FGF23 is a hormone your bones produce that controls mineral balance in your body, but when levels become abnormal, it increases the risk of heart disease, weak bones, kidney damage, and anemia. According to Gram Research analysis, elevated FGF23 is linked to heart enlargement, heart attacks, strokes, and increased mortality, while low FGF23 causes soft bones and fractures. New medications can now treat FGF23 imbalances, offering hope for people with these conditions.
Scientists have discovered that your bones produce a hormone called FGF23 that does much more than just manage minerals in your body. According to Gram Research analysis, this hormone controls how your body uses phosphate and vitamin D, but when levels get too high or too low, it can cause serious problems including weak bones, heart disease, and kidney damage. Researchers are now developing new treatments to fix FGF23 imbalances, which could help millions of people with bone and heart conditions. Understanding this hormone is changing how doctors think about bone health and its connection to heart and kidney disease.
Key Statistics
A 2026 review in Reviews in Endocrine & Metabolic Disorders found that elevated FGF23 levels are associated with left ventricular hypertrophy, cardiovascular events, vascular calcification, and increased mortality across multiple patient populations.
Research shows that FGF23 dysregulation causes both hypophosphatemic disorders (when FGF23 is too high) and hyperphosphatemic disorders (when FGF23 is too low), with the former now treatable through medical therapies targeting FGF23 excess.
A 2026 review identified that FGF23 exerts direct effects on organs beyond bone, contributing to left ventricular hypertrophy, anemia, and fibrosis in both cardiac and renal tissues through mechanisms not yet fully understood.
The Quick Take
- What they studied: How a hormone called FGF23 that your bones make affects not just your bones, but also your heart, kidneys, and blood vessels
- Who participated: This is a review article that summarizes findings from many different studies about FGF23, rather than a single study with participants
- Key finding: FGF23 controls mineral balance in your body, but when levels are abnormal, it increases the risk of heart disease, weak bones, anemia, and kidney damage
- What it means for you: If you have bone disease or heart problems, your doctor may soon be able to test your FGF23 levels and use new medicines to fix the imbalance. However, more research is needed to fully understand how this hormone works in different parts of your body
The Research Details
This is a review article, which means researchers gathered and summarized information from many previous studies about FGF23 instead of conducting their own experiment. The authors looked at 25 years of research since FGF23 was first discovered and identified as a cause of a bone disease called hypophosphatemic rickets. They organized the findings into two main categories: FGF23’s classical role in managing phosphate and vitamin D levels, and its newer discovered effects on the heart, blood vessels, and kidneys.
The review focuses on how FGF23 works by binding to special receptors on cells throughout your body. These receptors require a partner protein called α-KLOTHO to function properly. When FGF23 levels are too high or too low, it disrupts the normal balance of minerals and can trigger problems in multiple organs at once.
This type of review is valuable because it brings together scattered research findings and helps doctors and scientists see the bigger picture of how one hormone affects the whole body. It also identifies gaps in our knowledge where more research is needed.
Understanding FGF23 is important because it connects bone health to heart and kidney health in ways doctors didn’t fully appreciate before. For decades, bone disease and heart disease were treated separately, but this research shows they may share a common cause. By reviewing all available evidence, researchers can identify patterns and develop better treatments that address the root problem rather than just treating symptoms.
This review was published in a respected scientific journal focused on hormones and metabolism. The authors examined decades of research, which gives the summary strong credibility. However, because this is a review rather than a new study, the findings depend on the quality of the original research being summarized. The authors note that some mechanisms of how FGF23 affects different organs are still not fully understood, which means some conclusions are preliminary.
What the Results Show
FGF23 is a hormone produced by bone cells that acts like a messenger throughout your body. Its main job is to regulate phosphate (a mineral) and vitamin D levels by telling your kidneys how much phosphate to keep or release. When FGF23 works properly, it maintains the right mineral balance for healthy bones and normal body function.
However, when FGF23 levels become abnormally high, serious problems develop. Research shows that elevated FGF23 is linked to enlarged heart muscle (left ventricular hypertrophy), heart attacks and strokes, hardening of blood vessels, anemia (low red blood cells), and kidney scarring. These complications can lead to increased risk of death, especially in people with kidney disease.
On the opposite end, when FGF23 levels are too low, bones become weak and soft, a condition called hypophosphatemic rickets or osteomalacia. This causes bone pain, fractures, and deformities. The good news is that doctors now have medicines that can treat FGF23-related bone diseases by either blocking excess FGF23 or replacing missing FGF23 function.
The review emphasizes that FGF23 affects multiple organ systems simultaneously, which explains why people with FGF23 imbalances often have problems in their bones, heart, kidneys, and blood at the same time.
Beyond its main role in mineral metabolism, FGF23 appears to have direct effects on heart muscle cells, blood vessel cells, and kidney cells that are independent of its mineral-regulating function. This means high FGF23 can damage these organs through multiple pathways, not just by changing mineral levels. The review also notes that FGF23 may contribute to anemia by affecting how the body produces red blood cells. Additionally, elevated FGF23 is associated with fibrosis (scarring) in both the heart and kidneys, which reduces their ability to function properly.
