Autism spectrum disorder (ASD) is a complex neurodevelopmental condition and is characterized by difficulties in social interaction, communication, and repetitive behaviors. It is thought that ASD is a disorder resulting from the complex interaction of genetic, environmental and metabolic factors rather than a single cause. Intellectual disability is a common condition in ASD patients. The co-occurrence of ASD and intellectual disability makes the diagnosis and treatment processes of the disease more complex. Intellectual disability is a condition that restricts the adaptive abilities of individuals and involves significant limitations. Folate plays an important role in processes such as neural tube development, DNA synthesis and repair, and methylation. In particular, the methylation cycle is a very important process for the regulation of gene expression and neurotransmitter synthesis. Imbalances in the methylation cycle may cause negative consequences in brain development and function. Since folate metabolism is regulated by enzymes such as methylenetetrahydrofolate reductase, it is thought that genetic variations in the genes of these enzymes may also affect folate bioavailability and metabolism. As a result of these genetic variations, a disrupted methylation cycle occurs. As a result, nervous system development may be affected and an increased risk of ASD may arise. Therefore, disorders in folate metabolism may affect brain development and synaptic plasticity in early stages and lead to intellectual disability and ASD. Low folate levels have also been linked to neurotransmitter imbalances, oxidative stress, and mitochondrial dysfunction. It is thought that these mechanisms may also be effective in the pathophysiology of ASD and intellectual disability. When this complex network of relationships is evaluated, it is predicted that ASD and intellectual disability may arise from the interaction of many genetic, environmental, metabolic, and biochemical factors, including folate metabolism.