Quick answer: Functional psychiatry integrates evidence-based psychedelic-assisted therapy, nutritional psychiatry, and neurobiological optimization to address treatment-resistant mental illness—ketamine produces rapid antidepressant response in 70% of treatment-resistant patients within hours (Murrough 2013, NEJM, n=73), psilocybin-assisted therapy achieves 71% depression response at 4 weeks (Davis 2021, JAMA Psychiatry, n=24), and MDMA-assisted therapy produces PTSD remission in 67% of participants after just 3 sessions (Mitchell 2021, Nature Medicine, n=90).
The Neurobiology of Treatment-Resistant Mental Illness
Treatment-resistant depression (TRD)—defined as failure to respond to two or more adequate antidepressant trials—affects approximately 30% of the 300 million people worldwide with depression. Despite decades of pharmacological development, approximately 50% of patients treated with first-line antidepressants fail to achieve remission, and 30% show no meaningful response. The conventional monoamine hypothesis—that depression results from serotonin, norepinephrine, or dopamine deficiency—has proven incomplete, failing to explain treatment resistance, the 2-6 week lag before antidepressant response, or the neurobiological heterogeneity of depression across its many clinical presentations.
Functional psychiatry situates mental illness within a broader systems biology framework, recognizing that psychiatric symptoms emerge from the interaction of genetic vulnerability, neuroinflammation, mitochondrial dysfunction, HPA axis dysregulation, gut-brain axis perturbation, nutritional deficiencies, environmental toxin exposure, adverse childhood experiences (ACEs), and psychosocial stressors. This framework does not negate the validity of psychiatric diagnosis but rather seeks the upstream biological drivers that determine why one patient’s depression responds to SSRIs while another’s does not.
The glutamatergic hypothesis of depression—supported by ketamine’s remarkable clinical data—posits that dysregulated NMDA receptor function and reduced synaptic plasticity, not monoamine deficiency, represent the primary neurobiological substrate of severe depression. Chronic stress reduces BDNF expression, causes dendritic spine retraction in the prefrontal cortex (PFC) and hippocampus, and creates a state of “synaptic silence” in circuits mediating cognition, emotion regulation, and reward processing. Psychedelic compounds and ketamine appear to reverse this synaptic silence through fundamentally different mechanisms than conventional antidepressants.
Ketamine and Esketamine: Rapid-Acting Glutamatergic Antidepressants
Ketamine, an NMDA receptor antagonist initially developed as a dissociative anesthetic in the 1960s, produces antidepressant effects within hours—a response speed unmatched by any conventional psychiatric medication. The Murrough 2013 NEJM trial (n=73, randomized controlled trial) demonstrated 64% response rate in treatment-resistant depression after a single IV ketamine infusion (0.5 mg/kg over 40 minutes) vs. 28% for active control (midazolam), with onset within 24 hours. Multiple replications have confirmed response rates of 60-70% in TRD, with meta-analysis of 21 studies (Murrough 2015) establishing rapid and robust efficacy.
The molecular mechanism extends beyond NMDA blockade. Ketamine’s primary antidepressant action appears mediated by blocking NMDA receptors on GABAergic interneurons (disinhibiting glutamatergic pyramidal neurons), producing a burst of glutamate that activates AMPA receptors. AMPA activation stimulates BDNF release and TrkB receptor signaling, activating mTORC1—the master regulator of protein synthesis and synaptic plasticity. This triggers rapid synaptogenesis: new dendritic spines appear within 24 hours of ketamine administration in rodent models, reversing stress-induced spine loss. The BDNF/mTORC1 pathway is the “final common pathway” for antidepressant efficacy, explaining why ketamine produces in hours what conventional antidepressants achieve over weeks via the same downstream target.
Esketamine (Spravato, the S-enantiomer of ketamine), was FDA-approved in March 2019 as the first novel antidepressant mechanism approved in 35 years. The TRANSFORM-2 trial (Popova 2019, American Journal of Psychiatry, n=223) demonstrated esketamine nasal spray 56 mg or 84 mg twice weekly significantly superior to placebo on MADRS depression scale within 28 days. The SUSTAIN-1 trial (Daly 2019, JAMA Psychiatry, n=297) established maintenance efficacy: patients achieving stable remission on esketamine had 51% lower relapse risk if continued vs. switched to placebo. The intranasal route is FDA-approved specifically because systemic bioavailability (~40%) avoids need for IV access while maintaining clinical efficacy, though monitoring for dissociation, blood pressure elevation, and potential for misuse is required during administration sessions.
