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Furthermore, excess LA might elevate pro-inflammatory eicosanoid levels (e.g. , prostaglandin E2) and disrupt gut microbiota, fostering dysbiosis and immune dysregulation. Evidence, however, derives primarily from preclinical studies, with limited human data but epidemiological signals are strongest for breast (age-standardized incidence, approximately 130\/100000 women), colorectal (approximately 39\/100000), prostate (approximately 112\/100000 men) and cutaneous melanoma (approximately 26\/100000) cancers, where higher LA biomarkers or intakes have been repeatedly observed. Ketogenic diets, historically prioritized for metabolic benefits, reduce blood glucose, an effect possibly beneficial in cancer contexts, but may impair gut health by restricting fermentable fiber, potentially decreasing short-chain fatty acid production. This review explores LA\u2019s hypothetical role in cancer-related pathways and the trade-offs of carbohydrate restriction. A proposed \u201cterrain restoration\u201d protocol, emphasizing reduced LA intake, gradual carbohydrate reintroduction to support microbiota, and nutrients like pentadecanoic acid (C15:0) for mitochondrial function, lacks clinical validation. 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