by Hilal Tokat
art by Gabriela Bentolila
Imagine feeling sad, hopeless, and disinterested…not just occasionally, but in a way that permeates your daily life. This is the harsh reality for those living with Major Depressive Disorder (MDD), a condition affecting approximately 280 million individuals worldwide [1]. Approximately 21 million Americans suffered from a major depressive episode in 2021 [2]. Moreover, individuals with MDD are 20 times more likely to die from suicide than the average person [3]. This condition is more than feeling down; it is a complex and life-disrupting disorder that permeates many aspects of existence [4].
Depression manifests differently for everyone, with varying emotions and physical symptoms. According to the DSM-5, MDD is diagnosed if a person experiences a major depressive episode and at least five of the following symptoms for two or more years: depressed mood, diminished interest or pleasure in activities for more than two weeks, loss or gain of appetite, insomnia or hypersomnia, psychomotor agitation or retardation, fatigue, feelings of worthlessness and excessive guilt, and decreased concentration [5]. Various factors, from life events, trauma, and social circumstances to genetic, neurochemical, and hormonal influences, contribute to the complexity of depression [6]. MDD often coexists with anxiety, substance use, and other mental health disorders [7]. Individuals diagnosed with MDD have a 15 to 18 percent risk of having lifetime depression symptoms, which can also significantly impact physical health [8].
Antidepressants, such as selective serotonin reuptake inhibitors (SSRIs), aim to boost serotonin, a neurotransmitter associated with mood regulation. SSRIs block serotonin reuptake in the synaptic cleft, the intermediary connection between two neurons, by increasing serotonin availability at the postsynaptic membrane [9]. Drugs such as buspirone and tandospirone stimulate the 5-HT1A receptor, acting on presynaptic receptors in the raphe nucleus, a group of serotonin-containing neurons [10]. However, their delayed therapeutic effect—taking weeks to improve mood —and side effects like insomnia, skin rashes, headaches, joint and muscle pain, stomach upset, nausea, and diarrhea underscore why novel therapeutics for treating depression are so necessary [11].
Eight-week SSRI treatments have been linked to increased activity in the amygdala, a brain region involved in emotional and behavioral regulation [12]. Using functional magnetic resonance imaging (fMRI) and positron emission tomography (PET) scans, researchers found decreases in amygdala activity in response to harmful stimuli after 6 to 12 weeks of SSRI treatment. However, studies show no significant differences in efficacy among SSRIs like sertraline, citalopram, and escitalopram, emphasizing that depression is not simply a one-size-fits-all disorder [13].
While treatment for MDD exists, it is not effective for everybody. Thirty percent of patients do not experience relief from conventional treatments such as electroconvulsive therapy, psychotherapy, cognitive-behavioral therapy, and interpersonal therapy and are diagnosed with treatment-resistant depression (TRD) [14]. While a universally agreed upon definition for TRD does not currently exist, the US Food and Drug Administration (FDA) and the European Medicines Agency have defined it as a poor treatment response to at least two antidepressants despite participating in an adequate treatment trial [14]. Factors like inflammation, stress, or altered brain glucose metabolism may contribute to TRD. Research on cerebral glucose metabolism—the process of using glucose and other substrates to generate energy for sustaining neurological functions in the brain—found differences in the rostral anterior cingulate between responders and non-responders to antidepressants, with hypometabolism linked to non-response [15, 16]. Patients who were not responsive to medication exhibited hypometabolism (lower glucose metabolism) compared to healthy individuals, whereas those who were responsive exhibited hypermetabolism (increased glucose metabolism) in the same location [16]. Psychosocial risks, such as early trauma, physical illness, or social isolation, also complicate TRD in older adults [17]. Genetics may further influence TRD, as a family history of antidepressant resistance is linked to increased suicide risk [18].
More effective treatments are urgently needed for depression. The limitations of SSRIs, the complexity of TRD, and the consequences of untreated depression underscore this gap. Recent clinical research on psychedelics is revolutionizing mental health treatment, paving the way for new therapeutic possibilities [19].