FGF23 was discovered about 25 years ago as the cause of a rare genetic bone disease. Early research focused only on its role in mineral metabolism. This review shows how scientific understanding has expanded dramatically, researchers now recognize FGF23 as a hormone with effects throughout the body. Previous studies treated bone disease, heart disease, and kidney disease as separate problems. This research suggests they may be connected through FGF23 dysregulation, which is a major shift in how doctors think about these conditions.
The authors acknowledge that while elevated FGF23 is clearly associated with heart and kidney problems, the exact mechanisms of how it causes damage are not fully understood. Some of the effects may be indirect, working through changes in mineral levels, while others appear to be direct effects on organ cells. More research is needed to clarify these pathways. Additionally, most studies have focused on people with kidney disease or rare genetic bone disorders; less is known about FGF23’s effects in otherwise healthy people. The review also notes that while new treatments exist for FGF23-related bone disease, long-term safety data and effectiveness in preventing heart and kidney complications are still being studied.
The Bottom Line
If you have chronic kidney disease, bone disease, or a family history of hypophosphatemic rickets, ask your doctor about testing your FGF23 levels. If levels are abnormal, new medications are available that can help restore balance (moderate confidence: these are newer treatments still being studied). For people with normal kidney function and no bone disease, FGF23 testing is not routinely recommended at this time. Maintaining adequate vitamin D and phosphate intake through diet supports normal FGF23 function, though this doesn’t prevent genetic forms of FGF23 disease.
People with chronic kidney disease should care about this research because they often have elevated FGF23, which increases their heart attack and stroke risk. People with hypophosphatemic rickets or osteomalacia (soft bones) should care because new FGF23-targeting treatments may help them. People with unexplained heart enlargement or heart failure should discuss FGF23 testing with their cardiologist. People with normal kidney function and no bone disease don’t need to worry about FGF23 at this time, though maintaining good nutrition supports overall bone and heart health.
If you start FGF23-targeting medication for bone disease, improvements in bone strength typically appear over months to years. Heart and kidney benefits may take longer to develop and are still being studied. If you have elevated FGF23 due to kidney disease, controlling it may help slow heart and kidney damage, but this is a long-term process requiring ongoing monitoring and treatment.
Frequently Asked Questions
What is FGF23 and why should I care about it?
FGF23 is a hormone your bones make that controls how your body uses phosphate and vitamin D. When levels are abnormal, it increases risk of heart disease, weak bones, and kidney damage. If you have kidney disease or bone problems, your doctor may test your FGF23 levels.
Can high FGF23 cause heart problems?
Yes. Research shows elevated FGF23 is linked to heart enlargement, heart attacks, strokes, and hardened blood vessels. This connection is especially important for people with kidney disease, who often have high FGF23 levels and increased heart disease risk.
Is there treatment for FGF23 imbalances?
New medications are now available to treat FGF23-related bone diseases by blocking excess FGF23 or replacing missing FGF23 function. These treatments can improve bone strength, though long-term benefits for heart and kidney health are still being studied.
How does FGF23 affect the kidneys?
FGF23 normally tells kidneys how much phosphate to keep or release. When FGF23 is abnormal, it disrupts this balance and can cause kidney scarring and reduced kidney function. People with kidney disease often have elevated FGF23, creating a harmful cycle.
Should I get my FGF23 levels tested?
Testing is recommended if you have chronic kidney disease, bone disease, or a family history of hypophosphatemic rickets. For people with normal kidney function and no bone disease, routine FGF23 testing is not necessary at this time.
Want to Apply This Research?
- If your doctor has tested your FGF23 levels, track the results over time in your health app. Record the date, FGF23 value, and any medications you’re taking. Note any symptoms like bone pain, fatigue, or shortness of breath. This helps you and your doctor see if treatment is working.
- If you have kidney disease or bone disease, use your app to set reminders for taking FGF23-targeting medications exactly as prescribed. Also track your vitamin D and phosphate intake through food logging, as these minerals affect FGF23 levels. Set monthly reminders to check in with your doctor about lab results.
- Create a dashboard that shows your FGF23 trend over time alongside your kidney function tests and heart health markers. If you’re on treatment, track whether symptoms improve. Share this data with your healthcare team at each visit to guide treatment adjustments.
This article summarizes scientific research about FGF23 and is for educational purposes only. It is not medical advice. If you have kidney disease, bone disease, heart disease, or symptoms like bone pain, fatigue, or shortness of breath, consult your healthcare provider about whether FGF23 testing or treatment is appropriate for you. Do not start, stop, or change any medications without medical supervision. The mechanisms of how FGF23 affects different organs are still being researched, and treatment recommendations may evolve as new evidence emerges.
This research translation is published by Gram Research, the science division of Gram, an AI-powered nutrition tracking app.