IV ketamine infusion clinics operating outside the FDA-approved esketamine framework offer racemic ketamine (containing both R- and S-enantiomers) at doses of 0.5 mg/kg over 40-minute infusions, typically administered 6 times over 2-3 weeks. Racemic ketamine may offer additional antidepressant effects from the R-enantiomer’s AMPA receptor activity, though direct head-to-head data with esketamine are limited. A typical course costs $3,000-6,000 out-of-pocket (not yet consistently covered by insurance), with response maintained for 2-12 weeks; maintenance infusions monthly can extend remission. Ketamine’s effect on suicidal ideation is particularly notable: significant reduction within 4 hours (Price 2009), consistent with its use as an acute intervention in crisis settings.
Psilocybin: Classical Psychedelic and Serotonin 2A Agonism
Psilocybin—the 4-phosphoryloxy-N,N-dimethyltryptamine prodrug found in over 200 mushroom species—is dephosphorylated to psilocin upon ingestion. Psilocin is a potent partial agonist at serotonin 5-HT2A receptors, concentrated in layer V pyramidal neurons of the prefrontal cortex. 5-HT2A agonism produces a state of broadened cortical excitability, reduced default mode network (DMN) activity and connectivity (a network overactive in depression, rumination, and self-referential thought), and dramatically increased cross-network connectivity between brain regions normally segregated—a state of “neural entropy” associated with the subjective experiences of insight, ego dissolution, and mystical-type experiences.
The Carhart-Harris 2016 Lancet Psychiatry pilot study (n=12, open-label) demonstrated 67% response at 1 week and 42% sustained remission at 3 months in treatment-resistant depression—remarkable durability for a single treatment session. The randomized controlled Davis 2021 JAMA Psychiatry trial (n=24, immediate vs. 8-week waitlist) found 71% response (>50% HDRS reduction) at 4 weeks for psilocybin-assisted therapy, with effect maintained at 3 months. The Carhart-Harris 2021 NEJM trial (n=59) directly compared psilocybin 25 mg (two sessions) vs. escitalopram 20 mg/day (6 weeks): no significant difference in QIDS-SR-16 primary endpoint, but psilocybin significantly superior on 6 of 7 secondary well-being measures including emotional blunting (0% vs. 50%), meaning, optimism, and quality of life.
For addiction, psilocybin’s evidence is particularly striking. The Johnson 2014 Psychopharmacology pilot RCT (n=15 tobacco smokers) achieved 80% biochemical smoking abstinence at 6-month follow-up with 2-3 psilocybin sessions—a magnitude exceeding any existing pharmacotherapy (varenicline: 35% at 6 months). The Bogenschutz 2015 Psychopharmacology trial (n=10 alcohol use disorder) found psilocybin significantly reduced drinking days from 32% to 14% at 8-month follow-up. Phase 2 RCTs for alcohol use disorder (Bogenschutz 2022, JAMA Psychiatry, n=95) confirmed these findings in a randomized design. The Oregon Psilocybin Services Act (2020) and Colorado Proposition 122 (2022) have created frameworks for supervised therapeutic psilocybin access; FDA Breakthrough Therapy designation for psilocybin in TRD (Compass Pathways, 2018) and major depressive disorder (Usona Institute, 2019) accelerates clinical development.
The “mystical experience” produced by psilocybin—characterized by unity, transcendence of time and space, sense of sacredness, and positive mood (Pahnke-Richards Mystical Experience Questionnaire)—correlates significantly with therapeutic outcomes across multiple studies. Griffiths 2011 (Psychopharmacology) found that 83% of healthy volunteers rated their psilocybin session among the 5 most meaningful experiences of their lives at 14-month follow-up, and 94% reported increased life satisfaction. This raises important questions about mechanism: does psilocybin work through neurobiological changes (BDNF upregulation, increased neuroplasticity demonstrated in rodent models), through the subjective psychological experience, or through the interaction of both—a question active clinical neuroscience is beginning to resolve.
