A rising body of scientific evidence points to an unanticipated link between a common vitamin, birth abnormalities, and nerve damage in adults—particularly those with diabetes. A new laboratory study revealed that folic acid, a B vitamin long associated with prenatal health, may also play an important role in safeguarding nerves later in life. 

Peripheral neuropathy, characterised by tingling, numbness, weakness, or searing pain, affects an estimated 2–8% of the general population and more than 14% of those over 40. Nearly one-third of cases are associated with type 2 diabetes, making it one of the most prevalent and severe diabetic complications. 

The mouse study focused on a gene called Shmt1, which helps the body produce fundamental DNA building blocks. Researchers discovered that mice with decreased activity of this gene experienced not only neural tube abnormalities (severe birth malformations of the brain and spine) but also early symptoms of peripheral neuropathy. This result shows that the same biological flaw might impact nerve development before birth and nerve maintenance decades later. 

Simply put, nerves require ongoing repair, much as electrical cables require proper insulation. DNA creation is required for the repair process. When it is interrupted, nerves are more sensitive to harm. 

The researchers also investigated if folic acid could protect nerve health. Mice fed a high-folic-acid diet were protected from nerve injury, even if they had diabetes. Nerve signal speed, an important indicator of nerve health in diabetic mice, improved considerably. The researchers pointed out, "These results indicate a special nutritional requirement for folic acid in diabetes and implicate impaired de novo thymidylate synthesis in PN." 

In simple terms, the result suggests that diabetes may make the body need more folic acid to keep nerve cells working properly. 

The study also found big differences between men and women. Female mice with the Shmt1 deficiency sustained more severe nerve damage compared to males. Further research showed that male mice activated natural defensive mechanisms that help nerves recover, while female mice did not respond as well. 

In another unexpected discovery, uridine, a dietary component that has been related to birth abnormalities in the past, harmed the nerves of healthy mice. In women, it reduced myelin, the protective layer around nerves, by more than 40%. The consequence is like taking the insulation off a wire, which makes signals weaker or fail. 

Although the study was performed on animals and cannot be directly extrapolated to humans, scientists believe it offers valuable insights. It suggests that nerve damage from diabetes is not inevitable and that nutrition, especially folic acid, can aid in its prevention alongside standard diabetes treatment. 

The results pave the way for forthcoming human investigations and pose a critical inquiry: may individualised nutritional protocols eventually aid in preventing nerve damage prior to the manifestation of symptoms?