Vitamin B12 (hydroxycobalamin) is scientifically validated for use in supporting and treating certain types of nerve damage, especially those resulting from vitamin B12 deficiency. B12 is essential for normal neurological function, playing a critical role in myelin synthesis and neuronal health. Deficiency of B12 can result in demyelinating neuropathy, which may manifest as peripheral nerve damage, numbness, tingling, and even cognitive impairment.

Numerous clinical studies and case reports have demonstrated that correcting B12 deficiency with supplementation (including hydroxycobalamin) can halt progression and, in many cases, partially reverse neuropathic symptoms, particularly if treatment begins early. This is reflected in guidelines from neurology and hematology societies, which recommend B12 supplementation for deficiency-related neuropathy. There is strong mechanistic evidence: B12 is necessary for the functioning of methionine synthase, which is involved in methylation reactions vital for myelin maintenance.

However, the evidence for using B12 to treat nerve damage not associated with deficiency (such as diabetic neuropathy or traumatic nerve injuries in B12-replete individuals) is less robust, with only limited and inconsistent clinical trial data. Most of the scientific support is thus for B12’s role in deficiency-induced neuropathy, with widespread acceptance in clinical practice and medical literature.