Key moments, in order
GAD is a terrible diagnosis the way the community uses it, but there is something real there. It is its own disorder in a sense, and tighter criteria would capture a smaller proportion of the population.
For anxiety, psychological treatment is fundamentally the most important part for the vast majority of patients. The risk is that patients take high-dose medication, get good enough, and never do it.
Anxiety is a form of activation, a higher level of psychological energy. Suppress it entirely, as a benzodiazepine does, and you slow or stop motivation itself.
You have to know your algorithm. If you do not, you will not know when to deviate, and you will not have it in your head ready to use.
Mild anxiety can forgo treatment entirely.
The same risk carries more weight when the condition you are treating is less serious, or less responsive to that medication. That part often gets lost in the conversation.
Do not assume a patient remembers the side effects and problems, even with a medication they have taken before. Go over them again.
Several CYP enzymes metabolize sertraline, while escitalopram is broken down by 3A4 and 2C19, and 2C19 has a lot of variants. Ultra-slow and ultra-fast metabolizers have a really bad response to escitalopram more often than to sertraline.
Both are fine choices partly because they have relatively fewer interactions. Even in a young patient, you never know if another medication will be needed for a new medical condition down the line.
A basic start: sertraline 25 mg for a week, then 50 mg, stay there for a month, then judge the effect.
PRNs are not a good treatment plan. In the vast majority of cases a PRN adds a safety signal and forces that safety signal to be a medication.
The important teaching point in getting better from anxiety is learning to trust that you will be okay and that you can handle something. A PRN reduces that lesson.
Without a PRN, people develop other coping skills: going outside for a bit, a breathing practice.
Get used to accepting suffering. There is a minimum level of suffering and anxiety you have to live with, and if you accept it, you will not make it worse.
Do not underdose it. It is often written off because it was never adequately dosed. Titrate fairly aggressively and do not be afraid to take it to the max, but do not expect the moon and the stars: it gives a modest benefit. We have seen it work better at the higher dose range.
The starting dose is 30 mg a day, divided: at minimum 15 in the morning and 15 at night. The 7.5 mg tablet is deceptive; that is for titrating once you are already at the starting dose. Loading most of the dose at night is fine if tolerated.
Tell anxious patients that medication will not remove all anxiety, and that if it does something has gone wrong. Some anxiety is normal, and personality will not change with medication.
Anxious patients, especially with somatic tendencies, may react to medication with anxiety, a nocebo reaction that can make a drug fail. Head it off by explaining timing and what to expect.
The lowest-risk anxious patient for habituation is the medication hater: strong placebo effects and a negative emotional relationship with medications.
We do not do the classic benzodiazepine bridge for the first couple of weeks of an SSRI. If a patient really needs a PRN, use gabapentin or hydroxyzine.
We do not find SNRIs more effective than SSRIs (at most a very marginal improvement) and they have slightly more side effects, even if just duloxetine's slight blood pressure rise. Many patients have a really tough time getting off them, and venlafaxine's withdrawal is strong and uncomfortable enough that we avoid it entirely.
Another view: do not use it at all unless the patient is already on it, because the withdrawal is so bad. An elderly woman once came in with what was basically delirium, and it turned out to be Effexor withdrawal.
Use an SNRI first line only when a comorbidity gives it a second job: a diagnosed migraine disorder or chronic pain with a good medical explanation that is not adequately treated, or fibromyalgia. Then you might as well use a dual-use medication. In some cases true ADHD counts, but not apparent ADHD. They may also be a little better for hot flashes.
For anxiety, the studies needed much higher doses than the 100 or 300 mg people are usually on. It is more effective at about 900 to 3,600 mg a day, and because absorption is nonlinear, much less is absorbed at the higher doses than the number suggests.
Cap a single dose at about 1,200 mg and split anything more into a separate dose. We do not give a lot of gabapentin for anxiety disorders, but we are not opposed to it.
At high doses you are getting into broad suppression of neurons, so habituation is possible, though we have not seen it in our patients.
