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Current Dietary Phosphorus Intake: Are there Potential Implications for Public Health?

Current Dietary Phosphorus Intake: Are there Potential Implications for Public Health?

Tuesday, February 26, 2013

The New York Academy of Sciences

Presented By


Exploring the mechanisms responsible for risk associated with hyperphosphatemia in chronic kidney disease and cardiovascular disease, this symposium examines the potential health implications of these mechanisms at the population level if general intake is increased.

This conference will highlight changes in understanding of hormonal regulation of phosphorus homeostasis and how this may explain potential adverse health effects of phosphorus intakes beyond nutrient requirements, exploring in particular the relationship with kidney function, cardiovascular diseases, obesity, hypertension and cancer. A panel discussion will identify further areas of research and discuss how existing evidence should be considered as well as needs to new evidence for the upcoming review of dietary guidelines for Americans in 2015.

Reception to follow.

Registration Pricing

Student/Postdoc Member$25$30$35
Nonmember (Academia)$45$50$55
Nonmember (Corporate)$70$75$80
Nonmember (Non-profit)$45$50$55
Nonmember (Student / Postdoc / Fellow)$45$50$55


Presented by

  • Sackler"


* Presentation titles and times are subject to change.

February 26, 2013

8:30 AM

Registration & Breakfast

9:00 AM

Welcome Remarks
Mandana Arabi, MD, PhD, The Sackler Institute for Nutrition Science

SESSION I: Overview: the Current Intake of Phosphorus in the United States and Changing Understanding of the Hormonal Regulation of Phosphorus Homeostasis

Chair: Jaime Uribarri, MD, The Mount Sinai School of Medicine

9:15 AM

Historic Development of Health Concerns for the Current Phosphorus Intake in the United States
Jaime Uribarri, MD, The Mount Sinai School of Medicine

9:25 AM

Phosphorus Content of the United States Food Supply: Dietary Intake Guidelines, Current Intake Levels and Primary Dietary Sources
Mona S. Calvo, PhD, U.S. Food and Drug Administration

9:35 AM

The Essential Role of Phosphorus Containing Additives in Food Processing
Lucina E. Lampila, PhD, RD, Louisiana State University

10:15 AM

The Role of Phosphorus on the Pathogenesis of Secondary Hyperparathyroidism
Eduardo Slatopolsky, MD, Washington University in St. Louis

10:45 AM

Regulators of Phosphorus Homeostasis: Approaches to Control Phosphorus Excess
Harald W. Jüppner, MD, Massachusetts General Hospital and Harvard Medical School

11:15 AM


SESSION II: Discussing Evidence of Adverse Health Effects of Phosphorus Intakes Beyond Nutrient Requirements

Chair: Patrick Archdeacon, PhD, U.S. Food and Drug Administration

11:30 AM

Health Concerns for Phosphorus Intake: Historic Perspectives of Early Research Findings Concerning the Dietary Calcium to Phosphorus Ratio and Bone Health
Mona S. Calvo, PhD, U.S. Food and Drug Administration

11:50 AM

Phosphorus Intake and Kidney Function
Jaime Uribarri, MD, The Mount Sinai School of Medicine

12:10 PM

Is Dietary Phosphorus a Risk Factor for Cardiovascular Disease?
Joachim H. Ix, MD, University of California, San Diego; Veterans Affairs San Diego Healthcare System

12:40 PM

Potential Health Concerns of Dietary Phosphorus: Cancer, Obesity and Hypertension
John J.B. Anderson, PhD, University of North Carolina at Chapel Hill

1:10 PM


2:15 PM

Facilitated Discussion of Sessions I and II
Moderator: Jaime Uribarri, MD
Discussants: John J.B. Anderson, PhD; Mona S. Calvo, PhD; Joachim H. Ix, MD; Harald Jüppner, MD; Lucina Lampila, PhD, RD; Eduardo Slatopolsky, MD

SESSION III: Using Existing Evidence and Recommending Further Research to Inform Dietary Guidelines

