The Other Agents: Atypical, Repurposed, and Non-Classical Psychiatric Drugs

A high-level examination of bupropion, mirtazapine, trazodone, the MAOIs, and the growing list of non-psychiatric drugs — anti-inflammatories, antibiotics, anti-diabetics, hormones, and others — with real or emerging psychiatric uses

What This Document Covers, and Why It Matters

The preceding documents in this pharmacology series carve psychiatry's drugs into mechanistic families — serotonergic, glutamatergic, GABAergic, dopaminergic, and so on. But two large groups of clinically important agents fall outside those neat boundaries, and they are the subject here.

The first group is the atypical antidepressants — bupropion, mirtazapine, trazodone, and the MAOIs — drugs that are unambiguously psychiatric and genuinely useful, but that do not fit the SSRI/SNRI mold because they work through different mechanisms (dopaminergic-noradrenergic, receptor antagonism, broad enzyme inhibition). They are arguably the most underused effective antidepressants precisely because they are not the default class.

The second group is far more interesting theoretically and increasingly important clinically: drugs that are not classically psychiatric at all — anti-inflammatories and immune-modulators (including TNF-alpha inhibitors), antibiotics (minocycline, D-cycloserine), anti-diabetic and metabolic agents, hormones (thyroid, estrogen, testosterone, the neurosteroids), anti-inflammatory analgesics, and others — that have demonstrated or plausible psychiatric effects. This group matters for two reasons. First, practically: some are genuinely useful, off-label or emerging, for real patients now. Second, and more profoundly, theoretically: these drugs are windows into the biology of psychiatric illness. If a TNF-alpha inhibitor lifts depression in inflamed patients, that tells us something about what depression is in those patients — that the "chemical imbalance" framing was never the whole story, that immune, metabolic, and endocrine systems are woven into mood and cognition, and that the neurotransmitter-centric model of psychiatric pharmacology is incomplete. The repurposed drugs are not just alternative treatments; they are clues to the etiology the monoamine drugs never explained.

The honest framing throughout: the atypical antidepressants are effective, underused, and worth knowing well; the non-classical agents range from genuinely-useful-now (thyroid augmentation, the neurosteroids) through promising-but-unproven (anti-inflammatories in inflamed subgroups, NAC) to overhyped-and-thin (much of the antibiotic and metabolic-drug literature) — and their greatest value may be conceptual, as evidence that psychiatry's biology is broader than its drug classes suggest.

Bupropion: The Dopaminergic-Noradrenergic Antidepressant

What it is. Bupropion (Wellbutrin, and as Zyban for smoking cessation) is an antidepressant that acts on dopamine and norepinephrine rather than serotonin — a norepinephrine-dopamine reuptake inhibitor (NDRI), the mechanistic mirror image of the SSRIs. (Its precise pharmacology is more complex — relatively weak reuptake inhibition plus action on the dopamine and norepinephrine systems and nicotinic receptor antagonism — but the practical point is that it is the major non-serotonergic antidepressant.)

What it does, and why it matters clinically. Bupropion is comparably effective to SSRIs for major depression, but its non-serotonergic mechanism gives it a distinctive and valuable profile defined largely by what it lacks:

• No (or minimal) sexual dysfunction — the SSRI burden it most conspicuously avoids, making it a first choice for patients for whom sexual side effects are unacceptable, and a common add-on to SSRIs specifically to counter SSRI-induced sexual dysfunction.
• No weight gain (often weight-neutral or modestly anorexic) — another contrast with the SSRIs and mirtazapine.
• Activating rather than sedating — energizing, often helpful for the anergic, anhedonic, hypersomnic, "atypical" depressed patient, and for the fatigue and concentration problems depression brings.
• Smoking cessation — a genuine, separate indication (the nicotinic and dopaminergic actions reducing craving and withdrawal), useful given how often depression and smoking co-occur.
• ADHD (off-label) — the dopaminergic/noradrenergic mechanism gives it modest ADHD efficacy, useful in comorbid depression-plus-ADHD.

