Table of contents
Excess phosphate in modern foods block Calcium, which causes a vzriety of health problems - Aug 2024
Hidden Ingredient in Your Food Is Hurting Your Health: The Phosphate Problem
- "Modern diets often contain 2 to 3 times more phosphorus than recommended, while calcium intake frequently falls below recommended levels. Phosphate additives are prevalent in processed meats, cheese, baked goods, soft drinks, and even grocery store fresh meat"
- "Food labels aren't required to list phosphate content,..."
- "The relationship between calcium and phosphorus is so crucial that nutritionists often speak of the calcium to phosphorus ratio (Ca:P) as a key indicator of dietary health. Ideally, this ratio should be close to 1:1 or higher, meaning we should consume roughly equal amounts of calcium and phosphorus, or slightly more calcium than phosphorus in our diets."
- Food manufacturers use phosphate additives for various reasons:
- To increase water-holding capacity in meats
- To increase meat pH and slow discoloration
- To reduce cooking losses
- To retard oxidative rancidity
- To protect against microbial growth
Common Sources in Food
- Processed meats — Bacon, sausages, hot dogs, and deli meats often contain added phosphates as preservatives and to improve texture.
- Cheese — Many types of processed, industrial cheese and cheese spreads have added phosphates to enhance texture and melting properties.
- Baked goods — Packaged bread, cakes, cookies, and other baked items may have added phosphates as leavening agents.
- Soft drinks — Some carbonated beverages, especially colas, contain phosphoric acid, a type of phosphate.
- Ready-to-eat meals — Frozen dinners and other convenience foods can contain phosphates to improve shelf life and texture.
- Instant foods — Instant noodles and soups may contain phosphates to enhance flavor and texture.
See in VitaminDWiki Ultra-processed foods associated with worse health and lower Vitamin D - several studies
Phosphatonins: From Discovery to Therapeutics - Oct 2022
Endocr Pract . 2022 Oct 6;S1530-891X(22)00625-5. doi: 10.1016/j.eprac.2022.09.007
Kittrawee Kritmetapak 1 , Rajiv Kumar 2
Phosphate is crucial for cell signaling, energy metabolism, nucleotide synthesis, and bone mineralization. The gut-bone-parathyroid-kidney axis is influenced by parathyroid hormone (PTH), 1,25-dihydroxyvitamin D (1,25(OH)2D), and phosphatonins, and facilitates maintenance of phosphate homeostasis. Phosphatonins including fibroblast growth factor 23 (FGF23), secreted frizzled-related protein 4 (sFRP4), matrix extracellular phosphoglycoprotein (MEPE), and fibroblast growth factor 7 (FGF7) play a pathogenic role in several hypophosphatemic disorders. Excess FGF23 inhibits sodium-dependent phosphate cotransporters (NaPi-2a and NaPi-2c), resulting in hyperphosphaturia and hypophosphatemia. Additionally, FGF23 suppresses 1,25(OH)2D synthesis in the proximal renal tubule, and thus it indirectly inhibits intestinal phosphate absorption. Disorders of FGF23-related hypophosphatemia include X-linked hypophosphatemia (XLH), autosomal dominant hypophosphatemic rickets (ADHR), autosomal recessive hypophosphatemic rickets (ARHR), fibrous dysplasia/McCune-Albright syndrome, and tumor-induced osteomalacia (TIO). Complications of conventional therapy with oral phosphate and vitamin D analogs comprise gastrointestinal distress, hypercalcemia, nephrocalcinosis, and secondary/tertiary hyperparathyroidism. In both children and adults with XLH and TIO, the anti-FGF23 antibody burosumab exhibits a favorable safety profile and is associated with healing of rickets in affected children and improvement of osteomalacia in both children and adults. This review summarizes current knowledge regarding the phosphate homeostasis, phosphatonin pathophysiology, and clinical implications of FGF23-related hypophosphatemic disorders, with specific focus on burosumab treatment.
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Vitamin D and Phosphate Interactions in Health and Disease - March 2022, book chapter
DOI: 10.1007/978-3-030-91623-7_5 10 pages
Nuraly S. Akimbekov, Ilya Digel, Dinara K. Sherelkhan & Mohammed S. Razzaque
Vitamin D plays an essential role in calcium and inorganic phosphate (Pi) homeostasis, maintaining their optimal levels to assure adequate bone mineralization. Vitamin D, as calcitriol (1,25(OH)2D), not only increases intestinal calcium and phosphate absorption but also facilitates their renal reabsorption, leading to elevated serum calcium and phosphate levels. The interaction of 1,25(OH)2D with its receptor (VDR) increases the efficiency of intestinal absorption of calcium to 30–40% and phosphate to nearly 80%. Serum phosphate levels can also influence 1,25(OH)2D and fibroblast growth factor 23 (FGF23) levels, i.e., higher phosphate concentrations suppress vitamin D activation and stimulate parathyroid hormone (PTH) release, while a high FGF23 serum level leads to reduced vitamin D synthesis. In the vitamin D-deficient state, the intestinal calcium absorption decreases and the secretion of PTH increases, which in turn causes the stimulation of 1,25(OH)2D production, resulting in excessive urinary phosphate loss. Maintenance of phosphate homeostasis is essential as hyperphosphatemia is a risk factor of cardiovascular calcification, chronic kidney diseases (CKD), and premature aging, while hypophosphatemia is usually associated with rickets and osteomalacia. This chapter elaborates on the possible interactions between vitamin D and phosphate in health and disease.
97 references online
7 VitaminDWiki pages with PHOSPHATE etc in title
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