Chair: Mona S. Calvo, PhD, U.S. Food and Drug Administration

2:45 PM

Data Needs for Evidence Linking Dietary Phosphorus Excess to Health Problems in the General Population
Katherine L. Tucker, PhD, Northeastern University

3:15 PM

Introduction to the Dietary Guidelines for Americans and Possible Strategies for Action
Mona S. Calvo, PhD, U.S. Food and Drug Administration

3:30 PM

Panel Discussion: Research Gaps and Data Needs, Implications of Findings to the 2015 Dietary Guidelines for Americans

Moderator: Mona S. Calvo, PhD, U.S. Food and Drug Administration
Patrick Archdeacon, MD, U.S. Food and Drug Administration
Robert Burns, PhD, Grocery Manufacturers Association
Lucina E. Lampila, PhD, RD, Louisiana State University
Alanna J. Moshfegh, RD, Agricultural Research Service, United States Department of Agriculture
Katherine L. Tucker, PhD, Northeastern University

4:30 PM

Closing Remarks
Jaime Uribarri, MD
Mandana Arabi, MD, PhD

4:35 PM


5:30 PM




Jaime Uribarri, MD

The Mount Sinai School of Medicine

Dr. Jaime Uribarri is a practicing nephrologist and clinical investigator. He was born in Chile and received his medical degree from the University of Chile School of Medicine. He did all his postgraduate training in the United States. He began his academic career at Downstate Medical Center, SUNY at Brooklyn. He moved to The Mount Sinai School of Medicine in 1990, where he is currently Professor of Medicine and Director of the Home Dialysis Program. His main areas of research have been on acid-base and fluid and electrolytes disorders as well as nutrition in patients with chronic kidney disease. He has published well over one hundred papers in the nephrology literature. Together with Dr. Helen Vlassara, Dr. Uribarri was among the first to explore the question of food advanced glycation endproducts (AGEs) and their detrimental effects in healthy persons as well as in those with diabetes or with kidney disease of different causes. For the past decade he has also collaborated with Dr. Mona S. Calvo to bring attention to the potential public health impact of the increasing "unseen" dietary phosphorus intake in the US not only in renal failure patients, but also in the general population.

Mona S. Calvo, PhD

U.S. Food and Drug Administration

Dr. Mona S. Calvo is an Expert Regulatory Review Scientist in the Center for Food Safety and Applied Nutrition of the U.S. Food and Drug Administration. She is a graduate of the Nutritional Sciences Doctoral Program at the University of Illinois, Champaign-Urbana and received post-doctoral training in the endocrine regulation of calcium, phosphorus and vitamin D in the Endocrine Research Unit of the Mayo Clinic, Rochester, MN. As a doctoral student, she participated as a subject, as well as a researcher, in the first clinical study examining the physiologic effects of phosphate containing food additives on calcium homeostasis in healthy adults. As a Mayo Research Fellow and Associate, she designed and conducted prospective human studies examining the endocrine changes from consuming meals high in phosphate additives from common grocery store foods. In an 18 month feeding study using young female Beagles, she demonstrated that chronic consumption of a nutrient adequate diet with low calcium to phosphorus content ratio similar to that consumed by teens and young adults resulted in a sustained secondary hyperparathyroidism and lower bone mineral content when the dogs reached maturity. Working with nephrologist, Dr. Jaime Uribarri of the Mount Sinai School of Medicine, she continues to explore the health impact of the growing cumulative use of phosphorus containing ingredients in food processing, publishing research papers, reviews monitoring national intake, chapters and government reports bringing attention to hidden dietary sources of phosphorus and the potential health impact of the changing phosphorus content of the American diet.

Mandana Arabi, MD, PhD

The Sackler Institute for Nutrition Science


John J.B. Anderson, PhD

University of North Carolina at Chapel Hill

Dr. Anderson is Professor Emeritus in the Department of Nutrition at the University of North Carolina at Chapel Hill. He received his PhD in Physical Biology from Cornell University in 1966. Dr. Anderson conducts research in the field of calcium metabolism using laboratory-animal models, human subjects, and cells in vitro. Human studies are designed to examine the effects of nutritional factors on bone health of young adult women. Early reports have been on the relationship between dietary calcium intake and indices of bone health in late postmenopausal women. A study of female athletes at UNC has shown that nearly all of the gain in bone mass occurs before 18 years of age. Current work focuses on the effects of estrogen-like isoflavones from soy on osteoblasts. The mechanism of action of genistein on bone cells is being investigated in cell culture. Support for these projects comes from a variety of sources.

