A study in Life Metabolism reveals how intermittent fasting reduces blood clot risk by altering gut microbiota and increasing indole-3-propionic acid (IPA) levels.
Cardiovascular diseases, primarily caused by arterial blockages, claim over 20 million lives annually. Atherosclerosis, high cholesterol, and glucose levels contribute to platelet aggregation, heightening thrombosis risk. Intermittent fasting (IF), which involves reducing energy intake by 60% on certain days, has been linked to improved cardiovascular health. Patients practicing IF exhibited increased IPA levels, which correlated with reduced platelet activation.
Spectrometric analysis identified gut bacteria as key players in this process. Elevated IPA levels were observed in fasting individuals, with Clostridium sporogenes emerging as the primary microbial producer. “IPA derived from C. sporogenes may mediate the beneficial effects of IF through inhibition of platelet activation and blood clot formation,” researchers noted. IPA interacts with the pregnane X receptor (PXR) in platelets, suppressing activation pathways that lead to clot formation.
Mouse studies confirmed these findings—animals treated with C. sporogenes exhibited higher IPA levels and reduced platelet aggregation. IF increased gut C. sporogenes levels, while antibiotic treatment elevated platelet activity. The effects of IPA were comparable to clopidogrel, a standard antithrombotic drug, with a combination of IPA and clopidogrel demonstrating a synergistic effect.
These results suggest intermittent fasting as a potential adjunct therapy for coronary atherosclerosis. While promising, further clinical trials are necessary to validate its long-term cardiovascular benefits.
