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  • Writer's pictureTeresa Rodríguez

The phosphate additives- a threat to life and limb.

Updated: Jan 19



Phosphate additives

 

Phosphorus is the most abundant mineral in the human body after calcium. In today’s modern world, when processed food, canned, or bottled drinks, fast food items, and spreadable cheese are in demand at every dining table, maintenance of phosphate balance is extremely essential for a healthy body. Phosphorus serves as a structural component of adenosine triphosphate, nucleic acids, and phospholipids of cellular membranes. It plays a key role in cellular signaling through phosphorylation reactions. 

 

Phosphate additives or inorganic phosphorus are used by the food industry to extend the shelf life of food. It makes the food creamy and easy to melt.  The human body absorbs phosphate additives more easily than the phosphorus that comes from organic food sources. About 40-60% of organic phosphorus is absorbed by your body, however; up to 100% of phosphorus present in food additives gets absorbed easily. Phosphorus doesn’t get stored in extracellular fluid because bones act as reservoirs for life-essential phosphorus and calcium.


Hyperphosphatemia

 

Since extra phosphorus can have toxic effects, kidneys regulate extracellular phosphate concentration by filtering and stimulating phosphate excretion through urine. This sophisticated system of excretion can tightly regulate the phosphate homeostasis in your body. So, the prevention and correction of hyperphosphatemia have been increasingly recognized as an important strategy for CKD patients because hyperphosphatemia can be a risk factor for cardiovascular diseases, progression of kidney disease, and high mortality rate.

 

Even individuals with normal kidney function can develop vascular calcification and cardiovascular diseases with consistent inorganic phosphorus intake. High phosphorus levels in your body can also lead to itching, red eyes, calcium-phosphorus deposits in the heart, brain, and lungs, and certain bone diseases.

 

In human beings, around 85% of phosphorus is present in teeth and bones, 10-15% in soft tissues, and less than 1% in extracellular fluid. The delicate balance of the chain between intestinal absorption, renal excretion, and influx-efflux through bones maintains phosphate homeostasis. Two hormones named fibroblast growth factor 23 and parathyroid hormone play a crucial role in phosphate homeostasis. 

 

An average human daily diet contains more than 1500 mg of phosphorus and approximately 40-80% of it is absorbed through the sodium-dependent phosphate cotransporter Npt2b. In addition, 1,25-dihydroxy vitamin D regulates the active transport of phosphorus by inducing the expression of Npt2b on the apical membrane of intestinal epithelial cells.


Intestinal phosphate absorption

 

A low phosphate diet also regulates the expression of Npt2b. Furthermore, the type of diet also has a great impact on intestinal phosphate absorption as the modern diet contains phosphate preservatives and salts that are easily absorbed. On the contrary, phosphate in the form of phytic acid, present in plants isn’t generally bioavailable to humans due to the absence of the enzyme phytase that degrades phytic acid. 


Renal excretion of phosphorus 

 

During glomerular filtration in kidneys, the majority of the phosphorus is reabsorbed in proximal tubules which are mediated by Npt2a and Npt2c. The expression of Npt2a on the apical membrane of tubular cells is regulated by two hormones called FGF23 and PTH. PTH decreases the Npt2a expression in the proximal tubules by driving its internalization and decreasing gene transcription while FGF23 exerts its biological function by binding to its cognate factor FGF in the presence of cofactor klotho. The major role of Klotho is to promote urinary phosphate excretion by suppressing the expression of Npt2a. The high phosphate blood level increases PTH gene expression and serotonin which acts as a phosphate-sensing mechanism. A recent study suggested that an infusion of phosphorus in the duodenum acts as a stimulus to enhance urinary phosphate excretion without any changes in hormonal balance. 




 

The serum phosphate levels are usually normal in early to moderate CKD. The PTH and FGF23 induce phosphate excretion in this case. Plus, Fetuin-A prevents the precipitation of calcium phosphate by forming fetuin mineral complexes that are removed by phagocytic cells of the reticuloendothelial system. In end-stage renal disease, there’s an extreme reduction in phosphate excretion. Other than that, bone metabolism in CKD patients can also lead to hyperphosphatemia. Various studies have shown a link between hyperphosphatemia and increased risk of death in kidney patients.