Dr. Anderson is a member of the American Nutrition Society, the American College of Nutrition, the American Society for Clinical Nutrition, the American Society for Bone and Mineral Research, and the International Conference on Calcium-Regulating Hormones. Dr. Anderson is on the editorial boards of several journals and he is the past president of the American College of Nutrition.

Patrick Archdeacon, MD

U.S. Food and Drug Administration

Patrick Archdeacon is a medical officer in the Office of Medical Policy with the Center for Drug Evaluation and Research (CDER) at FDA. His serves as the FDA chair for the Kidney Health Initiative (KHI), a consortium founded by FDA and American Society of Nephrology that includes stakeholders from across the kidney community, including patients, regulators, other government agencies, pharmaceutical and device industry, dialysis providers, and health care professionals. The mission of KHI is to advance the scientific understanding of the kidney health and patient safety implications of new and existing medical products and to foster development of therapies for disease that affect the kidney by creating a collaborative environment in which FDA and the greater nephrology community can interact to optimize the evaluation of drugs, devices, biologics, and food products. His work in the Office of Medical Policy also includes acting as FDA liaison to the Clinical Trials Transformation Initiative (a public-private partnership that identifies practices to increase the quality and efficiency of clinical trials) and medical lead for the Sentinel Initiative (a system that will draw on existing automated healthcare data from multiple sources to actively monitor the safety of medical products continuously and in real time). Dr Archdeacon originally joined FDA in 2008 as a medical officer in the Division of Special Pathogens and Transplant Products in the Office of New Drugs. He attended medical school at Columbia University’s School of Physicians and Surgeons. Prior to joining FDA, he completed his training in internal medicine at the New York Presbyterian Hospital and in nephrology and transplant nephrology at the University of North Carolina.

Robert Burns, PhD

Grocery Manufacturers Association

Robert Burns has a BS in Biochemistry from Queen’s University, Belfast, Northern Ireland. He also attended graduate school at Queen’s and received a PhD in Nutritional Biochemistry as a result of his work on folic acid metabolism. He was a postdoctoral research fellow in the laboratory of Peter Buttery, a leading expert on nitrogen metabolism in animals, at Nottingham University, UK, and at the University of Illinois in the laboratory of John Milner, a world expert on nutrition and cancer. In 1982, Burns joined Mead Johnson Nutritionals, where he conducted research on nutrient bioavailability and established standards for the content and communication of nutrient aspects of infant formulas, toddler foods and adult nutritional products. He joined Cadbury Schweppes in 2005, assuming global responsibility for nutrition and scientific issues relating to the beverage, chocolate, candy and gum product portfolios. In 2011, he joined Grocery Manufacturers Association where he is responsible for the application of balanced science to health and nutrition policy. His primary interest is the development of sound scientific basis for impactful public health policy. Burns is actively involved and has held leadership roles in professional societies including the American Society for Nutrition and Institute of Food Technologists.

Mona S. Calvo, PhD

U.S.Food and Drug Administration

Joachim H. Ix, MD

University of California San Diego

Dr. Ix graduated from the University of California San Francisco. He is currently an Associate Professor and Interim Head of the Division of Nephrology-Hypertension at the University California, San Diego, and the Veterans Affairs San Diego Healthcare System. His research focuses on the contribution of abnormalities in calcium and phosphorus homeostasis with cardiovascular disease. This research focuses on populations with kidney disease and those in the general population with normal kidney function. His research has demonstrated the relationship of higher serum phosphorus concentrations with subclinical and clinical cardiovascular disease in the general population. Recent work has evaluated novel methods to lower serum phosphorus in the general population, including evaluation of dietary phosphorus restriction. His presentation will review the current state of literature evaluating urine phosphorus (a marker of dietary phosphorus absorption) with cardiovascular disease in patients with and without kidney disease.

