Proco Products and Mental Health Medications: Interactions to Know Before You Combine Them

If you take a prescription medication for depression, anxiety, bipolar disorder, or another mental health condition, and you're also considering magnesium, omega-3, or one of our sleep or cognitive blends, this is worth ten minutes of your time before you combine them. Some of these interactions are minor and just mean "you might feel extra drowsy." A couple are worth a real conversation with the person who prescribes your medication.

This article is general education, not personalized medical advice. It cannot know your dose, your diagnosis, your other medications, or your health history — only your prescriber or pharmacist can weigh all of that together. Mental health medications in particular should never be started, stopped, or adjusted based on something you read online. If you're on one, the right move is to bring this list to your next appointment or call your pharmacist before adding anything new.

Why these interactions happen at all

Most of what follows falls into one of three buckets. First, additive sedation — two things that both make you drowsy, taken together, can make you more drowsy than either alone. This is the most common issue on this list and usually the least serious, but it matters if you drive or operate machinery. Second, changes to how your body processes a drug — a supplement that affects liver enzymes or a hormone system can raise or lower how much of your medication is actually active in your body. Third, and rarest, a supplement that competes for the same biological pathway as the medication, which is the category the L-tyrosine and MAOI concern below falls into.

None of this is a reason to be afraid of supplements. It's a reason to have one more conversation before you combine them.

SSRIs and SNRIs

SSRIs (like sertraline, escitalopram, fluoxetine) and SNRIs (like venlafaxine, duloxetine) are the most commonly prescribed class of mental health medication, so they're the one most Proco customers will actually be checking against. If you want the drugs themselves explained rather than just the interactions — what an SSRI does mechanically, what the efficacy evidence actually shows, and why published withdrawal estimates range from about 15% to 55% — that is in what SSRIs actually do. The main thing to know about is melatonin. The best-documented case is fluvoxamine, and the size of the effect is striking. In a controlled pharmacokinetic study, five healthy volunteers took 5mg of melatonin with and without 50mg of fluvoxamine; co-administration raised melatonin's total exposure roughly 17-fold and its peak blood concentration roughly 12-fold. That is a five-person study rather than a large trial, but the mechanism is clear — fluvoxamine strongly inhibits the liver enzyme that clears melatonin. Fluvoxamine is the outlier here; the other SSRIs and SNRIs are not established to do this to anything like the same degree. The broader additive-sedation concern is a pharmacological expectation rather than a measured interaction, and it is worth keeping in proportion: across 19 randomised trials in 1,683 people, melatonin's own effect on sleep was real but modest — about 7 minutes faster to fall asleep and 8 minutes more total sleep. This isn't a dangerous interaction, but it's a real one — if you're on an SSRI or SNRI and want to try melatonin (found in our Sleep Support and Sleep Formula blends), it's worth starting at a lower intake and asking your prescriber or pharmacist whether your specific medication is one that tends to interact.

Magnesium and omega-3 don't have documented direct interactions with SSRIs or SNRIs. Omega-3's main interaction concern is with blood-thinning medications, covered briefly below.

MAOIs and L-tyrosine

Monoamine oxidase inhibitors (phenelzine, tranylcypromine, isocarboxazid, and the selegiline patch) are prescribed less often today than they used to be, but if you're on one, this is the item on this page worth clearing with your prescriber before you start anything: L-tyrosine, an amino acid in our Cognitive Support blend.

Tyrosine is the direct precursor your body uses to build dopamine and norepinephrine. MAOIs work by blocking the enzyme that normally breaks those neurotransmitters down. Put the two together and you can end up with more dopamine and norepinephrine activity than your body is used to regulating — the same basic mechanism behind the well-known tyramine/MAOI food interaction, just via a different amino acid. The published human evidence here is thinner than the interaction databases suggest, and it is worth stating plainly rather than hiding behind a severity rating. The only documented report of supplemental tyrosine given alongside an MAOI is a 2024 case in the European Journal of Clinical Nutrition: a 67-year-old woman on the transdermal selegiline patch received parenteral nutrition containing tyrosine, was monitored closely for hypertensive crisis, and tolerated the combination without incident. Those authors describe a tyramine pressor response from tyrosine as a theoretical possibility rather than an established one, and their recommendation is to introduce it gradually with monitoring rather than avoid it. So the mechanism is real and the caution is standard, but the direct human evidence is one patient who was fine. What that means in practice: if you're on an MAOI, don't start L-tyrosine or Cognitive Support without clearing it with your prescriber first, and know the warning signs of a hypertensive reaction — severe headache, visual changes, chest pain, unexplained nausea. What we shouldn't have told you, and previously did, is that this is a documented major interaction with a settled answer.

