Depression & Mood Disorders
Comprehensive integrative medicine approach for lasting healing and complete recovery
Understanding Depression & Mood Disorders
Depression and Mood Disorders represent a spectrum of psychiatric conditions characterized by persistent disturbances in emotional regulation, motivation, and cognitive function. Major Depressive Disorder (MDD) involves dysregulation of monoamine neurotransmitters (serotonin, norepinephrine, dopamine), HPA axis hyperactivity, impaired neuroplasticity, chronic neuroinflammation, and disrupted circadian rhythm. These disorders significantly impair daily functioning, relationships, and quality of life, affecting over 280 million people globally.
Recognizing Depression & Mood Disorders
Common symptoms and warning signs to look for
Persistent sadness, emptiness, or feeling 'blue' most of the day, nearly every day for 2+ weeks
Loss of interest or pleasure in all or almost all activities (anhedonia) - hobbies, relationships, work
Sleep disturbances - either insomnia with difficulty falling/staying asleep OR sleeping too much (hypersomnia)
Significant appetite changes - weight loss or gain without intentional changes
Overwhelming fatigue and loss of energy that persists despite rest
What a Healthy System Looks Like
In a healthy mood regulatory system: (1) Monoamine neurotransmission - serotonin, norepinephrine, and dopamine are produced in appropriate quantities, released at synapses, bind to receptors, and are efficiently recycled through reuptake transporters, maintaining stable mood, motivation, and reward processing; (2) HPA axis function - the hypothalamic-pituitary-adrenal axis responds to stress appropriately, with cortisol rising during acute stress and returning to baseline through proper negative feedback via glucocorticoid receptors in the hippocampus and hypothalamus; (3) Neuroplasticity - brain-derived neurotrophic factor (BDNF) supports hippocampal neurogenesis, synaptic plasticity, dendritic branching, and healthy neural circuit formation in the prefrontal cortex and amygdala; (4) Circadian rhythm - the suprachiasmatic nucleus coordinates melatonin secretion from the pineal gland and cortisol rhythms, maintaining healthy sleep-wake cycles, energy fluctuations, and optimal neurotransmitter production timing; (5) Inflammatory homeostasis - balanced cytokine production (IL-6, TNF-alpha) without chronic elevation, with proper resolution of inflammatory responses; (6) Healthy gut-brain axis - proper vagal signaling, neurotransmitter production in the enteric nervous system (95% of serotonin is produced in the gut), and healthy microbiome diversity supporting neurotransmitter metabolism.
How the Condition Develops
Understanding the biological mechanisms
Depression results from multiple interconnected neurobiological mechanisms that form a self-perpetuating cycle: (1) Monoamine dysfunction - reduced serotonin, norepinephrine, and dopamine signaling due to decreased synthesis (tryptophan hydroxylase, tyrosine hydroxylase limitation), increased reuptake (elevated SERT expression), receptor downregulation (5-HT1A, 5-HT2A, beta-adrenergic), and impaired second-messenger systems; (2) HPA axis dysregulation - chronic stress leads to sustained cortisol elevation, impaired negative feedback, glucocorticoid receptor resistance (glucocorticoid receptor heterozygosity) in the hippocampus and prefrontal cortex, and altered CRH/ACTH dynamics; (3) Neuroinflammation - elevated pro-inflammatory cytokines (IL-6, TNF-alpha, IL-1beta, CRP) cross the blood-brain barrier via saturable transport, activate microglia (microglial priming), reduce serotonin synthesis (IDO enzyme activation diverts tryptophan to kynurenine pathway), impair neurogenesis in the dentate gyrus, and directly affect mood-regulating neural circuits; (4) Neuroplasticity impairment - decreased BDNF levels reduce hippocampal volume (3-5% reduction documented in MRI studies), impair synaptic plasticity, reduce dendritic spine density in prefrontal cortex, and affect mood regulation circuits; (5) Circadian rhythm disruption - altered melatonin secretion (delayed phase, reduced amplitude), flattened cortisol rhythm (loss of morning peak), disrupted sleep architecture (reduced REM latency, decreased slow-wave sleep), and altered circadian gene expression (PER, CLOCK, BMAL1); (6) HPA axis hyperactivity - elevated baseline cortisol, impaired dexamethasone suppression (DST non-suppression in 30-50% of melancholic depression), and elevated CRH levels in CSF; (7) Hypothalamic-pituitary-thyroid (HPT) axis dysregulation - low Free T3 levels despite normal TSH, elevated Reverse T3, and impaired peripheral T4 to T3 conversion can contribute directly to depressive symptoms; (8) Reduced prefrontal cortex activity - neuroimaging (fMRI, PET) shows decreased metabolic activity in the dorsolateral prefrontal cortex (dlPFC), increased amygdala reactivity, and altered default mode network connectivity; (9) Elevated glutamate - increased glutamate levels and NMDA receptor dysfunction contribute to excitotoxicity and impaired synaptic plasticity; (10) Mitochondrial dysfunction - reduced ATP production, increased oxidative stress, and impaired cellular energy metabolism affect neuronal function.
