A population-based analysis found that men who consume higher amounts of dietary calcium may face an increased risk of developing benign prostatic hyperplasia, a non-cancerous enlargement of the prostate gland that affects urinary function.
The researchers analyzed data from 590 men aged 40 and older who participated in the U.S. National Health and Nutrition Examination Survey between 2003 and 2008.
Each additional 100 mg of calcium consumed through food was associated with a 5% higher likelihood of having BPH, after adjusting for age, race, body mass index (BMI), income, smoking, alcohol use, hypertension, and diabetes. BPH diagnosis was based on self-reported physician confirmation.
Participants were divided into four groups based on their calcium intake. Men in the highest intake group (more than 1,135.25 mg/day) had significantly greater odds of BPH compared to those in the lowest group (less than 508.25 mg/day). In the fully adjusted model, the odds ratio for BPH in the highest intake group was 2.47.
Dose-response analysis showed a non-linear relationship. When calcium intake was below 1,114.11 mg/day, each 100 mg increase was associated with a 20% higher BPH risk. Above that threshold, no further significant increase was observed, suggesting a threshold effect.
Subgroup analysis showed stronger associations among men aged 60 and older, those with a BMI under 25, higher income levels, and no hypertension. No significant associations were found in younger men or those with higher BMIs, lower income, hypertension, or diabetes.
The study, led by Hongyuan Chang of the Department of Andrology, Xiyuan Hospital of China Academy of Chinese Medical Sciences, Beijing, China, and colleagues,did not include calcium supplements and relied on two 24-hour dietary recall interviews per participant. Although standardized, these methods may introduce recall bias. Because the data are cross-sectional, causality could not be established.
Biological mechanisms potentially linking dietary calcium to BPH include activation of androgen receptors and stimulation of fibroblast growth factors, which promote prostate cell growth. Calcium may also influence inflammatory pathways and suppress vitamin D production, which has protective effects against prostate enlargement.
While earlier research has primarily examined calcium in relation to prostate cancer, this study highlights a possible link between dietary calcium and non-cancerous prostate enlargement.
Further longitudinal studies are needed to confirm these findings and clarify the underlying mechanisms. Men with BPH or at higher risk may benefit from avoiding high levels of calcium intake and limiting calcium supplementation.
The authors reported no conflicts of interest.