Vitamin B12 (adenosylcobalamin) is scientifically validated as a treatment and supportive therapy for certain types of nerve damage, especially those related to vitamin B12 deficiency. B12 is crucial for the maintenance of myelin sheaths, which insulate nerve fibers and are essential for proper nerve conduction. Deficiency in B12 can result in demyelination and subsequent neurological symptoms such as paresthesia, numbness, and even irreversible nerve damage if untreated.

The evidence base includes numerous clinical studies and case reports demonstrating that B12 supplementation (including adenosylcobalamin and other forms such as methylcobalamin) can halt progression and, in some cases, partially reverse neurological symptoms when deficiency is the underlying cause. Treatment is especially effective when administered early. A well-documented cause of B12 deficiency-related nerve damage is pernicious anemia, an autoimmune condition that impairs B12 absorption.

However, for nerve damage unrelated to B12 deficiency (for example, in diabetic neuropathy without B12 deficiency), the evidence for benefit is less robust. Some small studies suggest possible symptomatic relief, but meta-analyses and reviews generally conclude that B12 is most effective only in deficiency states. Guidelines from neurology and hematology societies support B12 supplementation for nerve damage secondary to deficiency, but not as a general treatment for all neuropathies.