Key Laboratory Markers
Important values for diagnosis and monitoring
| Test | Normal Range | Optimal | Significance |
|---|---|---|---|
| Serotonin (Whole Blood) | 50-200 ng/mL | 100-150 ng/mL | Mood regulation; often low in depression; precursor to melatonin; 95% of body serotonin in gut |
| Morning Cortisol | 6.2-19.4 mcg/dL | 8.0-12.0 mcg/dL | HPA axis function; elevated in chronic stress/depression; indicates adrenal overactivation |
| DHEA-S (Dehydroepiandrosterone Sulfate) | 80-560 mcg/dL | 200-350 mcg/dL | Anti-stress hormone; low levels associated with depression, chronic fatigue; precursor to sex hormones |
| Vitamin B12 | 200-900 pg/mL | 500-900 pg/mL | Essential for neurotransmitter synthesis (serotonin, dopamine) and methylation; deficiency common in depression |
| Folate (Serum) | 3-20 ng/mL | 10-20 ng/mL | Required for serotonin synthesis via methylation; deficiency worsens depression and treatment response |
| Vitamin D (25-OH) | 30-100 ng/mL | 60-80 ng/mL | Modulates neurotransmitter synthesis, neuroinflammation, and neuroprotection; deficiency highly prevalent |
| TSH (Thyroid Stimulating Hormone) | 0.4-4.0 mIU/L | 1.0-2.0 mIU/L | Thyroid dysfunction can mimic or cause depression; subclinical hypothyroidism common contributor |
| Free T3 | 2.3-4.2 pg/mL | 3.0-4.2 pg/mL | Low T3 (even with normal TSH) can cause depression; affects brain neurotransmitter function |
| High-Sensitivity CRP | <3.0 mg/L | <0.5 mg/L | Inflammatory marker; elevated CRP correlates with treatment-resistant depression |
| IL-6 (Interleukin-6) | <5.0 pg/mL | <2.0 pg/mL | Pro-inflammatory cytokine; elevated in inflammatory depression; crosses blood-brain barrier |
| TNF-alpha | <8.1 pg/mL | <4.0 pg/mL | Pro-inflammatory cytokine; elevated in depressed patients; affects neurotransmitter metabolism |
| Homocysteine | <15 micromol/L | <8 micromol/L | Elevated indicates methylation dysfunction; linked to depression, cognitive impairment |
| Hemoglobin A1c | 4.0-5.6% | 4.5-5.3% | Blood sugar dysregulation affects mood stability; diabetes doubles depression risk |
| Magnesium (RBC) | 3.5-6.5 mg/dL | 5.0-6.5 mg/dL | Required for neurotransmitter function, HPA axis regulation, NMDA receptor modulation |
| Zinc | 50-150 mcg/dL | 80-120 mcg/dL | Essential for neurotransmitter synthesis and function; deficiency common in depression |
| Omega-3 Index | 4-8% | 8-12% | Measures EPA+DHA in red blood cell membranes; low levels associated with depression |
| DHEA (Dehydroepiandrosterone) | 130-980 ng/dL | 300-500 ng/dL | Precursor to sex hormones; low levels correlate with depression, especially in older adults |
| Melatonin (Salivary, Night) | 10-40 pg/mL | 20-40 pg/mL | Low nocturnal melatonin linked to depression; affects sleep and circadian rhythm |
Root Causes We Address
The underlying factors contributing to your condition
{"cause":"Genetic Predisposition","contribution":"30-40% - Family history increases risk 2-3x; variations in serotonin transporter gene (5-HTTLPR s-allele), BDNF gene (Val66Met), COMT enzyme (Val158Met), and other polymorphisms","assessment":"Family history screening; genetic testing for 5-HTTLPR, BDNF Val66Met, COMT polymorphisms; personal history of depression episodes"}
{"cause":"Trauma and Adverse Childhood Experiences (ACEs)","contribution":"30% - Childhood trauma increases depression risk 2-4x; alters HPA axis set-point permanently; affects stress response programming; changes attachment patterns; epigenetic modifications","assessment":"ACEs questionnaire (Adverse Childhood Experiences); trauma history assessment; developmental history; attachment style evaluation"}
