Diabetic peripheral neuropathy (DPN) remains among the most common, disabling, and therapeutically unresolved complications of diabetes. Current management can reduce neuropathic pain and improve cardiometabolic risk, but reliable disease-modifying therapy capable of restoring damaged peripheral nerves remains unavailable. Palm-derived tocotrienols represent an intriguing candidate because experimental evidence supports antioxidant, anti-inflammatory, neurotrophic, vascular, and membrane-protective effects, while clinical trials have reported improvements in selected sensory and motor nerve-conduction velocities. These electrophysiological effects, however, have not been accompanied consistently by proportional improvements in glycated hemoglobin, nerve-actionpotential amplitudes, pain, or patient-reported outcomes. This critical qualitative literature review synthesizes contemporary evidence published primarily from 2020–2026 to examine this apparent nerve-conduction–clinical-recovery paradox. The analysis distinguishes large-fiber conduction, axonal integrity, small-fiber pathology, Schwann-cell and myelin dysfunction, neuroinflammation, autonomic neuropathy, pain mechanisms, and functional disability. The synthesis proposes a glycemia-independent neuroprotection hypothesis in which tocotrienols may preferentially preserve or improve myelin–Schwann-cell function and neural microenvironment without necessarily regenerating lost axons. It further argues that future trials should abandon single-surrogate efficacy models and combine nerve-conduction studies with corneal confocal microscopy, intraepidermal nerve-fiber density, quantitative sensory testing, autonomic measures, gait, balance, quality of life, falls, and foot-ulcer outcomes. Tocotrienols should presently be viewed as a biologically plausible adjunct requiring phenotype-enriched, longer-duration trials before disease-modifying claims can be justified.