Benzodiazepines and other calming medications

Benzodiazepines (like alprazolam, lorazepam, clonazepam) and related sedative-hypnotics are prescribed for anxiety and sleep, and the concern here is additive sedation from several of our ingredients at once.

Valerian has the clearest mechanism. Laboratory work shows valerian extracts act at the GABA_A receptor's benzodiazepine binding site — the same site alprazolam and lorazepam act on — although the effect is biphasic, enhancing binding at low concentrations and inhibiting it at higher ones. That shared target is the reason for caution, and it is worth being clear that it is a mechanistic concern rather than a measured clinical interaction. Valerian's own sedative effect in people is in fact modest: in a head-to-head trial against midazolam before third-molar surgery, valerian produced less drowsiness than the benzodiazepine, and a meta-analysis of 18 randomised placebo-controlled trials found valerian improved sleep quality subjectively while having no measurable effect on how long people took to fall asleep. Ashwagandha carries a similar mechanistic caution — its botanical name, Withania somnifera, literally translates to "sleep-inducer," and rodent work attributes its sleep-promoting effect to GABA_A and GABA_B receptor activity, again overlapping with where benzodiazepines act. Melatonin, as noted above, is the same kind of expectation rather than a documented interaction.

GABA is a slightly different story, and worth being honest about: the research on GABA supplements and medication interactions is genuinely incomplete, and — as we've written about separately — how much orally supplemented GABA actually reaches GABA receptors in the brain (the same receptors benzodiazepines act on) is a real open question, not a settled one. That doesn't mean assume it's automatically safe to combine with a benzodiazepine; it means the evidence to reassure you either way just isn't there yet, so it belongs in the same "ask first" conversation as everything else here. See our piece on what oral GABA supplements can and can't do for more on that.

None of this means these ingredients are off-limits if you're on a benzodiazepine — plenty of people manage both. It means the sensible order of operations is: ask your prescriber, start with one new thing at a time, and pay attention to how sedated you feel, especially before driving.

Lithium

Lithium has one of the narrowest therapeutic windows of any commonly prescribed psychiatric medication — the gap between an effective blood level and a toxic one is small, and lithium levels are sensitive to hydration, sodium balance, and kidney function. That's the context worth knowing if you're on lithium and considering magnesium. We could not find a confirmed direct pharmacological interaction between oral magnesium and lithium — not in the primary literature, and not in the NIH Office of Dietary Supplements' professional fact sheet on magnesium, which is where the interactions magnesium does have are catalogued; we go through those in our own piece on how magnesium interacts with medications. But because lithium's safety margin depends so heavily on your fluid and electrolyte status, and because higher doses of magnesium can cause loose stools or diarrhea in some people, meaningful fluid loss from any cause is a legitimate reason to loop in whoever monitors your lithium levels — not because magnesium itself is dangerous, but because anything that changes your hydration is relevant when you're on a drug this dose-sensitive.

If ashwagandha is also part of the picture, there's a second, unrelated reason to mention it to your care team: lithium itself is well known to affect thyroid function over time, and ashwagandha raises thyroid hormone levels in people. That second half is not theoretical. In an eight-week randomised, double-blind, placebo-controlled trial in 50 adults with subclinical hypothyroidism, 600mg of ashwagandha root extract daily significantly raised T3 and T4 and lowered TSH compared with placebo. That trial treated the effect as a benefit — and for those patients it was — but it is the same effect that becomes a complication if your thyroid is already being watched for another reason. A separate placebo-controlled study in bipolar disorder picked up the same direction of change in the handful of participants who had thyroid bloods taken, and there are published case reports of ashwagandha-associated thyrotoxicosis. Neither drug nor herb is dangerous here on its own, but if you're on lithium and someone is already monitoring your thyroid, raise ashwagandha at your next check rather than after.