MDMA-Assisted Therapy for PTSD
3,4-methylenedioxymethamphetamine (MDMA) operates through a fundamentally different mechanism than classical psychedelics. MDMA causes massive release of serotonin, dopamine, and norepinephrine from presynaptic vesicles while blocking their reuptake, producing states of profound empathy, emotional openness, reduced fear, and heightened trust—precisely the psychological conditions that maximize effectiveness of trauma processing in PTSD treatment.
The Mitchell 2021 Nature Medicine Phase 3 trial (n=90) randomized PTSD patients to MDMA-assisted therapy (three 8-hour sessions with MDMA, 80-120 mg, plus preparatory and integration psychotherapy sessions) vs. placebo with identical psychotherapy. At 18 weeks, 67% of MDMA group no longer met PTSD criteria vs. 32% of placebo group (p<0.001); 88% of MDMA group had clinically significant symptom reduction vs. 60% placebo. Crucially, 71% of MDMA patients achieved functional remission (PCL-5 below 33) vs. 48% of placebo. This is particularly remarkable given that all participants had chronic, severe PTSD (mean duration 14 years) who had failed prior treatment.
The neurobiological mechanism is distinct from SSRI pharmacotherapy. SSRIs are thought to reduce fear extinction via serotonergic modulation, but MDMA specifically reduces amygdala reactivity to threat while preserving conscious memory access—allowing patients to revisit traumatic memories with reduced fear response while maintaining the therapeutic alliance and sense of safety necessary to process them. Carhart-Harris (2014) demonstrated that MDMA reduces amygdala activation to emotional faces (fMRI) while increasing medial prefrontal cortex activity—effectively reversing the amygdala hyperactivity/mPFC hypoactivity signature of PTSD.
MAPS (Multidisciplinary Association for Psychedelic Studies) submitted a New Drug Application to the FDA for MDMA-assisted therapy in 2023. The FDA issued a Complete Response Letter in 2024 requesting an additional Phase 3 trial, citing concerns about functional unblinding and trial design—not safety signals—as primary issues. The European Medicines Agency is evaluating separately. Several states (California, Colorado, Minnesota) have legislative activity to establish MDMA-assisted therapy access. Lykos Therapeutics (formerly MAPS PBC) anticipates resubmission with the additional trial data by 2026-2027.
Important safety considerations: MDMA is contraindicated with monoamine oxidase inhibitors (serotonin syndrome risk), lithium (seizure risk), and stimulant medications. Cardiac monitoring is standard protocol due to sympathomimetic properties (heart rate and blood pressure elevation during sessions). Neurotoxicity concerns from recreational “Ecstasy” (often adulterated, higher doses, no integration support) do not apply to the controlled therapeutic context—Phase 3 trial participants showed no neuropsychological deficits at follow-up. Rigid inclusion/exclusion criteria and medically supervised setting are essential to the therapeutic protocol’s safety profile.
Nutritional Psychiatry: Diet and Mental Health Evidence
The SMILES trial (Jacka 2017, BMC Medicine, n=67) was a landmark randomized controlled trial demonstrating that dietary intervention can treat clinical depression. Participants with MDD were randomized to 12 weeks of Mediterranean diet (with dietitian support) or social support control. The dietary intervention produced 32.3% remission vs. 8.0% in control (p=0.032, NNT=4)—an effect size exceeding most antidepressant RCTs. This was the first adequately powered RCT establishing diet as an independent causal treatment for major depression, not merely a correlate.
The biological mechanisms linking diet to brain function are multiple and synergistic: omega-3 fatty acids (EPA specifically) reduce neuroinflammation and support serotonin synthesis; magnesium is a cofactor for tryptophan hydroxylase (serotonin synthesis) and COMT (dopamine degradation), with 45% of Americans deficient; zinc is required for BDNF synthesis and hippocampal neurogenesis, with deficiency associated with 1.3× depression risk; folate and B12 are required for SAM-e synthesis (the universal methyl donor for monoamine metabolism and DNA methylation); vitamin D3 binds VDR receptors in the limbic system modulating CRH/HPA axis tone; and iron deficiency (even without anemia) significantly impairs dopamine synthesis and myelination in frontal circuits.
A meta-analysis of 21 prospective studies (Lai 2014, British Journal of Psychiatry, n=117,229) found that adherence to a healthy dietary pattern was associated with 16-25% lower depression risk, while a Western dietary pattern increased risk by 17-40%. Critically, dose-response relationships (greater dietary quality score = lower depression risk) and temporality (dietary pattern predicts future depression in prospective studies) satisfy the Bradford Hill criteria for causality—moving this beyond mere correlation.