The problems. Bupropion's activating profile is double-edged: it can worsen anxiety, agitation, and insomnia, making it a poor choice for prominently anxious patients (a real limitation given how often depression and anxiety coexist). Its signature serious risk is a dose-dependent lowering of the seizure threshold — contraindicated in seizure disorders, in eating disorders (bulimia/anorexia, where electrolyte disturbance compounds the risk), and in conditions predisposing to seizures. It does little for anxiety disorders or OCD (the serotonergic territory). The honest summary: an effective, distinctively-profiled antidepressant whose dopaminergic-noradrenergic mechanism makes it the natural choice when sexual side effects, weight, sedation, or comorbid smoking/ADHD matter — and a poor choice when anxiety dominates or seizure risk is present.

Mirtazapine: Antidepressant by Receptor Blockade

What it is. Mirtazapine (Remeron) is a noradrenergic and specific serotonergic antidepressant (NaSSA) that raises monoamine transmission by a mechanism opposite to the reuptake inhibitors: instead of blocking transporters, it blocks inhibitory receptors. It antagonizes presynaptic α2-adrenergic autoreceptors and heteroreceptors (releasing the brake on norepinephrine and serotonin release) and blocks postsynaptic 5-HT2A, 5-HT2C, and 5-HT3 receptors (so the increased serotonin is steered toward 5-HT1A while the receptors mediating SSRI side effects — anxiety/insomnia via 5-HT2A, sexual dysfunction via 5-HT2, nausea via 5-HT3 — are blocked). It is also a potent histamine H1 antagonist, which drives its prominent sedation and appetite effects.

What it does, and its distinctive niche. Mirtazapine is an effective antidepressant whose receptor profile gives it a profile almost photo-negative to the SSRIs, and a clear niche:

• Strongly sedating and appetite-stimulating (the H1 blockade) — making it valuable for depressed patients with prominent insomnia and weight loss/poor appetite, where these "side effects" become therapeutic. It is frequently chosen for the depressed patient who cannot sleep and is not eating, and used (off-label) for sleep and for appetite stimulation in medical/geriatric/oncology settings.
• Low sexual dysfunction and low GI/nausea (the 5-HT2 and 5-HT3 blockade) — another contrast with the SSRIs, and a reason it is added to SSRIs both to counter sexual side effects and to augment efficacy (the "California rocket fuel" combination of an SNRI plus mirtazapine, exploiting complementary mechanisms).
• Fast-ish onset of the sleep/appetite benefits and a generally favorable tolerability for the right patient.

The problems. The same H1 blockade that helps sleep and appetite causes sedation and weight gain — unwelcome in patients for whom these are not desired, and the weight/metabolic effect is a real long-term concern. Daytime grogginess, and (paradoxically) more sedation at low doses than high (because at low doses the antihistamine effect dominates before the noradrenergic activation kicks in — a useful clinical pearl). Rare agranulocytosis. The honest summary: an effective antidepressant whose receptor-antagonist mechanism makes it the natural choice for the depressed patient with insomnia, poor appetite, and intolerance of SSRI sexual/GI effects — and a poor choice when sedation and weight gain are unwanted. Like bupropion, it illustrates that "serotonergic antidepressant" need not mean reuptake inhibition.

Trazodone, the MAOIs, and Other Atypical Antidepressants

Trazodone is a serotonin antagonist and reuptake inhibitor (SARI) — it blocks the serotonin transporter and antagonizes 5-HT2A receptors, plus potent H1 and α1 antagonism. At antidepressant doses it is effective but sedating and now rarely used as a primary antidepressant; its overwhelming real-world use is off-label, low-dose, as a hypnotic — among the most prescribed sleep medications precisely because it promotes sleep without the dependence of benzodiazepines/Z-drugs (the sedation comes from H1 and 5-HT2A blockade, non-addictive). Its specific hazards: orthostatic hypotension (α1 blockade), and the rare but classic priapism (also α1-mediated). Nefazodone, a relative, fell out of use over hepatotoxicity.