Other mood stabilizers

For anticonvulsant-type mood stabilizers such as valproate/valproic acid and lamotrigine, two of our ingredients are worth raising with your prescriber — one for a shared liver risk, one for shared drowsiness. Ashwagandha and valproate share a rare but genuinely documented liver risk. For ashwagandha that is not hypothetical: a case series drawn from Iceland and the US Drug-Induced Liver Injury Network described five patients who developed jaundice, nausea, lethargy and prolonged itching two to twelve weeks after starting ashwagandha-containing supplements, with cholestatic or mixed liver injury that resolved over one to five months and no liver failure; further case series have been published since. Valproate's own potential for liver injury is long established and is why it carries a boxed warning. Combining two things that each carry that risk is usually a reason to monitor rather than avoid outright — but it is a real reason to tell whoever prescribes the valproate. Valerian and lamotrigine comes down to the additive-sedation point described above, and not much else. An earlier version of this article also said there was early laboratory evidence that valerian may affect an enzyme pathway involved in clearing lamotrigine. We have removed that, because it does not survive checking. The laboratory finding is that valerian root extracts inhibit CYP3A4 and P-glycoprotein in a test tube — but when valerian was given to twelve healthy volunteers for 28 days and their CYP1A2, CYP2D6, CYP2E1 and CYP3A4/5 activity was measured directly, there was no significant change. And lamotrigine is not cleared by CYP3A4 in the first place: it is cleared by glucuronidation via UGT1A4, which that laboratory work did not test. The sedation overlap is still worth mentioning to your prescriber. The enzyme story was not ours to pass on.

A quick note on omega-3 and blood thinners

This isn't a mental-health-medication interaction, but it comes up often enough for people managing both a mood disorder and cardiovascular health that it's worth a mention: high-dose omega-3/fish oil can have a mild antiplatelet effect, and periodic monitoring is reasonable if you're on an anticoagulant. We've covered this in detail separately rather than duplicate it here — see does fish oil interact with blood thinners.

Bacopa and the Cognitive Support blend

Bacopa monnieri, the other standout ingredient in our Cognitive Support blend alongside L-tyrosine, has two preliminary findings worth flagging honestly rather than ignoring. In mice, bacopa extract raised T4 by around 41% — the same direction as the ashwagandha effect above, though this is an animal study at a dose that does not translate directly to a human capsule. And in a laboratory assay using human enzymes, standardised bacopa extract inhibited CYP2C19, CYP2C9, CYP1A2 and CYP3A4; the authors noted that the relevant concentrations are plausible in the gut rather than the liver, which is where an orally taken extract is most concentrated. Several psychiatric medications are cleared by those enzymes. Neither finding has been tested in people taking both, so this is not cause for alarm — but if you're on an antipsychotic or another medication sensitive to enzyme activity, mention bacopa to your prescriber before adding it.

Bottom line

Supplements aren't inert just because they're sold over the counter, and mental health medications aren't a category to guess around. If you take an SSRI, SNRI, MAOI, benzodiazepine, lithium, or another mood stabilizer, the safest way to add any supplement — ours or anyone else's — is to tell your prescriber or pharmacist what you're taking and let them check it against your specific medication, dose, and health history. Never stop, skip, or reduce a prescribed mental health medication based on anything in this article or anywhere else online.

This article is for informational purposes only and has not been evaluated by the FDA. It is not intended to diagnose, treat, cure, or prevent any disease. It is not a substitute for advice from your doctor or pharmacist, especially regarding any medication you take for a mental health condition — never stop or change a prescribed medication without talking to the prescriber first.

References

Primary literature where it exists, plus government fact sheets. Consumer drug-interaction databases were removed in September 2026 and are not cited here.

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20. CDC/NCHS Data Brief No. 377 — Antidepressant Use Among Adults: United States, 2015–2018.
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22. NIH Office of Dietary Supplements — Omega-3 Fatty Acids: Fact Sheet for Health Professionals.

Related reading: Can supplements help with anxiety and low mood? and Is it safe to take multiple Proco products together?.

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