline data from three human intervention studies between 2006 and 2014 regarding intake and excretion of phosphorus and calcium. All subjects documented their nutritional habits in weighed dietary records. Fasting blood samples were drawn, and feces and urine were quantitatively collected. Dietary phosphorus intake was estimated based on weighed dietary records and urine phosphorus excretions. Food sources were identified by allocation to defined food product groups. Average phosphorus consumption was 1338 mg/day and did not change from 2006 to 2014, while calcium intake decreased during this period (1150 to 895 mg/day). The main sources for phosphorus intake were bread/cereal products, milk/milk products and meat/meat products/sausage products and the main sources of calcium intake included milk/milk products/cheese, bread/cereal products and beverages. There was no difference between estimated phosphorus intake from the weighed dietary records and urine phosphorus excretion. In conclusion, we demonstrated constant phosphorus intakes far above the recommendations and decreasing calcium intakes below the recommendations in three German collectives from 2006 to 2014. Furthermore, we could show in case of usual intakes that an estimated phosphorus intake from urine phosphorus excretion is similar to the calculated intake from weighed dietary records.

Nutritional therapy in autosomal dominant polycystic kidney disease.

CKD-related nutritional therapy (NT) is a crucial cornerstone of CKD patients' treatment, but the role of NT has not been clearly investigated in autosomal dominant polycystic kidney disease (ADPKD). Several clinical studies have focused on new pharmacological approaches to delay cystic disease progression, but there are no data on dietary interventions in ADPKD patients. The aim of this paper is to analyze the evidence from the literature on the impact of five nutritional aspects (water, sodium, phosphorus, protein intake, and net acid load) in CKD-related ADPKD extrapolating-where information is unavailable-from what occurs in CKD non-ADPKD patients Sodium intake restriction could be useful in decreasing the growth rate of cysts. Although further evidence is needed, restriction of phosphorus and protein intake restriction represent cornerstones of the dietary support of renal non-ADPKD patients and common sense can guide their use. It could be also helpful to limit animal protein, increasing fruit and vegetables intake together with a full correction of metabolic acidosis. Finally, fluid intake may be recommended in the early stages of the disease, although it is not to be prescribed in the presence of moderate to severe reduction of renal function.