This may shed some light onto how omega-3 fatty acids might work in psychiatric disorders. Recall that autophagy was recently implicated as a key factor in the pathophysiology of schizophrenia.[1] Oxidative stress also seems to be important in psychiatric disorders, and, normally, high levels of ROS or prolonged stress up regulates p53 and provokes a pro-oxidant response to further increase ROS, which subsequently elicits the p53-dependent apoptotic processes to eliminate cells that have been damaged beyond recovery.[2][3][4] Furthermore, I recall that Lithium stimulates the rapid degradation of p53, which in turn up-regulates the autophagy processes; deletion, depletion, or inhibition of p53 induces autophagy in human cells, i.e. the clearing out of damaged cellular components for continued cell survival.[5][6] i.g. lithium may help increase gray matter by salvaging cells through the up-regulation of autophagy; perhaps some psychiatric disorders are the result of a defect in the p53 pathway, as this also can explain gray matter atrophy as the result of p53 induced cellular apoptosis.

The omega-3 polyunsaturated fatty acid DHA induces simultaneous apoptosis and autophagy via mitochondrial ROS-mediated Akt-mTOR signaling in prostate cancer cells expressing mutant p53.
Biomed Res Int. 2013;2013:568671. doi: 10.1155/2013/568671 pmid: 23841076
Shin S1, Jing K, Jeong S, Kim N, Song KS, Heo JY, Park JH, Seo KS, Han J, Park JI, Kweon GR, Park SK, Wu T, Hwang BD, Lim K.

Abstract:
Docosahexaenoic acid (DHA) induces autophagy-associated apoptotic cell death in wild-type p53 cancer cells via regulation of p53. The present study investigated the effects of DHA on PC3 and DU145 prostate cancer cell lines harboring mutant p53. Results show that, in addition to apoptosis, DHA increased the expression levels of lipidated form LC3B and potently stimulated the autophagic flux, suggesting that DHA induces both autophagyand apoptosis in cancer cells expressing mutant p53. DHA led to the generation of mitochondrial reactive oxygen species (ROS), as shown by the mitochondrial ROS-specific probe mitoSOX. Similarly, pretreatment with the antioxidant N-acetyl-cysteine (NAC) markedly inhibited both the autophagy and the apoptosis triggered by DHA, indicating that mitochondrial ROS mediate the cytotoxicity of DHA in mutant p53 cells. Further, DHA reduced the levels of phospho-Akt and phospho-mTOR in a concentration-dependent manner, while NAC almost completely blocked that effect. Collectively, these findings present a novel mechanism of ROS-regulated apoptosis and autophagy that involves Akt-mTOR signaling in prostate cancer cells with mutant p53 exposed to DHA.

References:

• [1]: Molecular Psychiatry - Autophagy has a key role in the pathophysiology of schizophrenia
  
• [2]: Savior and slayer: the two faces of p53
  
• [3]: Does Nrf2 Contribute to p53-Mediated Control of Cell Survival and Death?
  
• [4]: p53/HMGB1 Complexes Regulate Autophagy and Apoptosis
  
• [5]: A dual role of p53 in the control of autophagy
  
• [6]: Antioxidants Accelerate Lung Cancer Progression in Mice