The MAOIs (monoamine oxidase inhibitors) — phenelzine, tranylcypromine, isocarboxazid, and the selective/reversible selegiline (transdermal) and moclobemide — are the oldest antidepressant class and, by some assessments, among the most effective, particularly for atypical depression (with mood reactivity, hypersomnia, hyperphagia, rejection sensitivity) and treatment-resistant depression. They inhibit monoamine oxidase, raising serotonin, norepinephrine, and dopamine broadly. They have been driven to near-obsolescence not by inefficacy but by their dietary and drug interactions: the tyramine reaction (hypertensive crisis from aged/fermented foods, requiring dietary restriction) and dangerous serotonin syndrome with serotonergic drugs (a long washout required when switching). The transdermal selegiline patch (which bypasses gut MAO at low doses, relaxing dietary restrictions) and the reversible moclobemide reduce these risks. The MAOIs are a cautionary tale of a highly effective class abandoned for interaction-management burden rather than efficacy — and an option worth remembering for the genuinely treatment-resistant patient, in expert hands.

Other notable atypicals: agomelatine (a melatonergic MT1/MT2 agonist and 5-HT2C antagonist, available in Europe — a genuinely novel mechanism targeting circadian disruption in depression, limited by hepatotoxicity monitoring); vortioxetine and vilazodone (covered in the serotonergic document); tianeptine (an atypical agent, glutamatergic/opioid actions, with a serious emerging abuse/dependence problem via its mu-opioid agonism — "gas station heroin" — a cautionary case); and esketamine and the neurosteroids (covered in the glutamatergic/rapid-acting document).

The Conceptual Pivot: Why Non-Psychiatric Drugs Have Psychiatric Effects

Before cataloguing the repurposed drugs, the theoretical frame that makes them coherent. The monoamine model of psychiatric illness — too little serotonin, too much dopamine — was always incomplete (see the serotonergic document's account of its collapse). The drugs in the rest of this document work because psychiatric illness, especially depression, is increasingly understood as involving systems the neurotransmitter model ignored:

• The immune-inflammatory system. A large body of evidence links depression (in a subset of patients) to chronic low-grade inflammation — elevated inflammatory cytokines (IL-6, TNF-alpha, CRP), the observation that inducing inflammation (interferon therapy, vaccines, endotoxin) reliably produces depressive symptoms ("sickness behavior"), and that inflammation is elevated in treatment-resistant and atypical depression. This is the inflammatory hypothesis of depression, and it predicts that anti-inflammatory drugs should help — in inflamed patients.
• The metabolic system. The tight, bidirectional links between depression and metabolic dysfunction (diabetes, insulin resistance, obesity), and the shared inflammatory and mitochondrial substrates, suggest metabolic drugs might have mood effects.
• The endocrine system. Thyroid, gonadal, and stress (cortisol/HPA-axis) hormones profoundly influence mood and cognition — hypothyroidism mimics depression, the perimenopause and postpartum periods are windows of mood vulnerability, and the neurosteroids (covered elsewhere) are a proven endocrine-psychiatric link.
• The microbiome-gut-brain axis and oxidative stress — further systems implicated, with their own candidate drugs.

The repurposed drugs, in other words, are predicted by a broader, systems-level model of psychiatric illness in which immune, metabolic, and endocrine dysfunction contribute — and their successes and failures are tests of that model. The crucial recurring theme: these drugs tend to work, when they work, in biologically-defined subgroups (the inflamed, the metabolically dysfunctional, the hormonally deficient), not in unselected patients — which is both why the trials are often negative in general populations and why they point toward a more stratified, biomarker-guided psychiatry than the one-size monoamine era allowed.

