I think all of us here would like to avoid cognitive decline. Probably the most feared condition.
Article in Nature
The article above is an association article, but probably valid. There can be the argument that the population with high riboflavin diets probably tend to do more healthy things - but looking at sources of riboflavin, a lot of it is from things I’d consider unhealth generally.
The study looked at Riboflavin intake vs. Cognitive testing on 2893 individuals over age 60 years. The confidence interval on all 3 tests, and in combination seems to favor higher Riboflavin intake.
Vegetable/Fungi Sources:
Fortified Tofu
Mushrooms
Spinach
Almonds
Avocados
Meat/Animal Sources:
Beef-Steak
Low fat milk
Non-fat yogurt
Cottage cheese
Pork Chops
Salmon
Eggs
The details on amounts of Riboflavin per serving is available here
It would seem pretty sensible to make sure this is adequately represented in your diet.
As an aside, it really hasn’t been on my list of things I recommend for decreasing homocysteine, but I saw another post on the forum regarding this, and Vera-Health.ai seems to agree that it can decrease homocysteine. The text below is their summary on that topic:
That post was from @Dr.Bart
BTW, Tommy Woods also recommended Riboflavin for homocysteine on one of his podcasts
Riboflavin, or vitamin B2, can indeed decrease homocysteine levels, particularly in individuals with specific genetic backgrounds. The relationship between riboflavin and homocysteine is significantly influenced by the methylenetetrahydrofolate reductase (MTHFR) C677T polymorphism. Individuals with the MTHFR 677TT genotype often have elevated homocysteine levels due to reduced enzyme activity, which is dependent on riboflavin as a cofactor.
Research indicates that riboflavin supplementation can lead to a significant reduction in homocysteine levels in these individuals. For instance, a study demonstrated a 22% reduction in homocysteine levels with riboflavin supplementation in subjects with the MTHFR 677TT genotype, especially those with low baseline riboflavin status. The effect of riboflavin is further modulated by folate status. In individuals with low folate levels, riboflavin can have a more pronounced effect on reducing homocysteine concentrations. This is because riboflavin acts as a cofactor for MTHFR, which is crucial for converting homocysteine to methionine, a process that also requires folate.
However, the impact of riboflavin on homocysteine levels in the general population or those without the MTHFR 677TT genotype is less clear. Some studies suggest that riboflavin alone may not significantly lower homocysteine levels unless combined with folate supplementation. In populations with adequate riboflavin and folate status, the effect of riboflavin on homocysteine might be minimal.
In summary, riboflavin can decrease homocysteine levels, particularly in individuals with the MTHFR 677TT genotype and low folate status. Its efficacy in the general population without these specific genetic and nutritional factors is not well-established.
