5 Myths About Depression

Depression is a mental health disorder that affects millions of people worldwide. Despite its prevalence, misconceptions and myths about depression persist, in-turn, leading to misunderstandings, stigma, and barriers to care and support. By addressing some common myths about depression, we hope to contribute  to a more compassionate and informed dialogue surrounding depression, fostering a supportive environment.

Myth #1: Depression always disrupts everyday life.

Fact: While it is true that mental health disorders can have a profound impact on individuals’ lives, it is important to note that experiencing depression does not render a person incapable of engaging in daily activities. Contrary to the misconception that mental health disorders disrupt every aspect of life, individuals with depression can continue to maintain jobs, pursue hobbies and participate in meaningful relationships. It may require additional effort and support, but with quality treatment and self-care, individuals with depression can navigate their daily lives while managing their symptoms.

Myth #2: Every depression diagnosis is treated the same way.

Fact: There is no magical cure or one-size-fits-all solution for treating depression. Depression is a multifaceted condition with various underlying causes, including genetic predispositions, environmental factors, nutrition, hormones, etc. Comprehensive and individualized treatment plans that incorporate therapy, medication, self-care practices, and a strong support network can be effective in managing depression.

Myth #3: Depression is the same as feeling sad and you can just “snap out of it”.

Fact: Feeling sad is a normal and temporary emotional response to specific life events or circumstances. In contrast, depression is a distinct mood disorder characterized by persistent feelings of sadness, hopelessness, and a loss of interest in activities. Depression goes beyond fleeting moments of unhappiness; it encompasses a pervasive and long-lasting state of despair that significantly impairs daily functioning. Other symptoms of depression may include changes in appetite and sleep patterns, difficulty concentrating, fatigue, and thoughts of self-harm or suicide. Depression is not a condition that can be overcome by sheer willpower or determination. Telling someone with depression to “snap out of it” or “just think positive” can be harmful and dismissive of their struggles.

Myth #4: Depression is not a serious condition and will go away on its own.

Fact: Depression is a serious medical condition that requires attention and treatment. Without appropriate intervention, it can worsen over time and significantly impact an individual’s quality of life. Seeking professional help is vital to effectively managing depression, improving well-being, and developing effective coping strategies.

Myth #5: Antidepressant medication is the only effective treatment for depression.

Fact: While antidepressant medication can be beneficial for many people with depression, it is not the only option. Talk therapy is a widely recognized and evidence-based treatment for depression. It provides individuals with a safe and supportive environment to explore their thoughts, emotions, and experiences. Different therapeutic approaches, such as cognitive behavioral therapy (CBT) or interpersonal therapy (IPT), can help individuals with depression identify negative thinking patterns, develop healthier coping mechanisms, and work toward recovery. Talk therapy can be used as a standalone treatment or in conjunction with medication, depending on the severity of the depression and the individual’s unique needs.

Debunking the Simple Fix for Depression 

For decades, the narrative surrounding depression has centered on “chemical imbalances” in the brain. When the first antidepressants were discovered, it was unknown how they reduced depression symptoms. Since the medications had notable effects on neurotransmitters, Imbalances in serotonin, dopamine and norepinephrine were put forward as a hypothesis as to how they worked. This narrative was further developed with the introduction of Prozac, where the pharmaceutical industry leaned heavily into the idea, marketing Prozac and other serotonin reuptake inhibitors (SSRIs) as a fix for these hypothetical imbalances.

While the serotonin hypothesis was an amazingly successful marketing strategy, the research does not support the idea that depression is a simple serotonin deficiency that can be reversed with medication.

Delayed Medication Response

One of the first red flags around the idea that a deficiency in serotonin underlies depression comes from the delayed effects of antidepressant medications (Malhi, 2020). These medications alter serotonin levels quickly, starting with the first dose. Yet weeks often pass before mood symptoms improve. If low serotonin was the cause of depression, wouldn’t the first dose bring relief? Why are the benefits of antidepressants delayed? This delayed response is highly suggestive of other factors underlying depression symptoms.

Levels of Serotonin

Most of the body’s serotonin is produced in the gut and serotonin from the bloodstream can’t directly enter the brain (Hardebo,1980). Measuring blood levels of serotonin doesn’t accurately reflect the brain’s levels of the neurotransmitter. As a workaround, researchers have focused on measuring serotonin breakdown products in the cerebrospinal fluid, as these levels more directly reflect brain levels of the chemical.

A meta-analysis of the published human studies on the levels of different metabolites in spinal fluid found no correlation between depression and serotonin (Mousten, 2022). In other words, serotonin metabolite levels in depression were not reduced as compared to healthy controls. The idea that an overall deficiency of serotonin is the cause of depression symptoms was not supported.

Serotonin Transporters

In the brain, serotonin transporters clear serotonin from the synapse, decreasing serotonin activity. Blocking these transporters is the main mechanism of SSRI medications like Prozac and Paxil. If low serotonin levels are the cause of depression, transporter activity should be high in depressed patients. Surprisingly, studies reveal the exact opposite: transporter activity is often reduced in depressed patients (Kambeitz, 2015). The finding is counter to what we would expect if low serotonin levels were the cause of depression symptoms.

Serotonin Receptors

In order for serotonin to have a biochemical effect, it needs to interface with a receptor. Serotonin receptors come in multiple flavors. One of the most well-studied receptor types, the 1A receptor, inhibits serotonin release. Increasing the number of 1A receptors would decrease serotonin activity overall. However, research consistently shows a decrease in these receptors in depressed patients, again contradicting the idea that serotonin deficits underlie the condition (Wang, 2016).

A Multifaceted Puzzle

Mental health is a complex condition influenced by various factors, including nutritional deficiencies, hormonal levels, inflammation, genetics, chronic infections, toxicity and personal history. There is no “one-size” fits all treatment. While neurotransmitters can impact mood, the “chemical imbalance” narrative is overly simplistic and not well supported by the evidence.

Here at Blue Sky Medical, we move beyond the serotonin hypothesis and we pursue a more comprehensive understanding of depression. By delving deeper into the contributing factors, and taking a more personalized approach to treatment, we have identified more effective treatments that address the root causes of mental health conditions, not just the symptoms.

If you’re ready to learn about more personalized and effective functional treatments for depression and other mental health conditions, we encourage you to reach out to us by phone or email to learn more!


Hardebo JE, Owman C. Barrier mechanisms for neurotransmitter monoamines and their precursors at the blood-brain interface. Ann Neurol. 1980;8(1):1-31. doi:10.1002/ana.410080102

Kambeitz JP, Howes OD. The serotonin transporter in depression: Meta-analysis of in vivo and post mortem findings and implications for understanding and treating depression. J Affect Disord. 2015;186:358-366. doi:10.1016/j.jad.2015.07.034

Malhi GS, Bell E, Morris G, Hamilton A. The delay in response to antidepressant therapy: A window of opportunity?. Aust N Z J Psychiatry. 2020;54(2):127-129. doi:10.1177/0004867419900313

Mousten IV, Sørensen NV, Christensen RHB, Benros ME. Cerebrospinal Fluid Biomarkers in Patients With Unipolar Depression Compared With Healthy Control Individuals: A Systematic Review and Meta-analysis. JAMA Psychiatry. 2022;79(6):571-581. doi:10.1001/jamapsychiatry.2022.0645

Wang L, Zhou C, Zhu D, et al. Serotonin-1A receptor alterations in depression: a meta-analysis of molecular imaging studies. BMC Psychiatry. 2016;16(1):319. Published 2016 Sep 13. doi:10.1186/s12888-016-1025-0


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