The Anti-Inflammatory and Immune-Modulating Agents

The rationale (above): if inflammation contributes to depression in a subset, anti-inflammatories should help that subset.

TNF-alpha inhibitors. The most theoretically striking case. TNF-alpha is a key inflammatory cytokine, and its inhibitors (infliximab, etanercept, adalimumab) are established treatments for autoimmune disease. The landmark psychiatric finding (Raison and Miller): a trial of infliximab in treatment-resistant depression was negative overall — but in the subgroup with high baseline inflammation (elevated CRP), infliximab produced significant antidepressant effects, while in low-inflammation patients it did nothing (or slightly worsened mood). This is a paradigmatic result: it both supports the inflammatory hypothesis and demonstrates that the effect is restricted to the inflamed subgroup — a proof of concept for biomarker-stratified psychiatry. Patients with autoimmune diseases treated with TNF-alpha inhibitors also frequently report mood improvement, though disentangling this from relief of the underlying disease is difficult. The honest status: a genuinely important conceptual finding, not (yet) a treatment — TNF-alpha inhibitors are expensive, immunosuppressive, and not used for depression in practice, but they validated the inflamed-subgroup model that drives the whole field.

NSAIDs and cytokine inhibitors. Celecoxib (a COX-2 inhibitor) and other NSAIDs have been tested as antidepressant adjuncts with mixed-but-suggestive results, again strongest in inflamed patients; concerns about cardiovascular and GI risks and about NSAIDs possibly interfering with SSRI efficacy temper enthusiasm. Other cytokine-targeted approaches are in investigation.

Minocycline. This antibiotic (below) is also a potent anti-inflammatory and microglial inhibitor, and most of its psychiatric interest is on that basis rather than its antibacterial action.

The honest assessment of the anti-inflammatory approach: a strong, important theoretical advance — inflammation is genuinely part of the picture for some patients — with real but subgroup-restricted evidence, and no anti-inflammatory yet established as a routine psychiatric treatment. Its value is currently more as proof that depression is biologically heterogeneous and that a stratified, biomarker-guided approach is the future, than as a present prescription.

The Antibiotics

Several antibiotics have psychiatric interest, and the reasons differ instructively:

Minocycline. A tetracycline antibiotic that crosses the blood-brain barrier and has anti-inflammatory, antioxidant, neuroprotective, and microglia-inhibiting properties largely independent of its antibacterial action. It has been investigated as an adjunct in depression (signals in inflamed patients, paralleling the anti-inflammatory story), schizophrenia (mixed results, on the microglial/neuroinflammation rationale and possible negative-symptom benefit), and bipolar and OCD — a genuinely interesting repurposing candidate whose psychiatric mechanism is its anti-inflammatory, not antibiotic, action. Evidence is promising-but-inconsistent; not established.

D-cycloserine. An old tuberculosis antibiotic that happens to be a partial agonist at the NMDA-receptor glycine site — and thus a glutamatergic drug (relevant to the glutamatergic document). Its psychiatric use is mechanistically elegant: because NMDA-receptor activity is required for the learning that underlies extinction, D-cycloserine has been used as an augmenter of exposure therapy — given before exposure sessions to enhance the consolidation of fear extinction learning in anxiety disorders, OCD, and PTSD. The idea (a beautiful marriage of pharmacology and psychotherapy) is to make CBT work better by pharmacologically strengthening the new learning it depends on. Results have been mixed — early enthusiasm, then trials showing the effect is inconsistent and timing-dependent (it may enhance successful exposures and worsen unsuccessful ones, by strengthening whatever was learned) — but it remains a fascinating proof of concept for pharmacologically augmenting psychotherapy, a frontier that connects this whole pharmacology series back to the psychotherapy series.

The broader antibiotic story (microbiome). Beyond specific drugs, the gut-brain axis and the influence of the microbiome on mood and behavior have driven interest in antibiotics, probiotics ("psychobiotics"), and fecal transplantation — an active research area, mostly preclinical and early-clinical, where the psychiatric effects of altering gut flora are real in animals and suggestive but unproven in humans. The honest status: a genuinely interesting frontier, heavy on hype and preliminary data, light on established treatments.

