How lithium helps prevent suicide: a patient’s experience
Lithium is one of the most effective anti-suicide medications psychiatrists have to treat patients with mood disorders. http://www.bmj.com/content/346/bmj.f3646
How it works is unknown. [i]
Recently, a patient of mine with recurrent major depression had increasingly intense suicidal ideation. She was already taking lurasidone (Latuda), escitalopram (Lexapro) 10 mg/day, and trazodone 50 mg at bedtime, but they weren’t helping. She reported she was “terrible…desperately depressed…I can’t get out of this dark place…I go to bed early to escape the day…It would be easier if I wasn’t here.” She told me she was thinking of overdosing several times a day.
I started her on lithium 300 mg/day and met with her two weeks later. She reported she had been feeling so unsafe she had asked a series of family members to stay with her.
One week after she started the lithium, she was at home with her sister, standing in her living room, next to her couch, watching golf on television, when “it felt like a switch flipped, and the suicidal thoughts left me. It felt like a weight had been lifted. I knew it immediately.”
“Before this, the suicidal thoughts had been constant: how can I do it (which pills can I take), when can I do it, where should I do it (should I got go a hotel, so no one has to find me in the house?). It was overwhelming and very scary.”
“I still have the depression, I’m still feeling sluggish and sad, but I don’t have the suicidal thoughts. Things don’t seem as catastrophic. Before, everything seems like a dead end, hopeless”.
In a post about the Research Domain Criteria (RDoC), Thomas Insel notes “that symptoms alone rarely indicate the best choice of treatment” and that “mental disorders are biological disorders involving brain circuits”. [ii]
In this case, a symptom (increasing suicidal ideation) suggested a treatment (lithium) that appeared to cause my patient’s suicidal ideation (and hopelessness) to turn off like a switch turning off an electrical circuit.
[i] UpToDate lists the following under mechanisms of action: “Traditionally thought to alter cation transport across cell membranes in nerve and muscle cells, influence the reuptake of serotonin and/or norepinephrine, and inhibit second messenger systems involving the phosphatidylinositol cycle (Ward, 1994). May also provide neuroprotective effects by increasing glutamate clearance, inhibiting apoptotic glycogen synthase kinase activity, increasing the levels of antiapoptotic protein Bcl-2 and, enhancing the expression of neurotropic factors, including brain-derived neurotrophic factor.”