Harald W. Jüppner, MD

Massachusetts General Hospital

Dr. Jüppner’s received his MD from the Medizinische Hochschule Hannover (MHH), Hannover, Germany; during his studies, he spend one year as a fourth year medical student at Tufts University Medical School. After training in pediatrics at the Kinderklinik of the MHH, he joined the Endocrine Unit at MGH for post-doctoral training. His main research focus at the time was the molecular cloning of the PTH/PTHrP receptor. Besides subsequent studies to characterize this G protein-coupled receptor, he explored the regulation of mineral ion homeostasis and bone metabolism through the genetic analysis of different inherited disorders. He is particularly interested in parathyroid hormone (PTH) and fibroblast growth factor 23 (FGF23), and the role of these hormones in patients with phosphate-wasting disorders and chronic kidney disease. His laboratory identified the molecular defect of several inherited disorders, including pseudohypoparathyroidism type Ib, infantile cortical hyperostosis, hypoparathyroidism, and several hypophosphatemic disorders. To explore the molecular basis of these and other inherited human disorders, he has collaborated with a large numbers of investigators and clinicians.

Lucina E. Lampila, PhD, RD

Louisiana State University

Lucina Lampila earned a BS in Home Economics/Dietetics from the State University College at Oneonta (NY). She completed her MS in Human Nutrition at the University of Nebraska, Lincoln (UNL) conducting research on the impact of dietary fiber in controlled, human feeding trials. She was accepted into the UNL Food Science and Technology PhD program and conducted research under the guidance of the Mycologist, Dr. Lloyd Bullerman and while there worked on a fungal fermentation to produce β-carotene from whey. Lampila became a Post-Graduate Research Biochemist in the laboratory of Dr. W. Duane Brown and developed the on-board handling techniques to reduce sodium in canned tuna. She was later an Assistant Professor at the Oregon State University Seafood Laboratory in Astoria, OR where she worked with Dr. David Crawford on development of process protocol to manufacture surimi from Pacific whiting and the means to inhibit the heat stable enzyme commonly associated with this fish species. Lampila moved to the mid-Atlantic region to become the Superintendent of the Virginia (Tech) Seafood Agricultural Experiment Station to work with seafood safety and nutrition. She then moved into the private sector and worked as the Technical Service Manager for four European based ingredient manufacturers. Lampila returned to academia in 2008 as an Associate Professor in the LSU Department of Food Science and Seafood Specialist in the Louisiana Sea Grant College Program. Her interests include the role of seafood in nutrition, seafood safety, seafood preservation and post-mortem muscle biochemistry. Lampila was recognized as an expert on seafood safety after the 2010 BP oil spill and was an invited speaker on this topic at the National Museum of Natural History at the Smithsonian Institution. She is Co-Editor of the Seafood HACCP Compendium.

Alanna J. Moshfegh, RD

United States Department of Agriculture

Alanna Moshfegh is Research Leader, Food Surveys Research Group at the Beltsville Human Nutrition Research Center for the United States Department of Agriculture, a position she has held since 1994. She leads a staff including nutritionists, food technologists, and statisticians in planning and directing a national program of research in monitoring food consumption behavior and assessing nutritional adequacy of American diets. Her research interests and responsibilities focus on food consumption behavior and nutritional adequacy of American diets, food and nutrition policy, and dietary guidelines.

Ms. Moshfegh is responsible for directing What We Eat in America, the dietary interview component of the U.S. Federal government’s primary health survey—the National Health and Nutrition Examination Survey. For that program, she directed the development and validation of USDA’s Automated Multiple-Pass Method, a 5-step 24-hour dietary recall system that is used in What We Eat in America. What We Eat in America, NHANES has been in continuous data collection since 2002 providing thousands of dietary recalls on the U.S. population.

