With support from the AHA Strategically Focused Disparities Research Netowrk, CTMH investigators are working to determine how lack of access to food options low in dietary phosphates impact health and contribute to disease. We hypothesize that large amounts of phosphate-based additives, consumed through processed foods, contribute to heart failure (HF) and advanced chronic kidney disease (CKD), and that these risks are brought about by elevated levels of fibroblast growth factor 23 (FGF23) that contribute mechanistically to pathological cardiac remodeling and kidney injury.
Food Deserts and Public Health
Food deserts are defined by the U.S. Department of Agriculture as “urban neighborhoods and rural towns without ready access to fresh, healthy, and affordable food. Instead of supermarkets and grocery stores, these communities may have no food access or are served only by fast food restaurants and convenience stores that offer few healthy, affordable food options.” A lack of accessible and affordable fresh options leads to the disproportionate consumption of processed foods among populations who are economically disadvantaged. Our center contends that this is at the core of the disparately high risks of HF and CKD among these populations.
Phosphates, FGF23 and Health
Our current work proposes that elevated FGF23 is a novel and modifiable molecular mediator of disparities in cardiovascular disease (CVD) and CKD. This focus was developed through:
- Early patient-oriented clinical studies that characterized the central role of FGF23 in phosphate homeostasis in health and across the spectrum of CKD. These studies helped reshape our understanding of normal and disordered mineral metabolism.
- Population-based studies that first demonstrated that elevated circulating FGF23 levels are powerfully associated with mortality and CVD events across populations with and without kidney disease. These results suggested that elevated FGF23 was not only a risk factor but perhaps also a mechanism of adverse health outcomes.
- A multidisciplinary, three-year project that demonstrated that elevated FGF23 induces pathological left ventricular hypertrophy (LVH). Elevated FGF23 was independently associated with incident LVH in 4000 CKD patients (population/clinical), and experimentally increasing FGF23 levels was sufficient to induce hypertrophy of isolated cardiac myocytes and LVH in a series of rodent models (basic). This study provided the first evidence of direct end-organ toxicity of FGF23 and advanced a novel mechanism of CVD that is a major basis of the current proposal.
Phosphates in the News
Interested in learning more about phosphates, nutrition, and their impacts on health? Follow along with our research efforts by visiting the links below.
News: AHA Strategically Focused Disparities Research Network
July 2015, Is Phosphate the Next Sodium?