It has more evidence in anxiety than gabapentin. The usual thinking is that gabapentin may be a little more tolerable, with less abuse risk.
It is too effective: the speed and amount of its absorption are enough to make it possibly habit-forming, which also means a higher risk of withdrawal effects.
We will hand it out because it is low risk, and some people just seem to like it. The main dividing line is how sedated they get.
Pamoate versus hydrochloride: one of us pays zero attention to it, has seen no difference in practice, and found no evidence of one.
For anxiety, look for evidence that the fight-or-flight system is upregulated before using it. We do use it for trauma disorders, and certainly for akathisia, because it is low risk and effective.
For performance anxiety, 20 to 40 mg about an hour before the performance or other anxiety-provoking situation. It suppresses the autonomic response.
Explain that it treats the perception of physical arousal as a threat. If you can learn to read that arousal as non-threatening, or even as excitement, you can modulate your body's response yourself, but that takes practice, not one night.
The usual order: an SSRI, then another SSRI, then augmenting with buspirone or gabapentin. If they are still unresponsive, go by patient characteristics, such as mirtazapine for a lot of sleep trouble.
Vilazodone and vortioxetine are the two medications we have seen marketed as having slightly lower sexual side effects.
For a primary anxiety disorder not responding to SSRIs and SNRIs, tricyclics are the traditional answer.
Imipramine is the classic pick only because it was the most researched back in the day. Really, use whatever tricyclic is tolerated; nortriptyline is one of the classically better tolerated ones.
It helps anxiety that is part of the depression and is great for depression with anxious features. When anxiety is the predominant problem we tend to avoid it: in our opinion it does not help anxiety on its own and worsens generalized anxiety disorder long term.
Do not treat by algorithm alone. Any of these agents, including SSRIs and bupropion, can cause agitation in some people without bipolar disorder, and if someone gets worse, use buspirone, gabapentin or psychotherapy.
The patch is absorbed systemically, not through the gut, so in theory there is much less risk of a hypertensive reaction to tyramine-containing foods. We think following the diet is still recommended.
We hate anything that causes withdrawal and physical dependence when there are other options, but that is not 'never'. Be practical: consider what is reasonable for the patient's values, goals and functioning.
With longstanding benzodiazepines we may have iatrogenically caused physiological change that is permanent, and some patients just have to stay on them.
A recent big study showed higher mortality in patients who discontinued long-term benzodiazepines. The risks of tapering are genuine and need to be considered.
Before starting one, spell it out: a controlled substance that causes addiction, withdrawal, executive function and memory problems and sedation, and probably slows progress in psychotherapy. And if you change doctors, the next one may not continue it.
If you do use one for an anxiety disorder, make it a standing medication, not a PRN, and avoid the short-acting ones, which make addictive behavior more likely. Clonazepam or diazepam.
The goal of medication is to improve function and prevent decompensation, not to obliterate anxiety. Titrate by function and activities, not by the patient's reported feelings of anxiety.
Take the request not as manipulation but as coming from an innocent person who heard Xanax helps anxiety, and calmly lay out why it will not help long term and why you will not go that route.
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.
A very interesting choice now, and there are studies of lavender in anxiety. As far as we know it is only sold over the counter, with no insurance-covered prescription version.
Start with one pill for a week, then move up to two (we think that is about 160 milligrams). Almost everyone says it really helped.
For the effect size we perceive as clinicians, we can get patients somewhere similar with buspirone (BuSpar), so we are not huge fans.
Generalized anxiety disorder: grade A, almost a requirement to teach, and a standalone treatment. If a patient can tolerate and engage with it, it is a fast track to managing anxiety long term, with CBT the next option if it is not working.
Three necessary and sufficient parts: deliberate attention (on purpose), to the present moment (the ongoing now, not the past, the future or what should be), without judgment. And it is a practice, something you actively do.
For medication management, first assess fully for other physiological and medical causes, especially substances.
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.