Ms. Moshfegh received her M.S. in nutrition and food service management from the University of Nebraska and her B.S. in nutrition and dietetics from North Dakota State University. She is a member of the American Society for Nutrition and the Academy of Nutrition and Dietetics. She has published and presented numerous articles and reports on nutrition monitoring, food consumption, and dietary status of Americans.

Eduardo Slatopolsky, MD

Washington University in St. Louis

Eduardo Slatopolsky graduated from the University of Buenos Aires, Argentina and in 1963 joined the Renal Division at Washington University and was promoted to Professor of Medicine in 1975. He is the founder of the chronic dialysis program at Washington University. Dr. Slatopolsky clarified most of the mechanisms by which secondary hyperparathyroidism develops in chronic renal failure. He is the author of more than 500 publications and honorary member of more than 15 nephrological societies around the world. He received numerous awards, in particularly the Award of Excellence of the National Kidney Foundation, the Belding Scribner Award of the American Society of Nephrology and the Amgen Award of the International Society of Nephrology. He is a Fellow the St. Louis Academy of Science.

Katherine L. Tucker, PhD

Northeastern University

Dr. Katherine L. Tucker is Professor of nutritional epidemiology in the Department of Health Sciences at Northeastern University in Boston, MA, and Adjunct Professor at the Friedman School of Nutrition Science and Policy and the Jean Mayer USDA Human Nutrition Research Center on Aging at Tufts University. Dr. Tucker has contributed to more than 250 articles in scientific journals and has received over $20,000,000 in research funding. Her research focuses on dietary intake and risk of chronic disease, including osteoporosis, cognitive decline, obesity, metabolic syndrome, and heart disease. She is the director of an NHLBI funded center on Population Health and Health Disparities, studying the roles and interactions of stress, social support, diet, health behavior and genetic predisposition in relation to health disparities in Puerto Rican adults. She has collaborated for many years with the Framingham Studies, particularly the Framingham Osteoporosis Study, and she serves as a scientific advisor for, and leads a Vanguard data analysis center with the Jackson Heart Study. She currently serves on the NIH study section for Kidney disease, Nutrition, Obesity and Diabetes, is an associate editor for Public Health Nutrition, and is a co-editor of the 11th edition of the textbook, Modern Nutrition in Health and Disease. She recently completed a two-year term as chair of the Nutritional Sciences Council at the American Society for Nutrition and an eight-year term as Associate Editor for the Journal of Nutrition.

Jaime Uribarri, MD

The Mount Sinai School of Medicine



The Essential Role of Phosphorus Containing Additives in Food Processing
Lucina E. Lampila
, PhD, RD, Louisiana State University, Baton Rouge

The uses and functions of phosphorus containing food ingredients vary widely across the food industry. Ortho- and pyrophosphates are essential to the acid-base reaction for leaving of baked goods. Low levels of condensed phosphates act synergistically with salt in meat processing resulting in a reduction of sodium used in processing. This presentation will cover common uses of phosphorus containing food ingredients to include food quality, safety and nutrition.

The Role of Phosphorus on the Pathogenesis of Secondary Hyperparathyroidism
Eduardo Slatopolsky
, MD, Washington University, Department of Medicine, St. Louis

Alterations in phosphorus, calcium and vitamin D metabolism play a critical role in the development of secondary hyperparathyroidism (S.H.) in patients with chronic renal disease (CKD). Calcium regulates the secretion of PTH on a minute to minute basis. Active vitamin D compounds suppresses PTH at the transcriptional level. Phosphorus stimulates the secretion of PTH post-transcriptional by stabilizing the PTH mRNA in addition it induces parathyroid hyperplasia by activating the complex TGFalpha-Epidermal Growth Factor Receptor. Phosphorus stimulates FGF-23 that with its cofactor Klotho decreases the level of the renal 1, hydroxylase and increases the levels of 24 hydroxylase responsible for the catabolism of calcitriol. We had demonstrated in experimental animals with chronic renal disease that a low phosphorus diet prevents the development of S.H. and parathyroid gland hyperplasia, the opposite is seen when the animals are fed a high in phosphorus diet. Correction of hyperphosphatemia is imperative to reduce not only S.H. but vascular calcification and other morbid effects including death. Numerous epidemiological studies have demonstrated a correlation between serum phosphorus and death. These effects were also seen in patients with moderate renal failure. Thus, it is mandatory that we control serum phosphorus in patients with CKD by combining special diets, phosphate binders and effective hemodialysis to prevent or ameliorate the devastating effects induced by phosphorus retention.