{"cause":"Chronic Stress and HPA Axis Dysregulation","contribution":"40% - Prolonged stress exhausts cortisol regulation; flattened cortisol rhythm; impaired negative feedback at glucocorticoid receptors; adrenal fatigue pattern","assessment":"4-point cortisol curve (morning, noon, evening, night), DHEA-S to cortisol ratio, dexamethasone suppression test, ACTH levels"}
{"cause":"Neuroinflammation","contribution":"30% - Elevated cytokines (IL-6, TNF-alpha, IL-1beta, CRP) reduce serotonin synthesis (via IDO enzyme), impair neurogenesis, and affect mood circuits; chronic low-grade inflammation","assessment":"CRP, IL-6, TNF-alpha, neopterin; clinical correlation with inflammatory conditions; kynurenine/tryptophan ratio"}
{"cause":"Circadian Rhythm Disruption","contribution":"25% - Altered melatonin secretion, flattened cortisol rhythm, disrupted sleep-wake cycles impair mood regulation; shift work, jet lag common contributors","assessment":"Salivary cortisol curves at multiple timepoints, melatonin testing (night saliva), sleep diary, actigraphy, chronotype assessment"}
{"cause":"Neurotransmitter Imbalances","contribution":"35% - Serotonin, norepinephrine, and dopamine dysregulation at synthesis, receptor, and reuptake levels; amino acid precursor deficiencies","assessment":"Neurotransmitter panel (urine), symptom correlation, response to precursors (5-HTP, tyrosine trial)"}
{"cause":"Gut-Brain Axis Dysfunction","contribution":"25% - Reduced serotonin production (95% in gut); dysbiosis affects neurotransmitter metabolism; leaky gut increases neuroinflammation; vagus nerve signaling affected","assessment":"Stool microbiome analysis (GI-MAP, uBiome), leaky gut testing (zonulin), SIBO breath testing, food sensitivity testing"}
{"cause":"Methylation Dysfunction","contribution":"20% - Impaired MTHFR reduces neurotransmitter synthesis; affects cortisol metabolism; elevated homocysteine; SAMe deficiency affecting neurotransmitter production","assessment":"MTHFR genetic testing (C677T, A1298C), homocysteine levels, methylmalonic acid, B12 and folate levels"}
{"cause":"Nutritional Deficiencies","contribution":"25% - B12, folate, vitamin D, magnesium, zinc, and omega-3 deficiencies impair neurotransmitter synthesis and neuronal function","assessment":"Comprehensive micronutrient panel, vitamin D 25-OH, B12, folate, magnesium RBC, zinc, omega-3 index"}
{"cause":"Medication-Induced Depression","contribution":"15-20% - Beta-blockers, corticosteroids, interferon, some chemotherapy agents, benzodiazepines, some anticonvulsants can cause depressive symptoms","assessment":"Medication review, temporal correlation with medication start, dose-response relationship"}
{"cause":"Thyroid Dysfunction","contribution":"15% - Subclinical hypothyroidism (elevated TSH) and low T3 levels directly affect brain neurotransmitter function regardless of TSH","assessment":"Full thyroid panel (TSH, Free T4, Free T3, Reverse T3, TPO antibodies, thyroglobulin antibodies)"}
{"cause":"Heavy Metal Toxicity","contribution":"10-15% - Mercury, lead, arsenic, cadmium exposure can impair neurological function and neurotransmitter metabolism","assessment":"Heavy metal testing (blood, urine, hair), provocation testing if needed"}
{"cause":"Electromagnetic Field Exposure","contribution":"5-10% - Chronic EMF exposure from devices may affect sleep, cortisol, and neurological function","assessment":"Exposure history, sleep quality correlation with device use"}
Risks of Inaction
What happens if left untreated
{"complication":"Chronic and Recurrent Depression","timeline":"Within 1-2 years","impact":"Untreated first episode increases risk of recurrence to 50%; each subsequent episode raises recurrence risk to 70-80%; episodes become more severe, longer-lasting, and more treatment-resistant; kindling phenomenon"}
