Consumption of ultra-processed food (UPF) results in a distinct metabolic 'signature' in the blood, associated with potentially adverse health conditions, a new study by an international team of researchers finds.
The peer-reviewed paper, published in the journal Critical Reviews in Food Science and Nutrition , is the first to use targeted metabolomics (the scientific study of the chemical processes involved in cell metabolism) to examine the effects of UPF intake on a large European cohort.
While emerging evidence links consumption of UPF to higher risks of cancer, cardiovascular disease, type 2 diabetes, mortality and obesity, the biological explanations for this remain unclear. To gain insight into the potential metabolic pathways linking UPF to poor health, Dr Jessica Blanco-Lopez of the International Agency for Research on Cancer (IARC/WHO) and colleagues identified molecular signatures of UPF intake using data from 15,200 participants in the European Prospective Investigation into Cancer and Nutrition (EPIC) study.
The team questioned participants about their diet and classified the results using the Nova system which categorises foods into four groups, from unprocessed to ultra-processed. The researchers also measured levels of small molecules called metabolites (an intermediate or end product of metabolism) and fatty acids (FAs) in blood samples taken from the participants. Then, they used regression modelling to identify metabolite and FA 'signatures' associated with UPF consumption while taking into account demographic, lifestyle and other confounding factors.
UPF intake was found to be associated with 22 circulating metabolites. Higher UPF consumption was associated with higher occurrence of certain lipid derivatives that are biomarkers of impaired fatty acid oxidation and mitochondrial dysfunction, and lower occurrence of several other lipids that are essential for cell membrane stability, permeability and cell signalling. This metabolic signature suggests that UPF consumption may stimulate the synthesis of endogenous lipids (fatty compounds, such as cholesterol) and inhibit healthy lipid processing.
UPF intake was also associated with eight plasma FAs. Higher UPF consumption resulted in a pattern of high stearic acid levels (which indicate high saturated fat intake or metabolic issues) alongside high levels of long-chain polyunsaturated FAs, suggesting the metabolic impact of UPFs extends beyond their fat content to stimulate internal lipid synthesis from excess dietary carbohydrates. This association further confirms that even low levels of industrial fatty exposure persist in circulation.
Dr Jessica Blanco-Lopez, whose background is in paediatrics and oncology, which led her to become involved in studies related to nutrition and metabolism, says: "These findings have several implications. The simultaneous decline in protective FA and the increase of metabolic stress suggest that UPF consumption may contribute to health risks through nutritional displacement and inducing metabolic disruption.
"Our study underscores the potential metabolic impact of UPFs and highlights the need for further research using targeted and untargeted metabolomics approaches to clarify the biological pathways linking food processing with chronic diseases and mortality."
A limitation of the paper includes that this study observed people at one point in time rather than following them over many years. Because of this, the researcher team cannot definitively say that eating ultra-processed foods causes the metabolic changes they found
They can only show that these two things are associated or linked together.
"We spent considerable time evaluating and refining the analytical approach, testing several different methodologies and strategies throughout the process," adds Dr Blanco-Lopez.
"What was particularly reassuring was that, despite these different approaches, the results remained remarkably consistent. This gave us greater confidence in the robustness and reliability of the findings."