Regulators of Phosphorus Homeostasis: Approaches to Control Phosphorus Excess
Harald W. Jüppner
, MD, Massachusetts General Hospital and Harvard Medical School, Boston

Fibroblast growth factor 23 (FGF23) and parathyroid hormone (PTH) are the main regulators of phosphate homeostasis that promote urinary phosphate excretion and thus help maintain serum phosphorus levels within normal limits. Both hormones affect vitamin D metabolism differently; while PTH increases the renal 1-alpha vitamin D hydroxylase, FGF23 suppresses the synthesis of this enzyme and stimulates the 24-hydroxylase, thereby reducing 1,25(OH)2 vitamin D levels through two different mechanisms. Additional factors involved in the regulation of phosphate homeostasis were established by defining the molecular basis of different FGF23-dependent hypophosphatemic disorders. These efforts led to the identification of several proteins, including PHEX, DMP1, Fam20C, and ENPP1, that contribute to the regulation of FGF23 synthesis. Hypophosphatemia can occur also independent of FGF23, namely by homozygous or compound heterozygous mutations in the renal phosphate transporters NaPi-IIa or NaPi-IIc, or by homozygous mutations in the glucose transporter GLUT2, suggesting that these proteins could be therapeutic targets. FGF23 levels are elevated in patients with oncogenic osteomalacia (OOM) and several other inherited disorders, thus explaining the increase in urinary phosphate excretion and the inappropriately normal or reduced 1,25(OH)2 vitamin D levels observed in these disorders. FGF23 levels are furthermore dramatically elevated in the absence of membrane-bound Klotho (mKL), the FGF23 co-receptor, and when a cleaved form of Klotho (cKL) is produced in excess. The levels of C-terminal FGF23, but not of intact FGF23, are elevated in hyperphosphatemic tumoral calcinosis (TC) that is caused by homozygous inactivating mutations in GALNT3, the enzyme that initiates O-glycosylation of FGF23. The lack of this post-translational modification thus leads to abnormal FGF23 processing, which increases the secretion of biologically inactive C-terminal fragments; a similar increase in C-terminal FGF23 fragments is observed with severe iron deficiency. FGF23 levels rise early during the course of acute or chronic kidney disease indicating that this hormone is an early biomarker of abnormal phosphate homeostasis. Since elevated FGF23 levels are associated with kidney disease progression and cardiovascular disease/mortality, it would be important to prevent or limit the FGF23 rise early during the course of CKD, possibly through the use of oral phosphate binders or through PTH analogs/mimetics that selectively promote urinary phosphate excretion.

Health Concerns for Phosphorus Intake:  Historic Perspectives of Early Research Findings Concerning the Dietary Calcium to Phosphorus Ratio and Bone Health
Mona S.Calvo
, PhD, U.S. Food and Drug Administration, Laurel, Maryland

Phosphorus intake in the United States has been high relative to calcium intake since we began monitoring nutrient intakes of the healthy general population. For the majority, phosphorus intake greatly exceeds the established dietary guidelines for nutrient requirements (the average estimated requirement, EAR), while calcium intake often does not meet the EAR. Growing evidence suggests that phosphorus intakes are actually higher than reported and seemingly continues to rise as a result of the increasing consumption of highly processed foods that rely on the many functional properties of added phosphorus ingredients needed to achieve a desired outcome such as texture or other characteristics. Phosphorus intake in excess of the nutrient needs of healthy men and women and far exceeding the recommended calcium to phosphorus intake ratio of 1:1 (mg:mg) have long been thought to disrupt the hormonal regulation of phosphorus, calcium and vitamin D resulting in bone loss or impaired peak bone mass. To gain insight into the potential for bone health concerns, we review the evidence from studies examining high phosphorus, low calcium experimental diets and diets containing low calcium, high phosphorus from natural food sources reported in recent Gambian field studies, as well as, findings from studies using defined diets prepared exclusively from common grocery store purchased foods rich in phosphorus additives. Changes in hormonal factors negatively impacting bone accretion or evidence of a direct impact on bone associated with specific processed foods raise concern for phosphorus intakes that exceed nutrient requirements, especially when calcium intake is limited.

