A new study by researchers at the USC Leonard Davis School of Gerontology suggested that the health benefits of the Mediterranean diet may be partly driven by tiny proteins within our mitochondria, offering fresh insight into how diet influences aging and disease risk. The findings were published in the journal Frontiers in Nutrition.
Led by Roberto Vicinanza, instructional associate professor of gerontology at USC Leonard Davis, the study found that individuals who closely adhere to a Mediterranean-style diet have higher levels of two mitochondrial microproteins, namely, humanin and SHMOOSE. Both proteins have previously been linked to protection against cardiovascular disease and neurodegenerative conditions.
The Mediterranean diet—rich in olive oil, fish, legumes, fruits, and vegetables has long been associated with a reduced risk of heart disease, diabetes, and cognitive decline. However, the biological mechanisms behind these benefits are still being explored.
In this study, researchers analyzed blood samples from older adults with varying levels of adherence to the diet. Participants who followed the diet most closely showed significantly higher levels of humanin and SHMOOSE, along with lower oxidative stress, a major contributor to ageing and chronic disease.
"MIND-recommended foods rich in antioxidants, such as berries, and high-quality protein sources like poultry, may reduce oxidative stress and mitigate neuronal damage," the study authors noted.
"Conversely, fast fried foods, often high in unhealthy fats, trans fats and advanced glycation end-products, may contribute to inflammation and vascular damage."
The findings also highlighted the role of specific foods. Higher consumption of olive oil, fish, and legumes was associated with increased humanin levels, while greater intake of olive oil and reduced consumption of refined carbohydrates were linked to higher SHMOOSE levels.
The researchers plan to investigate further whether targeted dietary interventions can directly boost levels of these microproteins and whether such changes could ultimately help lower disease risk.
"Our goal is to move from observing associations to understanding causality," Vicinanza concluded. "If we can harness these pathways, we may be able to design nutritional strategies that promote healthy aging at the molecular level."
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