Reflections on Psychiatry & Psychology

The glymphatic system is a brain-wide waste-clearance pathway where CSF flows along vessels, exchanges with interstitial fluid via astrocytes, and drains metabolites. It is driven by vascular pulsation and enhanced during sleep. Dysfunction—linked to poor sleep or vascular issues—may promote buildup of proteins like amyloid-β and contribute to neurologic disease.

Drugs disrupt brain homeostasis by hijacking the dopamine reward system, producing intense pleasure that outweighs natural rewards. Repeated use rewires brain circuits, weakens self-control, and creates cravings, withdrawal, and relapse. Though genetics and environment influence risk, top-down control allows change and recovery.

A large Cochrane review of 67 randomized trials (>2,300 patients) found no clear evidence that ketamine or other NMDA-receptor antagonists reduce chronic non-cancer pain. Evidence quality was rated low to very low, so current data do not reliably support ketamine as an effective pain treatment.

tDCS is a noninvasive brain stimulation that modulates cortical activity via weak currents, promoting plasticity. Evidence is strongest for depression (~33% response vs 17% sham), especially as adjunct therapy. It’s well tolerated but investigational; effects in other disorders are uncertain.

Geroscience studies aging itself as a root cause of disease. It distinguishes life span (years lived) from health span (years lived in good health). Research explores lifestyle changes, drugs like metformin, and senolytics to slow biological aging and extend healthy, active years.

Debate over benzodiazepines persists because better treatments for severe anxiety are lacking. Recent media portrayals highlight both benefit and risk. Used carefully, they remain essential for some patients—illustrating medicine’s constant balance between helping and harming.

Prescription nutraceuticals sometimes used in psychiatry include Deplin and EnLyte (L-methylfolate formulations that support neurotransmitter production) and Vascepa and Lovaza (omega-3 fatty acids). They are not antidepressants but may be added to treatment to support mood and overall brain health.

Researchers found that amyloid plaques in Alzheimer’s brains trap lithium, creating early lithium deficiency that may contribute to disease onset. In mice, low lithium worsened plaques and memory loss, while low-dose lithium orotate improved them. Human studies are still needed.

Ketamine and postpartum depression: A landmark BMJ study found that a single dose of esketamine after childbirth reduced postpartum depression by 75% in at-risk mothers. Learn what this means for prenatal depression treatment and maternal mental health.

Does naltrexone block ketamine’s antidepressant effects? Stanford research shows opioid receptor blockade dampens ketamine’s mood and antisuicidal benefits. Point Loma Clinic in San Diego explains what this means for your treatment plan.

New research shows the aging brain remodels — not just declines. Discover how the somatosensory cortex changes with age, why some layers thicken while others shrink, and what parvalbumin neurons and myelin reveal about brain aging and touch processing.

Can clinicians predict who will respond to ketamine for depression? A UCSD Veterans Affairs study identifies key baseline symptoms that predict ketamine non-response, informing better treatment planning. Learn more from Point Loma Clinic in San Diego.

"Taking traditional medication was like wading through mud—constantly struggling to stay clean. Ketamine, however, felt like walking in gentle rain; any mud simply washes away."

Psychedelic psychiatry is moving from fringe research to mainstream clinical practice. An overview of psilocybin, MDMA, and ketamine — including benefits, risks, and what the evidence supports.

If multiple antidepressants haven't worked for you, you're not alone and you're not out of options. Why Antidepressants Fail: Lessons from the STAR*D Study Treatment-resistant depression (TRD) is a complex challenge in mental health, characterized by patients' inadequate response to standard antidepressant therapies. The landmark STAR*D study, which extensively evaluated treatment strategies for depression, revealed that a significant percentage of individuals do not respond

The lateral habenula (LHb) stands out as a critical structure in understanding depression. This blog explores the LHb's role in the intricate landscape of neuroscience, its connection to depressive symptoms, and how ketamine therapy offers new hope by affecting this brain structure. The Lateral Habenula: A Critical Brain Structure The lateral habenula (LHb) is a small, symmetrical, paired nucleus located deep within the brain, nestled between the two thalamic bodies. It is in

The 2024 Oxford Ketamine Conference gathered global experts to discuss ketamine’s science and clinical use in mental health. Key themes included its rapid antidepressant effects, mechanisms of action, and improving treatment approaches, highlighting interdisciplinary collaboration and future research.

Stress and bipolar disorder (BD) interact bidirectionally. Stress, particularly in early life, appears to have lasting effects and marks for early onset of BD, although the exact mechanism is poorly understood. The relationship of stress to the onset of the disorder and its course has implications for treatment and management — and perhaps even prevention.

Methylfolate, the active form of folate (B9), supports serotonin and dopamine production and may help depression, especially in people with MTHFR variants or treatment-resistant cases. It can cause GI upset or insomnia and should be used cautiously, especially with SSRIs, under medical supervision.

The serotonin theory of depression has been around for a good 60 years and is often used as justification for the use of antidepressants, specifically selective serotonin re-uptake inhibitors (SSRIs). Understandably, a review published recently by psychiatric researcher Joanna Moncrieff, which concluded that there was no consistent evidence of an association between serotonin and depression, and no support for the hypothesis that depression is caused by lowered serotonin act