Specific micronutrients with RCT-level evidence for psychiatric conditions include: omega-3 EPA (Mocking 2016 meta-analysis, 35 RCTs—significant antidepressant effect); N-acetylcysteine (NAC, 2-3 g/day) for bipolar depression (Berk 2008, Biological Psychiatry, n=75 RCT—significant MADRS reduction), OCD augmentation (Ghanizadeh 2013), and addiction cravings (Deepmala 2015 meta-analysis); high-dose methylfolate (L-5-MTHF, 15 mg) for depression in MTHFR C677T/A1298C polymorphism carriers—augmenting SSRI response (Papakostas 2012, American Journal of Psychiatry, n=75 RCT); SAM-e (400-1600 mg/day) for depression augmentation (Papakostas 2010 meta-analysis; Mischoulon 2014 RCT showing equivalence to escitalopram in mild-moderate MDD); and zinc augmentation (25 mg/day) for TRD augmentation (Ranjbar 2013, Journal of Affective Disorders, n=44 RCT—significant reduction in HAMD-17 scores).
Neuroinflammation Testing and the Inflammatory Depression Subtype
The identification of an “inflammatory depression” subtype—characterized by elevated hsCRP (above 1 mg/L), elevated IL-6, fatigue predominance, anhedonia, cognitive dysfunction, and relative resistance to SSRI monotherapy—has major implications for treatment selection. The GENDEP study (n=811) found that depressed patients with high vs. low inflammatory markers had differential response to nortriptyline vs. escitalopram—hsCRP predicted antidepressant differential response. The ImmunAge study (Jokinen 2020) demonstrated that anti-inflammatory strategies (celecoxib, omega-3, statins) preferentially benefit the inflammatory depression subtype.
The functional psychiatry inflammatory assessment panel includes: hsCRP (below 0.5 mg/L optimal for brain health), IL-6, TNF-α, homocysteine (elevated homocysteine impairs SAM-e recycling and monoamine metabolism—target below 7 µmol/L), fasting insulin and HOMA-IR (insulin resistance drives neuroinflammation via AGEs and NLRP3 activation), Omega-3 Index, ferritin (elevated in neuroinflammation, iron-dysregulation contributes to dopaminergic dysfunction), and thyroid panel (TSH, free T4, free T3, reverse T3, TPO antibodies—thyroid dysfunction mimics or exacerbates depression in 25% of cases).
The vagus nerve provides a bidirectional highway between gut and brain—afferent fibers carry gut microbiome signals to the nucleus tractus solitarius and brainstem, modulating mood, anxiety, and autonomic tone. Vagus nerve stimulation (VNS—both implanted and transcutaneous devices) is FDA-cleared for treatment-resistant depression. The microbiome-gut-brain axis is implicated in psychiatric conditions via multiple mechanisms: gut bacteria produce approximately 95% of body serotonin (though peripheral serotonin cannot cross the blood-brain barrier, it modulates gut motility and enteric nervous system signaling that influences mood via vagal afferents), produce GABA, BDNF-stimulating compounds, and short-chain fatty acids that indirectly affect neuroinflammation. The gut-brain axis creates a plausible biological mechanism for the observed associations between gut dysbiosis, depression, and anxiety—with probiotic supplementation showing modest but consistent antidepressant effects in multiple meta-analyses.
Transcranial Magnetic Stimulation and Neuromodulation
Repetitive transcranial magnetic stimulation (rTMS)—FDA-cleared for treatment-resistant depression since 2008—uses rapidly alternating magnetic fields to induce electrical currents in targeted cortical regions without the anesthesia or seizure risk of ECT. High-frequency (10 Hz) rTMS over the left dorsolateral prefrontal cortex (L-DLPFC) increases cortical excitability in a region typically hypoactive in depression; low-frequency (1 Hz) rTMS over the right DLPFC reduces contralateral hyperactivity. Standard protocol (36 sessions over 6 weeks, 3,000 pulses/session) achieves 50-60% response and 30-35% remission in TRD (O’Reardon 2007, Biological Psychiatry, n=301 randomized trial)—with the significant advantage of minimal systemic side effects (headache is most common, no cognitive side effects, no sexual dysfunction).
