RESUMO
BACKGROUND: LPS-type endotoxins, naturally found in the gut microbiota, are recognized as triggers of inflammation and emerge as detrimental factors of healthy aging. Nutrition represents a promising strategy to reduce LPS burden, yet little is known about the relation of diet to circulating LPS concentrations. OBJECTIVE: The aim was to evaluate the associations between food groups, dietary patterns, and circulating 3-hydroxy fatty acids (3-OH FAs), a proxy of LPS burden. METHODS: In a cross-sectional study of 698 French older community-dwelling individuals, 3-OH FA concentrations were measured by LC-tandem MS. Dietary patterns were determined using food-frequency questionnaires. Adherence to a Mediterranean-type diet was computed according to the consumption of 8 food groups (fruits, vegetables, legumes, cereals, fish, olive oil, meat, and dairy products) and alcohol intake (range: 0, low adherence, to 18, high adherence). Three a posteriori dietary patterns were derived from factor analysis: complex carbohydrate (rich in rice, pasta, eggs, poultry, and potatoes), traditional (rich in alcohol, meat, processed meats-cold cuts, and legumes), and prudent (rich in vegetables and fruits and low in cookies) diets. Linear regression models were applied. RESULTS: The frequency of consumption of each food group was not associated with 3-OH FA concentrations. Greater adherence to both the Mediterranean diet and the prudent diet were associated with lower circulating 3-OH FAs (ß [95% CI] for each additional point of score: -0.12 [-0.22, -0.01] and -0.27 [-0.48, -0.07], respectively). In contrast, greater adherence to the traditional diet was associated with higher concentration of 3-OH FAs (ß [95% CI] 0.22 [0.001, 0.46]). The adherence to the complex-carbohydrate diet was not associated with 3-OH FA concentrations. CONCLUSIONS: Based on 2 complementary approaches, the identified plant-based dietary patterns were associated with lower 3-OH FA concentrations, and thus a lower LPS burden, which is considered a potent trigger of inflammatory response.
