Acetyl-CoA carboxylase is a biotin-dependent enzyme that catalyzes the irreversible carboxylation of acetyl-CoA to produce malonyl-CoA. Malonyl-CoA inhibits the rate-limiting step in beta-oxidation of fatty acids. Malonyl-CoA inhibits fatty acids from associating with carnitine by regulating the enzyme carnitine acyltransferase.
Biotin supplementation would then both inhibit beta-oxidation and assist with chain elongation in fatty acid biosynthesis.
I have been arguing that increases is beta-oxidation that result from increased intakes of polyphenols can lead to difficulties in schizophrenia. Given the dual functions of malonyl-CoA in inhibiting beta-oxidation and assisting with fatty acid elongation if there is excessive beta-oxidation there would have to be difficulties in fatty acid elongation. Supplemental biotin would decrease beta-oxidation and increase fatty acid elongation which would be headed in the right direction. Biotin would not be supplemented at the same time as pantothenic acid as pantothenic acid is a competitive inhibitor of biotin transport.
Biotin is apparently necessary for the treatment of the negative symptoms of schizophrenia. Biotin, however, taken alone is not effective as with biotin there are still difficulties with fatty acid absorption. Negative symptoms of schizophrenia are due to dysregulation of fatty acid metabolism which is dysregulated in multiple ways in schizophrenia.