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Background: As fast food, high in phosphorus content, becomes a staple in the American diet, the population increases its dietary phosphorus intake above the recommended amount. According to the NIH guidelines, adults over 19 years and older are 700mg per day (NIH, 2021, Wickham). For context, a meal consisting of a big cheeseburger, medium fries, and a can of soda contains around 600mg of phosphorus (Arquette, 2014). Although phosphorus is essential for bone health as it is part of the structural component of bones, consuming excess amounts of phosphorus has been linked to vascular calcification, cardiovascular disease, kidney disease, and changes in bone metabolism, promoting bone loss (Uribarri et al., 2013; Vorland et al., 2017). As the population gets older and osteoporosis incidence increases, it is essential to understand the influence that different levels and ratios of phosphorus consumption have on bone health (Hejazi et al. 2020).

Methods: Peer-reviewed publications from 2014 to 2025 were found via PubMed, with a focus on clinical trials, animal models, cohort studies, and literature reviews. These were then used to examine the relationship between phosphorus consumption and bone health.

Results: Recent studies have shown evidence that suggests that excess phosphorus consumption leads to detriments in bone health. In human studies, patients exposed to high phosphorus diets showed significant elevations in enzymes linked to bone stress and damage (Turner et al.). Among these, high intact FGF-23 levels are indicative of increasing bone porosity and decreased bone mineral density over time via undermineralization (Guo et al., Rout et al.). Several human studies found that diets high in phosphorus increase intact FGF-23 (Gerber et al), with rodent studies finding a direct link between a high phosphorus diet and exacerbating porosity and cortical thinning (Wei Ling Lao et al.). On the opposite side of the spectrum, conditions that cause hypophosphatemia or low dietary intake of phosphorus also have substantial negative effects on bone health (Haffner et al.). These conditions can include acute kidney injuries and X-linked hypophosphatemia, both of which can ultimately lead to osteoporosis and fractures.

Conclusion: While phosphorus consumption is vital for the maintenance of bone health, both excess and deficiency lead to bone detriments with long-term density and porosity changes. High phosphorus content in the diet promotes bone turnover (Hamid et al.). Future studies should examine the relationships between excess phosphorus consumption in low income communities and with high incidence of osteoporosis and fractures.

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High Phosphorus Diets and Bone Health: A Hidden Risk​

Background: As fast food, high in phosphorus content, becomes a staple in the American diet, the population increases its dietary phosphorus intake above the recommended amount. According to the NIH guidelines, adults over 19 years and older are 700mg per day (NIH, 2021, Wickham). For context, a meal consisting of a big cheeseburger, medium fries, and a can of soda contains around 600mg of phosphorus (Arquette, 2014). Although phosphorus is essential for bone health as it is part of the structural component of bones, consuming excess amounts of phosphorus has been linked to vascular calcification, cardiovascular disease, kidney disease, and changes in bone metabolism, promoting bone loss (Uribarri et al., 2013; Vorland et al., 2017). As the population gets older and osteoporosis incidence increases, it is essential to understand the influence that different levels and ratios of phosphorus consumption have on bone health (Hejazi et al. 2020).

Methods: Peer-reviewed publications from 2014 to 2025 were found via PubMed, with a focus on clinical trials, animal models, cohort studies, and literature reviews. These were then used to examine the relationship between phosphorus consumption and bone health.

Results: Recent studies have shown evidence that suggests that excess phosphorus consumption leads to detriments in bone health. In human studies, patients exposed to high phosphorus diets showed significant elevations in enzymes linked to bone stress and damage (Turner et al.). Among these, high intact FGF-23 levels are indicative of increasing bone porosity and decreased bone mineral density over time via undermineralization (Guo et al., Rout et al.). Several human studies found that diets high in phosphorus increase intact FGF-23 (Gerber et al), with rodent studies finding a direct link between a high phosphorus diet and exacerbating porosity and cortical thinning (Wei Ling Lao et al.). On the opposite side of the spectrum, conditions that cause hypophosphatemia or low dietary intake of phosphorus also have substantial negative effects on bone health (Haffner et al.). These conditions can include acute kidney injuries and X-linked hypophosphatemia, both of which can ultimately lead to osteoporosis and fractures.

Conclusion: While phosphorus consumption is vital for the maintenance of bone health, both excess and deficiency lead to bone detriments with long-term density and porosity changes. High phosphorus content in the diet promotes bone turnover (Hamid et al.). Future studies should examine the relationships between excess phosphorus consumption in low income communities and with high incidence of osteoporosis and fractures.

 

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