Phosphorus Intake and Kidney Function
Jaime Uribarri
, MD, Department of Medicine, The Mount Sinai School of Medicine,
New York, New York

High serum phosphorus is linked to poor health outcome and mortality in chronic kidney disease (CKD) patients before or after the initiation of dialysis. Therefore, maintenance of normal serum phosphorus levels is a major concern in the clinical care of this population with dietary phosphorus restriction and/or use of oral phosphate binders considered the best corrective care. This subject has been the focus of several 2012 National Kidney Foundation conferences/ workshops, an International Consensus Conference on Dietary Phosphorus Intake in CKD, as well as numerous articles in prominent medical journals. Effectively limiting phosphorus intake is difficult for both the CKD patient and healthy individuals because of problems in estimating total dietary phosphorus intake. One such problem is the wide range in bioavailability of phosphorus from different food sources that prevents accurate estimates of absorbed phosphorus. A second problem in estimating the dietary phosphorus load is the increasing use of phosphate salts as functional ingredients in processed foods and as inert ingredients in commonly used medications and the lack of phosphorus content information on these product labels. In the current presentation, we will briefly review these and other phosphorus related issues with repercussion in kidney patients and those seemingly healthy patients in the general population. We will also review the current experimental evidence suggesting that dietary phosphorus excess is an important factor determining progression of renal disease.

Is Dietary Phosphorus a Risk Factor for Cardiovascular Disease?
Joachim H. Ix
, MD, MAS, Division of Nephrology, Department of Medicine, University of California San Diego and Veterans Affairs San Diego Healthcare System

Initial studies from end-stage renal disease (ESRD) patients demonstrated strong associations of higher serum phosphorus concentrations with all-cause and cardiovascular mortality. Animal and in vitro studies have delineated mechanisms through which higher extra-cellular phosphorus concentrations transform vascular cells into bone-like cells and contribute to deposition of calcium and phosphorus in the vascular wall. Recently, similar associations have been extended to the general population where higher serum phosphorus concentrations have also been associated with vascular calcification, arterial stiffness, cardiovascular disease events, and, all-cause mortality. Moreover, higher phosphorus concentrations stimulate higher concentrations of the counter-regulatory hormones, including parathyroid hormone (PTH), and fibroblast growth factor-23 (FGF23), which have themselves been linked with bone loss and cardiovascular disease. Most Americans consume phosphorus in excess of recommended daily allowance, andphosphorus is efficiently absorbed. Thus, it is possible that lowering dietary phosphorus consumption may translate into lowered serum phosphorus concentrations, and by extension, potential improvements in cardiovascular and bone health. However, in the general population, among persons with normal kidney function, there are only limited data linking dietary phosphorus intake with changes in serum phosphorus concentrations and cardiovascular disease. Such studies are critical before considering public health or policy interventions to alter phosphorus in the food supply. Thus, in this presentation, I will review recent studies evaluating (1) the link between dietary phosphorus consumption with serum phosphorus concentrations, and, (2) the link between dietary phosphorus consumption with adverse health outcomes in the general population.