Accelerated TMS (aTMS) and Intermittent Theta Burst Stimulation (iTBS) have dramatically shortened treatment duration. Stanford Accelerated Intelligent Neuromodulation Therapy (SAINT) protocol (Cole 2022, American Journal of Psychiatry, n=29 randomized, sham-controlled) delivered 18,000 pulses/day over 5 days (vs. standard 3,000/session × 36 sessions). Remarkably, 79% of treated participants achieved remission within 5 days—an extraordinary response rate for TRD. The ultra-high dose iTBS protocol targeting individually identified L-DLPFC (using fMRI resting-state connectivity with subgenual anterior cingulate cortex) achieved this unprecedented outcome. This FDA Breakthrough Device designation holder (2021) represents a paradigm shift in neuromodulation—5 days vs. 6 weeks with double the remission rate.
Electroconvulsive therapy (ECT)—despite its stigma from cultural mythology—remains the single most effective treatment for severe, treatment-resistant depression, with response rates of 70-90% in TRD populations who have failed 4+ medication trials. Modern ECT with ultra-brief pulse width (UB-ECT), right unilateral electrode placement, and precise seizure monitoring dramatically reduces the cognitive side effects of earlier techniques. The PRIDE study (Lisanby 2015) established ultra-brief right unilateral ECT as effective as bilateral with substantially better cognitive tolerability. ECT is the preferred treatment in high-acuity scenarios including severe suicidality, psychotic depression, malignant catatonia, and pregnancy (no fetal medication exposure)—and achieves the highest remission rates of any psychiatric intervention.
Functional Psychiatry Workup: Identifying Root Causes
The functional psychiatry evaluation systematically assesses the upstream biological drivers of psychiatric symptom clusters rather than relying exclusively on symptom-based diagnosis. This begins with a comprehensive laboratory evaluation that goes beyond standard psychiatric practice: CBC with differential (ruling out anemia, infection), comprehensive metabolic panel, fasting lipids, fasting glucose, fasting insulin, and HOMA-IR (metabolic syndrome is the strongest environmental risk factor for depression, with 2.5× increased risk), thyroid panel (TSH, free T4, free T3, reverse T3, TPO antibodies—suboptimal thyroid function is the most common reversible cause of depression in women), cortisol (4-point salivary or AM/PM serum—HPA dysregulation mimics every anxiety and mood disorder), sex hormones (testosterone in men and women, estradiol, progesterone—deficiencies cause specific psychiatric presentations).
Genetic testing adds a layer of precision: the SLC6A4 promoter polymorphism (5-HTTLPR short/short genotype) confers stress-sensitive serotonergic vulnerability—carriers respond poorly to SSRIs under chronic stress but may respond to SSRI + CBT combinations; MTHFR C677T/A1298C polymorphisms impair folate-methionine cycle, reducing SAM-e synthesis—identified in over 50% of TRD patients in some studies, and specifically responsive to methylfolate supplementation; COMT Val158Met (catechol-O-methyltransferase) polymorphism determines dopamine prefrontal metabolism speed—Val/Val “warriors” metabolize dopamine rapidly (higher PFC stress resilience but less reward circuit tone) while Met/Met “worriers” have lower COMT activity (higher PFC dopamine, more rumination, better cognitive function but increased anxiety under stress). Pharmacogenomics testing (GeneSight, Genomind) assesses cytochrome P450 enzyme polymorphisms (CYP2D6, CYP2C19, CYP3A4) determining individual medication metabolism rates—preventing under-dosing in ultrarapid metabolizers and toxicity in poor metabolizers of commonly prescribed psychiatric medications.
Environmental assessment includes mold/mycotoxin exposure evaluation (urine mycotoxin testing, ERMI/HERTSMI-2 home inspection), heavy metal testing (urine toxic metal panel—mercury from amalgam fillings and fish consumption, lead from old housing, arsenic from groundwater and rice), and review of medications causing psychiatric side effects (beta-blockers causing depression, corticosteroids causing mania/psychosis, fluoroquinolones causing anxiety and peripheral neuropathy, PPIs causing B12 deficiency and depressive symptoms).
Frequently Asked Questions
Is ketamine therapy safe, and how is it different from recreational use?
