Dietary and Lifestyle Patterns among Young Patients with Lung Cancer: Analysis of Mutation-Specific Phenotypes

Lung cancer in young adults is biologically distinct, with 84% harboring targetable mutations largely unassociated with active and passive tobacco exposure. Environmental risk factors remain poorly characterized in this predominantly female, non-tobacco smoking population.

We analyzed 187 patients in the Epidemiology of Young Lung Cancer study using biological pathway groupings: EGFR Pathway (EGFR + ERBB2), Fusion-Positive (ALK + ROS1 + RET + NTRK), and Other/Mixed Mutations (KRAS, BRAF, MET exon 14 skipping, TP53, and additional alterations). Dietary quality was assessed using the Healthy Eating Index (HEI)-2015 and compared with US reference values from National Health and Nutrition Examination Survey. Statistical comparisons used one-sample t tests.

Active and passive tobacco use diverged from traditional mutation associations. In the Other/Mixed Mutations group, 68.8% never used tobacco despite these mutations being linked to tobacco exposure. Conversely, the EGFR Pathway group included 32.9% with a history of tobacco use. Oral contraceptive use among females was consistently elevated (81.7%-90.2%). Dietary analysis revealed that EGFR Pathway and Fusion-Positive patients demonstrated higher HEI-2015 scores versus the US reference (64.9 ± 10.7 and 65.5 ± 9.8 vs. 58) and consumed more total vegetables (4.2 vs. 3.5), fruits (3.3 vs. 2.5), and whole grains (3.9 vs. 2.6).

Young patients with lung cancer demonstrated mutation-specific environmental exposure patterns distinct from older populations. EGFR Pathway and Fusion-Positive patients had the highest diet quality scores, driven primarily by higher intake of vegetables, fruits, and whole grains-food categories with established protective associations and documented pesticide residues.

These findings highlight nontobacco environmental exposures in young patients with lung cancer and support further investigation of dietary patterns and hormonal factors in mutation-specific disease pathways.