Is your diet aging you prematurely? Researchers at HSDM have found that high levels of phosphates, found in sodas and processed foods, may accelerate the aging process.
Their study, described in April in The FASEB Journal, used genetic and dietary manipulations in mice to investigate an emerging connection between phosphate toxicity and aging. Authors Mutsuko Ohnishi and M. Shawkat Razzaque looked at the effects of high phosphate levels in three groups of mice.
The first group, which lacked a gene associated with excessive phosphate levels called klotho, developed phosphate toxicity. These mice showed symptoms resembling premature aging, including growth retardation, sluggish movement and infertility, and they died prematurely.
The second group was generated to determine whether phosphate toxicity was directly responsible for the accelerated aging seen in the klotho-deficient mice. This group was missing both the klotho gene and a second gene, NaPi2a, related to phosphate balance maintenance; the double absence lowered the animals’ phosphate levels. This reversal in phosphate toxicity alleviated their symptoms of aging and increased their lifespan.
The third group, like the second one, was missing both the klotho and NaPi2a genes, but was also fed a diet high in phosphates. Symptoms of premature aging reappeared, and all of these mice, like those in the first group, died within 15 weeks. This demonstrated that high levels of phosphate, whether caused by genetic defect or induced through diet, could accelerate symptoms of aging.
The toxic effects of phosphates in mice may translate to humans. Phosphates are commonly used in soft drinks to create fizz and are added to processed foods as preservatives and flavor enhancers. “This study adds another reason to avoid so-called ‘junk foods,’” said Razzaque.
Ohnishi and Razzaque suggest that high levels of phosphate may accelerate aging by increasing the rate of atrophy and cell death in various organs, leading to age-related complications such as kidney disease, cardiovascular calcification and muscle and skin atrophy.
For more information, students may contact M. Shawkat Razzaque at mrazzaque@hms.harvard.edu.
Conflict Disclosure: The authors declare no conflicts of interest.
Funding Sources: The National Institute of Diabetes and Digestive and Kidney Disease; the content of the work is the responsibility solely of the authors.