{"complication":"Treatment Resistance","timeline":"After 2+ untreated episodes","impact":"Longer untreated periods correlate with poorer treatment response; neurobiological changes become entrenched through neuroplasticity; higher medication doses may be needed; reduces treatment options"}
{"complication":"Suicide Risk","timeline":"Increased at any point","impact":"15% of severe depression leads to suicide; depression is the leading cause of suicide worldwide; 20x increased risk vs. general population; 60% of suicides have depression"}
{"complication":"Cognitive Decline and Dementia","timeline":"10-20 years","impact":"Chronic elevated cortisol damages hippocampal neurons; depression doubles Alzheimer's risk; accelerated brain aging; executive function impairment; vascular dementia risk"}
{"complication":"Cardiovascular Disease","timeline":"5-10 years","impact":"Depression increases heart disease risk 1.5x and heart attack risk 2x; affects heart rate variability; increased platelet aggregation; inflammatory markers elevated; lifestyle factors compound"}
{"complication":"Relationship and Career Damage","timeline":"Progressive","impact":"Social withdrawal, irritability, and impaired concentration strain relationships; 35% reduced work productivity; increased absenteeism; job loss common; marital dissolution rates 3x higher"}
{"complication":"Substance Abuse and Addiction","timeline":"Within 1-3 years","impact":"30% of depressed individuals develop substance use disorders as self-medication; alcohol and drug use worsens depression significantly; creates dual diagnosis; complicates treatment"}
{"complication":"Physical Health Deterioration","timeline":"Progressive","impact":"Weakened immune function leads to more infections; increased inflammation; accelerated aging (telomere shortening); digestive disorders; pain syndromes; mortality increased 50-70%"}
{"complication":"Quality of Life Destruction","timeline":"Immediate","impact":"Inability to enjoy life; chronic suffering; isolation; loss of identity and purpose; daily functioning impaired; caregiver burden significant"}
{"complication":"Treatment Complexity Increase","timeline":"Progressive","impact":"Each year of untreated depression makes treatment more difficult; neurobiological changes become more entrenched; higher treatment costs; longer recovery time"}
How We Diagnose
Comprehensive assessment methods we use
{"test":"Comprehensive Blood Panel (150+ markers)","purpose":"Baseline assessment of all major organ systems","whatItShows":"CBC (anemia, infection), CMP (liver, kidney, electrolytes), lipid panel (cardiovascular risk), thyroid panel, inflammatory markers, vitamins, minerals reveal underlying contributors"}
{"test":"Advanced Adrenal/HPA Axis Panel","purpose":"Assess stress response system comprehensively","whatItShows":"4-point cortisol curve (morning, noon, evening, night), DHEA-S, cortisol/DHEA ratio reveals HPA axis dysregulation patterns, adrenal function, stress capacity"}
{"test":"Neurotransmitter Panel (Urine)","purpose":"Measure neurotransmitter levels and metabolites","whatItShows":"Serotonin, norepinephrine, dopamine, GABA, glutamate, 5-HIAA, HVA levels indicate neurotransmitter imbalances, synthesis capacity, and metabolism"}
{"test":"Inflammatory Marker Panel","purpose":"Assess neuroinflammation and systemic inflammation","whatItShows":"CRP (hs-CRP), IL-6, TNF-alpha, homocysteine, fibrinogen reveal inflammatory contributors to depression; guides anti-inflammatory treatment"}