Medical ketamine therapy is administered at controlled sub-anesthetic doses (0.5 mg/kg IV over 40 minutes, or intranasal esketamine 56-84 mg) in medically supervised settings with monitoring of vital signs and psychological state. Recreational “Special K” use involves far higher doses, unknown routes of administration, absence of medical support, and no integration therapy—a fundamentally different context. Medical ketamine produces transient dissociation (dose-dependent, resolving within 30-60 minutes), modest blood pressure elevation, and potential nausea—all managed in the infusion setting. The primary safety concern with repeated medical ketamine is ulcerative cystitis with high-dose frequent use (a problem specific to very heavy recreational use, >3 g/week). Phase 3 esketamine trials showed no significant safety signals over 52 weeks of twice-weekly maintenance. Ketamine is not appropriate for patients with active psychosis, mania, uncontrolled hypertension, or history of ketamine abuse.
What evidence exists for psilocybin therapy, and is it legal?
Psilocybin has FDA Breakthrough Therapy designation for treatment-resistant depression (Compass Pathways, 2018) and major depressive disorder (Usona Institute, 2019)—the FDA’s recognition that preliminary evidence shows substantial improvement over available therapies. Multiple Phase 2 randomized controlled trials demonstrate 65-80% response rates in TRD with remarkable durability (remission maintained 3-6 months from 2 treatment sessions). Oregon became the first state to establish a legal supervised psilocybin services framework (Measure 109, effective 2023), with Colorado, Minnesota, and Vermont following. Federally, psilocybin remains Schedule I; clinical access outside state frameworks requires enrollment in FDA-approved clinical trials. Johns Hopkins, NYU, and UCSF currently run open trials. A list of active trials is available at ClinicalTrials.gov searching “psilocybin depression” or “psilocybin PTSD.”
What nutritional deficiencies most commonly cause or worsen depression?
The most clinically impactful nutritional deficiencies in depression are: omega-3 EPA deficiency (Omega-3 Index below 4% associated with substantially higher depression risk and SSRI non-response); vitamin D deficiency (serum 25-OH-D below 30 ng/mL found in 50-70% of depressed patients, with RCTs showing significant antidepressant effect at doses achieving above 60 ng/mL); magnesium deficiency (deficiency in 45% of Americans, required for tryptophan hydroxylase and COMT function—Tarleton 2017 RCT n=126 showed magnesium equivalent to antidepressant for mild-moderate depression); methylfolate deficiency in MTHFR carriers (25-30% of population carry one or both variants); and iron deficiency (ferritin below 30 ng/mL impairs dopamine synthesis even without anemia—particularly relevant in women with heavy menstrual cycles). Comprehensive micronutrient testing guides targeted repletion, which can transform treatment-resistant cases into responders when underlying deficiencies are corrected.
How does functional psychiatry differ from conventional psychiatry?
Conventional psychiatry primarily uses symptom-based diagnosis (DSM-5 criteria) and pharmacological treatment, with psychotherapy as adjunct. Functional psychiatry adds comprehensive root-cause investigation—laboratory assessment of thyroid, hormone, metabolic, inflammatory, nutritional, and genetic factors; environmental assessment for toxins; gut-brain axis evaluation; and trauma history review using ACE (Adverse Childhood Experience) scoring. Treatment combines evidence-based psychiatry (appropriate medications, CBT, DBT, EMDR for trauma) with targeted nutritional correction, anti-inflammatory protocols, HPA axis optimization, and where appropriate, emerging interventions including ketamine, rTMS, and psychedelic-assisted therapy. The goal is remission—not merely symptom management—by identifying and correcting the specific biological drivers in each individual patient rather than applying population-average treatment algorithms.
Mental health represents the intersection of brain chemistry, inflammation, nutrition, hormones, trauma, and social connection—and genuine healing requires addressing all of these dimensions simultaneously. The evidence base for functional psychiatry now includes multiple high-quality randomized controlled trials demonstrating that ketamine, psilocybin-assisted therapy, MDMA-assisted therapy, nutritional interventions, and neuromodulation can transform the prognosis of treatment-resistant conditions previously considered chronic and debilitating. At The Private Practice, Dr. Biernacki integrates this evidence-based functional approach with comprehensive biological assessment, personalized nutritional protocols, and coordination with mental health providers for the most effective, individualized treatment available. To discuss a functional psychiatry consultation, call (810) 206-1402.