Metabolic, Hormonal, and Other Repurposed Agents

Anti-diabetic and metabolic drugs. On the metabolic-dysfunction hypothesis (above): metformin (for metabolic and possible mood/cognitive effects, and importantly for mitigating antipsychotic-induced weight gain — an established adjunct use), pioglitazone (a PPAR-gamma agonist with anti-inflammatory and insulin-sensitizing actions, tested as a depression adjunct with subgroup signals), and — of major current interest — the GLP-1 receptor agonists (semaglutide and relatives), whose dramatic metabolic effects, anti-inflammatory actions, and central reward-system effects have generated intense investigation into possible benefits for addiction (reducing craving for alcohol, nicotine, and other substances — a genuinely promising signal), mood, and cognition, alongside attention to possible psychiatric risks (the question of whether they affect mood or suicidality has been raised and is under active study). The GLP-1 agonists are the most-watched metabolic-psychiatric story of the moment, plausible on multiple mechanisms, with real early signals especially in addiction and as-yet-unsettled risk questions.

Thyroid hormone. The most established endocrine-psychiatric use: T3 (liothyronine) augmentation of antidepressants in treatment-resistant depression is a long-standing, evidence-supported (if modest) strategy (a STAR*D augmentation arm), and levothyroxine treats the depression of hypothyroidism (and is used adjunctively, sometimes at supraphysiologic doses, in bipolar). Thyroid-mood links are real and clinically actionable — every depressed patient warrants thyroid screening.

Gonadal hormones. Estrogen has mood effects relevant to perimenopausal depression (and is used adjunctively); testosterone has been investigated for depression in hypogonadal men; the neurosteroids (brexanolone, zuranolone) are the proven case of an endocrine-psychiatric drug (covered in the glutamatergic/rapid-acting document). Hormonal contributions to mood — postpartum, perimenopausal, premenstrual (PMDD) — are a major, real, and sometimes under-addressed dimension.

N-acetylcysteine (NAC). An over-the-counter antioxidant and glutamate-modulator (and mucolytic/acetaminophen-overdose antidote) with a surprisingly broad psychiatric investigation — OCD and related disorders (trichotillomania, skin-picking, where it has some of its best evidence), addiction (craving), bipolar depression, and schizophrenia — on antioxidant and glutamatergic rationales. Evidence is mixed and mostly modest, but its safety and availability make it a common adjunct; a reasonable low-risk add-on with realistic (modest) expectations.

Anti-inflammatory nutraceuticals and others. Omega-3 fatty acids (EPA-predominant, modest antidepressant adjunct evidence, again possibly inflammation-mediated), and a long list of investigational agents (statins for their anti-inflammatory effects, allopurinol, celecoxib as above) round out the repurposing landscape — collectively more promising as a research direction than as established treatments.

Anti-craving and addiction agents that cross categories: naltrexone (opioid antagonist — alcohol and opioid use disorder, and low-dose naltrexone's contested off-label uses), acamprosate (glutamatergic/GABAergic — alcohol), and disulfiram (aversive) — established addiction pharmacotherapy that sits outside the classic psychiatric categories.

A Theoretical Synthesis

The agents in this document, taken together, deliver a single large lesson: psychiatric illness is biologically broader than the neurotransmitter model, and the drugs that work outside that model are the evidence. The atypical antidepressants (bupropion, mirtazapine, trazodone, the MAOIs) make the narrower version of the point — that even within "antidepressant," there are multiple distinct mechanisms (dopaminergic-noradrenergic reuptake inhibition, receptor antagonism, broad MAO inhibition), and that matching mechanism to patient (sexual side effects → bupropion; insomnia and weight loss → mirtazapine; atypical/resistant → MAOI) is real, useful clinical reasoning that the SSRI-default obscures.