Psychedelics are powerful psychoactive substances that affect the mind and, as a result, influence our emotions and perception of the world. They work differently than traditional antidepressants. Psychedelics unlock specific serotonin receptors that lead to the activation of new pathways. A receptor is a molecule outside a cell that interacts with a particular chemical to enable a specific function [20]. Psychedelics have various receptor targets that they bind to as a result of their complementary chemical structures. Psilocybin and lysergic acid diethylamide (lysergide, LSD) are two examples of psychedelics that function by attaching to serotonin 2A receptors. Serotonin 2A receptors are one of 15 specialized receptor molecules the serotonin system utilizes to govern brain activity [21]. Although their mechanisms of action are not fully understood, serotonin 5-HT2A receptors mediate the main effect of psychedelics. A 5-HT2A receptor or a serotonin 2A Receptor is a type of receptor frequently expressed in the central nervous system, including the striatum, which is a structure of interconnected nuclei in the brain involved in decision-making functions [22]. The brain can reboot by activating receptors such as serotonin 5-HT2A receptors, which can reduce and diminish symptoms of depression for months at a time after a single treatment [23].
New findings also show that systemic inflammation could be one of the causes of TRD, and psychedelics can be effective in reducing it. When we have an injury or infection, the immune system produces information to alert the rest of the body to the ailment. Inflammatory cells and cytokines—signaling proteins—rush in to signal and regulate bodily responses. However, just as an overly sensitive fire alarm can lead to unnecessary chaos, excessive production of cytokines can cause harmful inflammation. Inflammation in otherwise healthy individuals can contribute to chronic autoimmune conditions [24]. Increased concentrations of pro-inflammatory cytokines are seen in MDD patients [25]. This inflammation not only serves as an underlying cause of depression but also contributes to why some patients may be unresponsive to treatment [26]. A recent study on 60 healthy volunteers found that psilocybin, a classic psychedelic, reduced the concentration of pro-inflammatory cytokines in patients but did not affect other inflammatory markers [25].
Psilocybin (4-phosphoryloxy-N, N-dimethyltryptamine), informally known as “magic mushrooms,” is a hallucinogenic tryptamine alkaloid [21]. Tryptamine is a monoamine alkaloid with an indole ring structure [27]. Chemical technicalities aside, what is important is tryptamine’s structure that enables it to bind efficiently to serotonin receptor 2A, improving mood, perception, and cognition regulation. This efficiency can amplify serotonin-like effects, resulting in altered consciousness, heightened emotions, and enhanced introspection. This efficiency may also allow quick changes in brain connection and plasticity, further aiding in the treatment of depression. Psilocybin was discovered by Swiss scientist Dr. Albert Hofmann in 1957 from the Central American mushroom Psilocybe Mexicana [28]. One year later, psilocybin was chemically produced. Psilocybin has been detected in numerous mushroom species. They are often recreationally consumed as herbal concoctions or smoked [21]. Despite not affecting other inflammatory markers, preliminary research poses promise, suggesting psychedelics could help relieve patients of symptoms in addition to reducing one of the causes of TRD, systemic inflammation [25].
Psilocybin is not the only naturally occurring psychedelic. N, N-Dimethyltryptamine (DMT or N, N-DMT), one of the main ingredients in ayahuasca, a psychedelic plant beverage, is a natural psychedelic. Ayahuasca has been used during indigenous religious
ceremonies in Central and South America for centuries. DMT’s potent psychedelic effects in humans have attracted much attention, and global interest in its medicinal potential has peaked [29].
Psychedelics such as LSD can be synthesized in a lab [30]. Although LSD shares a functional group with psilocybin and DMT, it has a unique chemical structure [31]. Psychedelics all impact various cognitive processes, or the brain’s mental operations, to process information. They achieve this by creating new connection routes between neurons—a type of nerve cell in the brain. Neurons communicate through synapses—small spaces between neurons [30, 32]. Synaptic transmission is the process by which a chemical signal is emitted from one neuron and diffuses to other neurons or target cells, producing a signal that stimulates, inhibits, or modifies cellular activity [33]. Synaptic loss and impairments in functional connectivity are thought to contribute to symptoms of MDD. A study used synaptic vesicle glycoprotein 2A (SV2A) as a marker to estimate synaptic density by counting the number of nerve terminals in the brain. The results displayed a significant negative correlation between the intensity of depressive symptoms and SV2A density, with people with higher degrees of depression having a reduced number of nerve terminals. Functional connectivity assessments from magnetic resonance imaging (MRI) revealed a correlation between SV2A density and abnormal network function [34].
