Key moments, in order
There is no free lunch with receptors. No receptor can be flicked on or blocked with only benefits, because biology is held in homeostasis by feedback loops, and any change involves a trade-off.
Expect medication to reduce symptoms by about 30 to 40 percent. We are not curing OCD; we are reducing symptoms so patients can engage in therapy.
Do not mistake the medication for the treatment. The primary treatment is psychological and behavioral; medication reduces symptoms, and sometimes symptoms are so disabling that you need it to get people into ERP.
ERP comes first. Medication is for severe symptoms or a patient unwilling to do therapy.
Inference-based CBT identifies the incorrect thoughts that generate the obsession and the deeper assumptions and biases behind them.
Sertraline and escitalopram are the favorites, because they tend to have fewer medication interactions, though any SSRI is fine. Sertraline gives more room to titrate: four steps up to 100 mg and four to 200 mg, versus two steps to 10 mg and two to 20 mg.
Across studies it does not look more effective for OCD, yet when a patient with OCD has failed one or two SSRIs, we go to it anyway. Practice runs ahead of belief here.
With a partial response to the first SSRI, consider a supratherapeutic dose. If switching, fluvoxamine is the usual next step.
Some antipsychotics, especially the pines (clozapine, olanzapine), can worsen OCD or cause new OCD symptoms, more often than expected.
We do not use antipsychotic augmentation for primary anxiety: the evidence is insufficient (OCD aside). Clinicians reach for antipsychotic augmentation first because they are primed to.
It is the most serotonergic tricyclic. CYP1A2 breaks it down into norclomipramine, a secondary tricyclic that is less serotonergic.
It brings strong anticholinergic effects, QTc prolongation, heavy sedation and weight gain. Not necessarily the greatest choice, but if it is viable, you can consider it.
Fluvoxamine inhibits CYP1A2, so adding it raises the ratio of serotonergic clomipramine and, in theory, gives more of the serotonergic activity that is better for OCD.
Augmentation options: lamotrigine is reasonable, N-acetylcysteine is particularly good, especially with skin picking, and ondansetron may be one of the most effective add-ons.
Worth an add-on for almost any kind of neurotic illness: very low risk, within FDA limits, relatively well tolerated, without a lot of side effects.
Clomipramine and Luvox are still within the primary treatment arm. For augmentation, go from least harmful to most harmful.
Going by the available studies of NAC in OCD, we usually target 2.4 to 3 grams. We use the Now Foods 600 milligram capsules: start with two, then go up to 1,200 milligrams twice a day after a few weeks, once it is tolerated.
Other than smell and taste, it has few adverse effects. The main risk is allergy, as with any other medication.
For extremely severe OCD, such as patients basically stuck at home needing therapist home visits, implant treatments or vagal nerve stimulation come into consideration.
In bipolar disorder with OCD, avoid SSRIs whenever possible and use sleep support and a second-generation antipsychotic instead, though some people can tolerate an SSRI.
OCD proper pairs recurrent intrusive obsessions with a mental or physical compulsion that is not satisfying, or barely, needs a lot of repetition, and often takes at least an hour a day.
Most clinicians do not include personality nearly enough in their formulations, but overdoing it is its own failure mode.
Violent impulses rooted in personality tend to be ego-syntonic. Look further when there is distress or no clear link to secondary gain.
Each moment is a point made in the episode, linked to the second it was said. The topic links open everything the podcast has said on that topic.