{"test":"Comprehensive Gut Assessment","purpose":"Evaluate gut-brain axis function","whatItShows":"Stool microbiome analysis (diversity, pathogenic organisms, beneficial bacteria), leaky gut markers (zonulin), calprotectin, SIBO breath testing reveal gut-related contributors"}
{"test":"Nutrient Optimization Panel","purpose":"Identify deficiencies affecting mood","whatItShows":"Vitamin D 25-OH, B12, folate, magnesium RBC, zinc, selenium, copper, iron studies, omega-3 index indicate nutritional contributors to depression"}
{"test":"Genetic Methylation Panel","purpose":"Assess genetic predispositions affecting mood","whatItShows":"MTHFR (C677T, A1298C), COMT (Val158Met), BDNF (Val66Met), VDR, and other polymorphisms affecting neurotransmitter metabolism and stress response"}
{"test":"Full Thyroid Panel","purpose":"Rule out thyroid as primary or contributing cause","whatItShows":"TSH, Free T4, Free T3, Reverse T3, TPO antibodies, thyroglobulin antibodies reveal thyroid dysfunction that can cause or worsen depression"}
{"test":"Heavy Metal Testing","purpose":"Assess toxic load contribution","whatItShows":"Blood heavy metals (lead, mercury, arsenic, cadmium), urine provocation testing reveal toxicity affecting neurological function"}
{"test":"Sleep Study (Polysomnography)","purpose":"Evaluate sleep architecture","whatItShows":"Sleep stages, REM behavior, apnea events, periodic limb movements reveal primary sleep disorders causing secondary depression"}
{"test":"Validated Depression Scales","purpose":"Quantify severity and track treatment response","whatItShows":"PHQ-9 (severity), BDI-II (Beck Depression Inventory), HAM-D (Hamilton Rating Scale), EPDS (Edinburgh Postnatal Depression Scale) provide objective measurement"}
Our Treatment Approach
How we help you overcome Depression & Mood Disorders
Healers Clinic Depression Recovery Protocol
Healers Clinic Depression Recovery Protocol
Diet & Lifestyle
Recommendations for optimal recovery
Recovery Timeline
What to expect on your healing journey
{"initialImprovement":"2-4 weeks - Sleep quality improves, energy levels stabilize, acute symptoms reduce in frequency and intensity, appetite normalizes somewhat","significantChanges":"3-6 months - HPA axis function normalizes, neurotransmitter balance improves, inflammatory markers decrease, symptoms significantly reduced, return to activities begins","fullRecovery":"6-12 months - Most symptoms resolve, coping skills developed, lifestyle changes integrated, relapse prevention in place","maintenancePhase":"12+ months - Continued practice of lifestyle modifications, maintenance supplementation as needed, building long-term resilience, regular self-monitoring"}
How We Measure Success
Outcomes that matter
Mood symptom score improves (PHQ-9 score <10, ideally <5)
Cortisol rhythm normalizes (morning peak 10-15 mcg/dL, evening decline <5)
DHEA-S to cortisol ratio improves (>200 indicates healthy stress response)
Inflammatory markers normalize (CRP <1.0 mg/L, IL-6 <2.0 pg/mL)
Sleep quality score improves (PSQI <5, sleep efficiency >85%)
Energy levels return to baseline (fatigue resolved)
Interest and pleasure in activities returns (anhedonia resolves)
Cognitive function improves (concentration, memory, executive function)
Social functioning restored (relationships improved, social activities resumed)
Work and productivity restored (able to focus, complete tasks)
Overall quality of life score improves (WHO-5 >50)
Reduced or eliminated need for acute interventions
Stable mood without major episodes for 6+ months
Resilience to stress (able to handle setbacks without relapse)
Meaning and purpose in life restored
Frequently Asked Questions
Common questions from patients
What is the difference between sadness and clinical depression?
