High-Protein Diet May Raise Risk of Cancer-Associated Venous Thromboembolism: Study

Published On 2025-08-29 02:30 GMT   |   Update On 2025-08-29 09:05 GMT
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A new study by researchers at Boston University Chobanian & Avedisian School of Medicine has found that a high-protein diet, particularly one rich in the amino acid tryptophan (Trp), may increase the risk of cancer-associated venous thromboembolism. The findings, based on experimental models, were published in the journal Blood Advances and could have important implications for nutritional strategies in cancer care.

Cancer patients are four to seven times more likely to develop venous thromboembolism, which is fatal in approximately one out of every seven affected individuals. In this study, researchers explored how a diet high in protein or tryptophan influenced thrombosis in experimental models with colon cancer.

The team discovered that models fed a high-protein or tryptophan-rich diet developed more severe vascular thrombosis than those on a balanced diet. Inhibiting the enzyme responsible for tryptophan metabolism reduced vascular injury, and the metabolite kynurenine—produced during tryptophan breakdown—was found to impact coagulation factors that promote clot formation.

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The findings are particularly relevant for cancer patients, who are often advised to increase protein intake to combat cancer-cachexia and the side effects of chemotherapy. Researchers emphasize the need for further investigation into how dietary protein and specific amino acids may influence thrombosis risk in cancer patients.

“Although our new findings are based on experimental models, we believe that knowledge gained from this study could prompt interest in further testing relevance to the human condition,” said co-corresponding author Katya Ravid, Barbara E. Corkey Professor at the university.

Reference: Lotfollahzadeh, S., Jose, A., Yang, X., Bathla, T., Lazowski, A., Hoekstra, I., ... & Chitalia, V. C. (2025). Dietary Tryptophan Augments Cancer-Associated Venous Thrombogenicity Mitigated by Indoleamine 2, 3-Dioxygenase 1 Inhibition. Blood Advances.

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Article Source : Blood Advances

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