Editing Openai/693cca0d-8c24-800e-bde2-ffa4c902003d (section)

=== TL;DR ===

• Cannabinoids (CBD and THC) — especially when delivered as a non-smoked, balanced 1:1 oil — show clear anti-inflammatory and antioxidant actions in lab and animal studies and encouraging signals in some human conditions (e.g., nabiximols/Sativex for MS spasticity). These actions are plausibly neuroprotective. PMC<ref>{{cite web|title=PMC|url=https://pmc.ncbi.nlm.nih.gov/articles/PMC9932048/|publisher=pmc.ncbi.nlm.nih.gov|access-date=2025-12-13}}</ref>
• Ethanol (drinking alcohol) is metabolized to acetaldehyde, a genotoxic chemical, and alcohol use is a well-established cause of multiple cancers, is linked to accelerated biological ageing and brain atrophy in population studies, and promotes oxidative stress. That makes alcohol far more clearly tied to DNA damage, ageing and cancer. New England Journal of Medicine<ref>{{cite web|title=New England Journal of Medicine|url=https://www.nejm.org/doi/full/10.1056/NEJMsr2306723|publisher=New England Journal of Medicine|access-date=2025-12-13}}</ref>
• Bottom line: for the specific harms you named (DNA damage, cancer risk, accelerated ageing, brain atrophy), the epidemiology and mechanisms point to alcohol as the larger, proven threat — while cannabinoids have biological properties (antioxidant, anti-inflammatory) that could protect neurons. That said, cannabis is not risk-free (adolescent exposure, heavy/high-THC use and some cognitive/psychosis risks), and the human clinical evidence for long-term neuroprotection is still limited. PMC<ref>{{cite web|title=PMC|url=https://pmc.ncbi.nlm.nih.gov/articles/PMC9932048/|publisher=pmc.ncbi.nlm.nih.gov|access-date=2025-12-13}}</ref>