By activating serotonin receptors, psychedelics increase neural excitability, subsequently enhancing neuroplasticity and promoting synaptic density. Neuroplasticity refers to the nervous system’s ability to adapt, typically to stimuli, by rearranging its structure and connections [35]. By measuring the number of surviving synapses in the brain, synaptic density is a proxy for how the central nervous system grows and works [36]. A study investigating whether psilocybin produces quick and lasting antidepressant-like effects in mice, as well as whether its potential mechanisms of action are linked to enhanced neuroplasticity, found that psilocybin has strong, fast, and long-lasting antidepressant effects while also promoting neuroplasticity in the PFC and hippocampus, crucial brain regions for decision-making [37]. Another study found increased activity in several brain locations ten minutes after psilocybin injection. A study of specific brain regions revealed enhanced connectivity between the dorsal striatum, which has conscious motor movements and executive functions, and limbic regions, implying better-coordinated activity. A detailed study indicated that the cingulate cortex, a limbic region especially important for affective-motivational aspects of pain, was more connected to cortical and striatal regions, which work together to regulate movement and cognition, implying that psilocybin stimulated a greater network of brain regions. Psilocybin increased levels of EGR1 (a measure of brain activity) throughout the brain, showing broad activation in cortical and striatal regions [38].
Psychedelics may revolutionize mental health treatment by potentially “resetting” the mind
rather than managing symptoms through chronic drug intake [39]. This interpretation is
supported by a study led by Dr. Robin Carhart-Harris at Imperial College London, which used
psilocybin to treat patients with depression unresponsive to conventional therapies. Published in Scientific Reports, the study revealed patient-reported improvements lasting up to five weeks and fMRI scans showing brain activity changes associated with reduced depression symptoms. Dr. Carhart-Harris noted that several patients described feeling “reset” after treatment, likening the effect to a computer reboot. He stated that psilocybin might provide a temporary “kick start” to help patients break free from depressive states, with imaging results tentatively supporting this analogy. Similar brain effects have been observed with electroconvulsive therapy.
This “reset” is possible when psychedelics bind to target receptors, causing the connections between areas within the Default Mode Network (DMN) to shift slightly from being hyper-connected and insular to generally becoming more connected with other brain networks [40]. The DMN can be thought of as a mental autopilot responsible for our inner voice and sense of self. It is a brain network that functions during self-directed thought and introspection and consists of several brain regions [23]. One interpretation of this is that
states of rumination or depression are related to higher inter-network DMN activity, and psychedelics (or other 5HT treatment) restore the optimal level of connection between this network and others [40]. This reset results in a shift in consciousness and perception. This new state of perception and fluid sense of self have tremendous implications for mental illnesses like depression, which are characterized by rigid thought patterns. Psychedelics help break these patterns down, allowing patients to experience a shift in awareness. This can help reduce symptoms significantly, allowing individuals to reconnect with positive experiences.
A 2022 study by Johns Hopkins Medicine researchers showed that psychedelic treatments last up to a year and also have an immediate effect compared to the 4 to 12 weeks of traditional treatments for depression [41]. Psychedelic therapy could close the gap left by conventional treatments like SSRIs by proposing an option for treatment where SSRIs fail. Early research by doctors across a range of institutions found psychedelic-assisted therapy to be both practical and long-standing with only a few treatments [41]. These studies, among others, have been so successful that the FDA has named psilocybin a breakthrough therapy [19].
Psychedelics were first recognized in the United States in the 1960s and affiliated with the counterculture movement. Despite promising results for the clinical use of psychedelics to treat psychiatric patients, the growing use of recreational psychedelics tainted their public perception, leading the federal government to classify it as a Schedule 1 drug: drugs without approved medical use and with a high risk of abuse [19]. This stopped all research until about 15 years ago. Institutions started conducting smaller experiments on the use of psychedelics to treat mental disorders like treatment-resistant depression. Promising results have sparked a greater interest in the potential of psychedelics today [19].
As psychedelics gain popularity as viable mental health treatments, numerous ethical and practical questions about their potential clinical usage arise. Psychiatrists must be cognizant of informed consent, patient fragility, the distinctions between clinical and nonclinical psychedelic uses, and off-label psychedelic use [42]. Misuse of power has been documented in several healthcare settings, underlining the importance of clear guidelines and ethical training [43]. To provide informed consent, psychedelics must be culturally contextualized, with a focus on minimizing epistemic harm and ensuring that risks and benefits are communicated effectively [44]. Equitable access and economic feasibility of psychedelic drugs remain significant obstacles that necessitate additional consideration [42]. Open data and independent commissions are essential to ensure a safe and equitable distribution of these treatments [44].
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