The repurposed non-psychiatric drugs make the larger and more important point. That a TNF-alpha inhibitor lifts depression specifically in inflamed patients, that D-cycloserine can augment fear extinction by strengthening NMDA-dependent learning, that GLP-1 agonists reduce addictive craving, that thyroid hormone augments antidepressants, that NAC helps compulsive behaviors — each is a window into a system (immune, glutamatergic-learning, metabolic-reward, endocrine, oxidative) that contributes to psychiatric illness and that the monoamine drugs never addressed. And the recurring finding that these drugs work in biologically-defined subgroups rather than unselected populations points toward the most important structural change coming to psychiatric pharmacology: a move from one-size-fits-the-diagnosis prescribing toward stratified, biomarker-guided treatment — giving the anti-inflammatory to the inflamed patient, the metabolic drug to the metabolically dysfunctional one, the hormone to the deficient one. The repurposed drugs are, in this sense, not a miscellaneous appendix to psychiatric pharmacology but a preview of its future: the recognition that "depression" and "psychosis" are heterogeneous syndromes with multiple biological contributors, and that the right drug depends on which biology is driving this patient's illness.

The honest caution that must accompany the excitement: most of this is promising rather than proven. The subgroup findings are real but small; the trials in unselected populations are mostly negative; the biomarkers to guide stratification are not yet validated for routine use; and the field is prone to over-extrapolating from a striking mechanism or a positive subgroup to a general treatment. The repurposing landscape is heavy with hype (the microbiome, the metabolic drugs, the nutraceuticals) and light on agents actually ready for routine prescription. Its current value is partly clinical (a real set of options for specific patients and subgroups) and largely conceptual (the demonstration that psychiatry's biology, and therefore its future pharmacology, extends far beyond the synapse).

The Clinical Bottom Line

The atypical antidepressants are effective, distinctively-profiled, and underused: bupropion for the patient where sexual side effects, weight, sedation, or comorbid smoking/ADHD matter (avoiding it in prominent anxiety or seizure risk); mirtazapine for the depressed patient with insomnia, poor appetite, and SSRI intolerance (accepting sedation and weight gain); trazodone mainly as a non-addictive hypnotic; the MAOIs as genuinely effective options for atypical and treatment-resistant depression in expert hands, their interaction burden respected. Matching mechanism to patient is real clinical value.

The repurposed non-psychiatric agents divide by readiness:

• Useful now, in the right patient: T3/thyroid augmentation and treatment of thyroid-related mood disorder; metformin for antipsychotic-induced weight gain; the neurosteroids (covered elsewhere) for postpartum depression; NAC as a low-risk adjunct for compulsive/addictive behaviors with modest expectations; established addiction pharmacotherapy (naltrexone, acamprosate).
• Promising, watch closely, mostly investigational: GLP-1 agonists for addiction and possibly mood (with attention to emerging risk questions); anti-inflammatories (including TNF-alpha inhibitors) in biomarker-defined inflamed subgroups; D-cycloserine and other psychotherapy-augmenters; minocycline.
• Early/hype-heavy: microbiome interventions, most nutraceuticals beyond omega-3, and the broader metabolic-psychiatric frontier.

The overarching message: these agents demonstrate that psychiatric illness involves immune, metabolic, endocrine, and learning systems beyond the classic neurotransmitters, that effective treatment increasingly depends on matching the drug to the specific biology of the specific patient (mechanism for the atypical antidepressants, subgroup for the repurposed drugs), and that the future of psychiatric pharmacology is likely a more stratified, biomarker-guided, systems-level enterprise than the monoamine era's one-size prescribing. For now, the disciplined position is to use the genuinely-useful atypical antidepressants more readily than the SSRI-default encourages, to deploy the established repurposed agents (thyroid, metformin, NAC, addiction drugs) where they fit, to watch the promising frontier (GLP-1 agonists, anti-inflammatories in inflamed patients) with interested skepticism, and to read the whole landscape as evidence that psychiatry's understanding of its own drugs — and its own illnesses — is still, encouragingly, expanding.

