The adolescent brain, with ongoing prefrontal maturation, may be more vulnerable to drug use‐related neurotoxic changes as compared to the adult brain. We investigated whether the use of methamphetamine (MA), a highly addictive psychostimulant, during adolescence affect metabolic and cognitive functions of the anterior cingulate cortex (ACC). In adolescent MA users (n = 44) and healthy adolescents (n = 53), the levels of N‐acetyl aspartate (NAA), a neuronal marker, were examined in the ACC using proton magnetic resonance spectroscopy. The Stroop color–word task was used to assess Stroop interference, which may reflect cognitive functions of behavior monitoring and response selection that are mediated by the ACC. Adolescent MA users had lower NAA levels in the ACC (t = −2.88, P = 0.005) and relatively higher interference scores (t = 2.03, P = 0.045) than healthy adolescents. Moreover, there were significant relationships between lower NAA levels in the ACC and worse interference scores in adolescent MA users (r = −0.61, P < 0.001). Interestingly, early onset of MA use, as compared to late onset, was related to both lower NAA levels in the ACC (t = −2.24, P = 0.03) as well as lower performance on interference measure of the Stroop color–word task (t = 2.25, P = 0.03). The current findings suggest that metabolic dysfunction in the ACC and its related cognitive impairment may play an important role in adolescent‐onset addiction, particularly during early adolescence. In this study using proton magnetic resonance spectroscopy, we found that the use of methamphetamine, a highly addictive psychostimulant, during adolescence may be associated with metabolic dysfunction in the anterior cingulate cortex and its related cognitive impairment. Interestingly, the age of exposure is critical for the methamphetamine‐induced neurotoxic consequences.