 

A study on a group of patients with stage 5 CKD showed that 12% of all deaths in this group of patients were attributable to an elevated phosphorus concentration in blood. Increased phosphate level induces endothelial dysfunction and vascular calcification. In vascular calcification, the smooth muscle cells in blood vessels are reprogrammed to become osteoblasts-like cells. Phosphate-induced vascular changes can contribute to premature aging and death. 


Food labeling

 

Polyphosphates are generally used as an additive in industrial food production. The main food additives are sodium phosphate, potassium phosphate, triphosphate, acidifying agents, acidity buffers, and emulsifying agents. Phosphate salts are also added as taste intensifiers and food stabilizers. Fast food and ready-to-eat processed foods are the main contributing factors to today’s rising phosphate consumption. According to a recent study, the consumption of phosphate-containing food additives has doubled since 1990 from 500 mg per day to 1000 mg per day. The phosphate content of processed meat and poultry products was nearly twice that of the natural products and instant absorption of this additive phosphate has added fuel to the fire. Thus, not only the patients with declined renal function and cardiovascular diseases need to be put on the low-phosphate diet but also the general population should consume low phosphate. Be careful with your toothpaste!


 

Every individual should eat carefully and learn about processed foods. By carefully reading the nutritional food composition of phosphate additives, you can make well-informed and appropriate food choices. Nutritional education on food additives can promote hyperphosphatemia control, whether using tools such as phosphate traffic lights or by adding nutritional information on food labeling. 



 

The phosphate additives must be declared on the ingredients list of the product label so that anyone wanting to know the phosphate content can read it easily. The detailed labeling of phosphate additives ideally with a traffic light scheme is the need of the hour. The amount of added phosphate should be indicated with a green, yellow, or red sign on the packaging as it has been currently implicated in Finland and the United Kingdom to indicate sodium chloride content. The high phosphate concentration can also reflect the pathological concentrations of phosphate-regulating hormones Klotho and FGF23. Therefore, Phosphate concentration is the surrogate parameter for the functioning of these hormones.


Be careful even with your toothpaste!


 

A comprehensive public education with a scientifically well-grounded explanation of the adverse effects of high phosphate intake and easily understandable food labeling can help considerably to control the damage and spread awareness. 






References

 

Sullivan C, et al. Effect of food additives on hyperphosphatemia among patients with end-stage renal disease: a randomized controlled trial. JAMA. 2009; 301:629–635. [PubMed] [Google Scholar]

 

 Block GA, et al. Mineral metabolism, mortality, and morbidity in maintenance hemodialysis. JASN. 2004; 15:2208–2218. [PubMed] [Google Scholar]

 

Kestenbaum B, et al. Serum phosphate levels and mortality risk among people with chronic kidney disease. JASN. 2005; 16:520–528. [PubMed] [Google Scholar]

 

 KDIGO. Kidney Int Suppl. 2009. clinical practice guideline for the diagnosis, evaluation, prevention, and treatment of Chronic Kidney Disease-Mineral and Bone Disorder (CKD-MBD) pp. S1–S130. [PubMed] [Google Scholar]

 

Noori N, et al. Association of dietary phosphorus intake and phosphorus to protein ratio with mortality in hemodialysis patients. CJASN. 2010; 5:683–692. [PMC free article] [PubMed] [Google Scholar]

 

Komaba, H., & Fukagawa, M. (2016). Phosphate—a poison for humans? Kidney International, 90(4), P753–763. https://doi.org/10.1016/j.kint.2016.03.039

 

Ritz, E., Hahn, K., Ketteler, M., Kuhlmann, M. K., & Mann, J. (2012). Phosphate additives in food—a health risk. Deutsches Arzteblatt International, 109(4), 49–55. 

Watanabe, M. T., Barretii, P., & Caramori, J. C. T. (2018). Dietary intervention in phosphatemia control–nutritional traffic light labeling. Journal of Renal Nutrition, 28(6), E45–E47. https://doi.org/10.1053/j.jrn.2018.04.005

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