Selected References and Further Reading

1. Stahl, S.M. (2021). Stahl's Essential Psychopharmacology (5th ed.). Cambridge University Press.
2. Patel, K., et al. (2016). Bupropion: A systematic review and meta-analysis of effectiveness as an antidepressant. Therapeutic Advances in Psychopharmacology, 6(2), 99–144.
3. Watanabe, N., et al. (2011). Mirtazapine versus other antidepressants in the acute-phase treatment of adults with major depression: Systematic review and meta-analysis. Journal of Clinical Psychiatry, 72(10), 1404–1415.
4. Cipriani, A., et al. (2018). Comparative efficacy and acceptability of 21 antidepressant drugs. The Lancet, 391(10128), 1357–1366.
5. Suchting, R., et al. (2021). Revisiting monoamine oxidase inhibitors for depression. Journal of Affective Disorders / contemporary MAOI reviews.
6. Raison, C.L., et al. (2013). A randomized controlled trial of the tumor necrosis factor antagonist infliximab for treatment-resistant depression: The role of baseline inflammatory biomarkers. JAMA Psychiatry, 70(1), 31–41.
7. Miller, A.H., & Raison, C.L. (2016). The role of inflammation in depression: From evolutionary imperative to modern treatment target. Nature Reviews Immunology, 16(1), 22–34.
8. Köhler-Forsberg, O., et al. (2019). Efficacy of anti-inflammatory treatment on major depressive disorder: A systematic review and meta-analysis. Acta Psychiatrica Scandinavica, 139(5), 404–419.
9. Dean, O.M., Data-Franco, J., Giorlando, F., & Berk, M. (2012). Minocycline: Therapeutic potential in psychiatry. CNS Drugs, 26(5), 391–401.
10. Ressler, K.J., et al. (2004). Cognitive enhancers as adjuncts to psychotherapy: Use of D-cycloserine in phobic individuals. Archives of General Psychiatry, 61(11), 1136–1144.
11. Mataix-Cols, D., et al. (2017). D-cycloserine augmentation of exposure-based CBT: A systematic review and meta-analysis. JAMA Psychiatry, 74(5), 501–510.
12. Berk, M., et al. (2013). The promise of N-acetylcysteine in neuropsychiatry. Trends in Pharmacological Sciences, 34(3), 167–177.
13. Grant, J.E., et al. (2009/2016). N-acetylcysteine in trichotillomania and grooming disorders. Archives of General Psychiatry / JAMA Psychiatry.
14. Cooper, J.A., et al. (2023). GLP-1 receptor agonists and substance use / mood: Emerging evidence. Molecular Psychiatry / Nature Medicine reviews.
15. Wang, W., et al. (2024). Semaglutide and risk of suicidality: Pharmacovigilance and cohort analyses. Nature Medicine / JAMA Internal Medicine.
16. Cooper-Kazaz, R., & Lerer, B. (2008). Efficacy and safety of triiodothyronine supplementation in patients with major depression. International Journal of Neuropsychopharmacology, 11(5), 685–699.
17. Meltzer-Brody, S., & Kanes, S.J. (2020). Allopregnanolone in postpartum depression: Role in pathophysiology and treatment. Neurobiology of Stress, 12, 100212.
18. Berk, M., et al. (2014). So depression is an inflammatory disease, but where does the inflammation come from? BMC Medicine, 12, 200.
19. Cryan, J.F., et al. (2019). The microbiota-gut-brain axis. Physiological Reviews, 99(4), 1877–2013.
20. Jha, M.K., & Trivedi, M.H. (2018). Personalized antidepressant selection and pathway to novel treatments: Clinical utility of targeting inflammation. International Journal of Molecular Sciences, 19(1), 233.