Potential Health Concerns of Dietary Phosphorus: Cancer, Obesity, and Hypertension
John J.B. Anderson
, PhD, University of North Carolina, Gillings School of Global Public Health, Chapel Hill

Typically Americans consume on average 1400 mg of phosphorus daily or more in meals, thus far exceeding the recommended dietary allowance (RDA). After a meal, phosphorus is efficiently (50% or higher) and rapidly absorbed, and hormonal mechanisms act swiftly to maintain the serum inorganic phosphate (Pi) concentration within fairly narrow limits. Both parathyroid hormone (PTH) and fibroblast growth factor-23 (FGF-23) reduce serum phosphate during postprandial periods through their actions on the kidney. However, exposure of cells to a brief high Pi concentration may alter cell functions that contribute to deleterious effects and, more likely, to elevated serum FGF-23 or PTH that may be harmful to specific cell types. FGF-23 is known to inhibit PTH secretion by a direct action on the parathyroids. Examples of adverse effects of one or the other of these two factors on three chronic diseases are reviewed in the context of potential mechanisms. In the case of high-phosphate induced cancer, phosphate ions are readily transported by NPT 2 or 3 across epithelial cells, e.g., lung, and participate in activating insulin receptors and participating in the Akt (protein kinase B) pathway that enhances glucose entry via production of GLUT 4 or 2 and insertion in cell membranes. This system supports the anaerobic degradation of glucose needed for cell transformation. Phosphate ions are also thought to contribute to tumorigenesis of altered cells. Less is known about the possible direct role of FGF-23 or PTH in cancer cells. In the case of obesity, adipocytes require inorganic phosphate for the phosphorylation of glucose. A ready supply of this ion supports glucose conversion to glycerol-P and entry into the lipogenic pathways. FGF-23 may play a supportive role with insulin in the expansion of fat cell size and possibly number, but little is known. An elevation of PTH has been found to be associated with an increased risk of obesity and obesity is typically accompanied by an increase in serum PTH in healthy elders. In the case of hypertension, smooth muscle cells of the vasculature (smooth muscle myocytes) require Pi to drive the energy pathways involving glucose and fatty acids that produce sustained contractions leading to chronic elevations of blood pressure. A diet high in Pi, however, has been shown in a 6-year prospective population-based study to be associated with a reduced risk of hypertension when most of the Pi is provided by dairy foods. The long term role of high dietary Pi in blood pressure regulation has not been evaluated in terms of non-dairy sources of phosphate. A specific role of FGF-23 or PTH in hypertension has not been assessed. In summary, high dietary phosphorus, especially from foods processed with phosphate salts, may contribute to two of these three chronic diseases, lung cancer and obesity, because of the direct actions of phosphate ions or from the indirect actions of FGF-23 or PTHon cells. The public health significance of the adverse effects of high phosphorus intakes on specific cell types remains under-appreciated, and further investigation is needed to establish its importance within the large segment of our population who regularly consume high-phosphate diets.

Data Needs for Evidence Linking Dietary Phosphorus Excess to Health Problems in the General Population
Katherine L. Tucker
, PhD, Northeastern University, Boston, Massachusetts

Changes in the food supply over recent decades have led to increasing amounts of phosphorus in our diets. Although phosphorus is an important nutrient found naturally in most foods, it is now also added as a preservative, emulsifier, acidificant, flavor enhancer or for other characteristics of processed foods. Although the phosphorus content of many of these foods is known, food analysis studies have shown that nutrient databases may underestimate phosphorus in some foods by 20% or more. Importantly, this added phosphorus is much more bioavailable, perhaps twice or more, than natural phosphate esters in animal foods, and phytates in plant foods. When assessing the dietary intake of phosphorus, however, it remains standard practice to sum the phosphorus measures in the nutrient database without adjustment. Using this approach, very few individuals appear to exceed the upper level (UL) for phosphorus. However, to the extent that the databases underestimate total phosphorus intake, and the UL does not consider enhanced bioavailability of added phosphorus ingredients, those with excess intakes are likely to be underestimated. Additionally, foods enhanced with phosphorus compounds may lack other minerals that exist in natural foods, and which work together to either slow absorption, or to clear phosphorus in the blood more quickly. Foods such as cola, with added phosphoric acid, but no calcium, magnesium or other minerals, may lead to short periods of highly bioavailable phosphorus exposure that may have more negative health effects than the same amount of phosphorus from natural sources. These variations, not dissimilar to variations in bioavailability of natural folate vs added folic acid, suggest the need to develop an algorithm to consider phosphate bioavailability when calculating total phosphorus exposure from nutrient databases for use in studies of diet and health.

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