Sadness is a normal emotional response to loss, disappointment, or frustration that gradually resolves over days to weeks. Clinical depression (Major Depressive Disorder) is a diagnosable medical condition with specific criteria: symptoms lasting 2+ weeks, significantly impairing daily functioning. Depression includes persistent sadness PLUS other symptoms like anhedonia (loss of pleasure), sleep changes, appetite changes, fatigue, excessive guilt, concentration problems, and sometimes thoughts of death. Unlike normal sadness, depression does not lift on its own and requires intervention. The key distinction is duration, intensity, and impact on functioning.
Can depression be cured without medication?
Many patients achieve complete symptom remission through functional medicine approaches addressing root causes. Treatment choice depends on severity: mild depression often responds well to therapy, lifestyle changes, and nutritional support. Moderate depression may benefit from combining medication (to reduce symptoms enough for other interventions to work) with functional approaches. Severe depression may require medication initially. The best approach is personalized based on comprehensive testing, symptom severity, patient preference, and history. Many patients successfully taper off medication once stable with proper support. Functional medicine can often help treatment-resistant depression by identifying underlying contributors (inflammation, HPA axis dysfunction, gut issues, thyroid problems) that standard treatment does not address.
What are the best supplements for depression?
Evidence-supported supplements include: Omega-3 fish oil (EPA+DHA 2000-4000mg - anti-inflammatory, membrane health), Vitamin D3 (correct deficiency, often present in depression - target 60-80 ng/mL), B-complex (B12, folate for methylation and neurotransmitter synthesis), St. John's Wort (300mg 3x daily - serotonin modulation, but interacts with medications), SAMe (400-800mg - neurotransmitter synthesis), Magnesium glycinate (300-400mg - nervous system support), 5-HTP (50-200mg - serotonin precursor, use cautiously), L-theanine (calm focus), and adaptogens like Ashwagandha (cortisol reduction). However, supplementation must be personalized based on lab testing - what works for one person may not work for another. Always consult a healthcare provider before starting supplements, especially if on medication.
How does gut health affect depression?
The gut-brain axis is crucial in depression through multiple mechanisms: The gut produces 95% of the body's serotonin. Gut dysbiosis reduces neurotransmitter production. Dysbiosis increases inflammatory molecules (LPS) that cross the blood-brain barrier, triggering neuroinflammation. The vagus nerve directly connects gut to brain, transmitting signals that influence mood. Leaky gut allows toxins and bacteria to trigger systemic inflammation. Specific gut bacteria produce neurotransmitters (GABA, dopamine). Healing the gut through diet (removing inflammatory foods, adding probiotics), addressing SIBO, and supporting gut lining often significantly improves depression symptoms. Research shows fecal microbiota transplantation can improve depression in some patients.
How long does depression treatment take to work?
Initial symptom reduction often occurs within 2-4 weeks with appropriate intervention (sleep improves first, then energy). Significant improvement typically happens within 8-12 weeks. Full recovery and root cause correction usually requires 6-12 months of consistent treatment. Some patients require longer maintenance phases. However, most patients notice meaningful improvement within the first month. Treatment duration depends on severity, adherence, underlying causes, and individual biology. Chronic or severe depression may require 12-24 months of treatment. Maintenance treatment is often recommended to prevent relapse, especially with history of multiple episodes.
What is treatment-resistant depression?
Treatment-resistant depression (TRD) is depression that does not respond adequately to at least two different antidepressant medications at adequate dose and duration (minimum 4-6 weeks each). It affects approximately 30% of depressed patients. Functional medicine approaches can help TRD by identifying underlying contributors: chronic inflammation, HPA axis dysfunction, thyroid issues (low T3), gut problems (SIBO, dysbiosis), methylation defects (MTHFR), nutritional deficiencies (B12, D, omega-3), and medication-induced causes. Comprehensive testing often reveals treatable biological factors. Other options include ketamine therapy, ECT, TMS, and medication combinations.
Medical References
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- 11.American Psychiatric Association. 'Practice Guideline for the Treatment of Patients With Major Depressive Disorder.' Am J Psychiatry. 2023;170(3):1-89.
- 12.National Institute for Health and Care Excellence. 'Depression in adults: treatment and management.' NICE Guidelines. 2024.
- 13.WHO. 'Depression and Other Common Mental Disorders.' Global Health Estimates. 2023.
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