this is completely news for me, but there is an arachidonic acid hypothesis of bipolar and depression:
Mood-Stabilizers Target the Brain Arachidonic Acid Cascade
Bipolar disorder (BD) is a severe psychiatric illness characterized by recurrent manic and depressive episodes, without a characteristic neuropathology or clear etiology. Drugs effective in BD target many key signaling pathways in animal and cell studies. However, their mode of action in the BD brain remains elusive. In the rat brain, some of the mood stabilizers effective in treating mania (lithium, carbamazepine, valproate) or depression (lamotrigine) in BD are reported to decrease transcription of cytosolic phospholipase A2 and cyclooxygenase-2 and to reduce levels of AP-2 and NF-κB, transcription factors of the two enzymes. The anti-manic drugs also decrease arachidonic acid (AA) turnover in brain phospholipids when given chronically to rats. Thus, drugs effective in BD commonly target AA cascade kinetics as well as AA cascade enzymes and their transcription factors in the rat brain. These studies suggest that BD is associated with increased AA signaling in the brain. Developing therapeutic agents that suppress brain AA signaling could lead to additional treatments for BD. In this review, we discuss the mechanisms of action of mood stabilizers and the effects of docosahexaenoic acid on AA cascade enzymes in relation to BD.
https://www.ncbi.nlm...les/PMC2825027/
furthermore:
NSAID induced hypomania in stable bipolar disorder
Some case reports have proposed the antidepressant role of the non-steroidal anti- inflammatory drugs. These effects might reflect the activation syndrome[1] induced by these agents.
We describe three patients of bipolar mood disorder currently in remission as per the DSM-IV criterion who were on treatment with mood stabilizers (lithium carbonate/sodium valproate). Patients experienced pain due to neuromuscular conditions and were advised treatment with NSAIDs (nimesulide/etoricoxib/celecoxib). While on treatment, they developed symptoms of hypomania. The symptoms were seen within 3 days of the administration of the agent and remitted when the NSAIDs were stopped. Symptoms reappeared with the drug rechallenge and disappeared within 2 days of drug discontinuation. All patients stabilized after that and did not restart the NSAID.
https://www.ncbi.nlm...les/PMC3512378/
amazingly, even low dose aspirin is effective:
The AA hypothesis for mood stabilizer action is consistent with reports that low-dose aspirin reduced morbidity in patients taking lithium, and that high n-3 and/or low n-6 polyunsaturated fatty acid diets, which in rats reduce brain AA metabolism, were effective in BD and migraine patients.
https://www.ncbi.nlm...pubmed/24786695
I personally never noticed any effects from aspirin or NSAIDs, but benefited from low dose Li. Now I know Li is COX2 inhibitor!