Vitamin B2 (Riboflavin) and Dementia Risk Reduction
Based on current evidence, vitamin B2 (riboflavin) supplementation is not recommended for reducing the risk of dementia in individuals without documented B2 deficiency. While recent research suggests a potential association between dietary riboflavin intake and reduced dementia risk, there is insufficient clinical trial evidence to support supplementation as a preventive strategy.
Evidence on B Vitamins and Dementia
Current Guidelines on B Vitamin Supplementation
- The European Society for Clinical Nutrition and Metabolism (ESPEN) explicitly recommends against B vitamin supplementation for prevention or correction of cognitive decline in persons with dementia when there is no indication of deficiency (Grade of evidence: low) 1
- This recommendation is based on multiple randomized controlled trials and systematic reviews that found no consistent benefit of B vitamin supplementation on cognition 1
- The 2024 updated ESPEN guideline maintains this position, stating that "no controlled intervention study has been able to demonstrate a cognitive benefit for persons with dementia from supplementing a single nutrient, neither folic acid, vitamin B, B12, D, E or selenium nor any other micronutrient" 1
Specific Evidence on B Vitamins
- While vitamin B6, B12, and folate have been extensively studied, specific evidence regarding vitamin B2 (riboflavin) and dementia is more limited 1
- Supplementation with B vitamins has been shown to reduce homocysteine levels (a potential risk factor for dementia), but this biochemical effect has not translated to meaningful cognitive benefits in clinical trials 1
- A Cochrane review examining B vitamin supplementation found no evidence that supplementation improves dementia or slows cognitive decline in subjects without vitamin deficiency 1
- Even in individuals with elevated homocysteine levels, the evidence for cognitive benefit from B vitamin supplementation remains inconsistent 2, 3
Recent Research on Riboflavin (B2)
- A 2025 prospective cohort study from Japan found that dietary intake of riboflavin was inversely associated with the risk of disabling dementia over a 15.4-year follow-up period (hazard ratio for highest vs. lowest quartiles: 0.51,95% CI 0.42-0.63) 4
- This same study also found similar inverse associations for dietary vitamin B6 and folate intake 4
- However, this observational evidence has not yet been confirmed in randomized controlled trials specifically examining riboflavin supplementation 1, 5
Clinical Implications
When to Consider B Vitamin Supplementation
- B vitamin supplementation, including riboflavin, should be considered only when there is a documented deficiency 1
- Existing deficiencies should be corrected with adequate supplementation, regardless of dementia status 1
- Normal doses (not mega-doses) should be used when supplementation is indicated to avoid potential toxic effects 1
Potential Pitfalls
- Relying on vitamin supplementation without addressing other modifiable risk factors for dementia may provide false reassurance 1, 6
- Supplementation in the absence of deficiency represents unnecessary cost and pill burden 1
- Long-term high-dose supplementation may have unintended consequences, as seen with other vitamins (e.g., increased prostate cancer risk with vitamin E supplementation) 6
Conclusion for Clinical Practice
- Despite the biological plausibility and some promising observational data regarding riboflavin, current clinical guidelines do not support B vitamin supplementation for dementia prevention or treatment in the absence of deficiency 1
- For patients concerned about dementia risk, focus should be placed on overall dietary quality rather than single nutrient supplementation 1, 5
- If considering B vitamin supplementation, priority should be given to patients with documented deficiencies or those at high risk for deficiency 1