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The Role of Dopamine in Major Depressive Disorder

(Image from Everyday Health)

Author: Whitney Elaine

Editors: Rayaan Dhar and Riyaa Sri Ramanathan

The most noticeable sign of Major Depressive Disorder (MDD) is a severe and prolonged low mood, profound sadness, or a sense of hopelessness. Sometimes, this mood can come off as irritability. Or the individual going through significant depression might not be able to take pleasure in activities that they regularly might. 

Major depression disorder is more than just a brief episode of melancholy or a "poor day." It’s characterized by symptoms that persist for at least two weeks, although these symptoms frequently last months or even years, significantly impacting how the person lives and how well the person can function (LeWine, 2022).

One of the most predominant theories that attempt to explain depression is that a chemical imbalance brings it on (Harvard Health, 2022). More recent explanatory theories claim otherwise, without discarding the role of SSRIs as effective interventions for a certain percentage of the population (Thomson, 2022). Selective serotonin reuptake inhibitors (SSRIs) are a class of drugs used to treat depression. Major depressive illness, anxiety disorders, and other psychological diseases are generally treated with them. The most often prescribed class of antidepressants, SSRIs (Mayo Clinic Staff, 2019) are effective in reducing the symptoms of mild to severe depression. They function by raising serotonin levels in the brain.

According to research, having too much or too little of a particular brain chemical does not necessarily cause depression. Instead, there are a myriad of other explanatory theories for depression, such as poor mood regulation by the brain, hereditary susceptibility, and traumatic life experiences. It is thought that a number of these factors combined to cause depression (Harvard Health, 2022).

Etymology of Depression

The etiology, or cause, of major depressive disorder is complex and includes several variables that are related to the prognosis of the disorder, including genetics, early life stress and trauma, anxiety, cognitive, socio-behavioral, and most recently discovered neurochemical components of an individual. The origins of depression's onset are as varied as the disorder's symptom clusters, ranging from hereditary vulnerability to early trauma and stress to co-occurring neurological illnesses (Remes et al., 2021).

The environmental element also contributes to depression because the risk of developing depression is increased by unfavorable social conditions, such as unemployment and unstable economies, which are key social determinants of health. Recent studies suggest that additional physical environmental factors, such as noise and chemical pollutants, may also have an effect on neurobiology and affect the risk of depression, especially in those who are genetically predisposed to it (Van Den Bosch & Meyer-Lindenberg, 2019).

There are many signs of depression. We highlight a few below.


Anhedonia is described in the DSM-V, or the fifth version of the Diagnostic and Statistical Manual of Mental Disorders, as “lack of enjoyment from, engagement in, or energy for life’s experiences; deficits in the capacity to feel pleasure and take an interest in things” (Watson et al., 2019).

Research has, for years, pointed to the role that dopamine plays in mood stability. Dopamine is a neurotransmitter in the brain that mediates pleasure. 

Anhedonia has been linked to imbalances in neurotransmitters, which are chemical messengers secreted by nerves. The reward-related neurotransmitter dopamine is highly expressed in the nucleus accumbens and is implicated in reward pathways. Higher anhedonia intensity correlates with decreased dopamine expression in the ventral striatum, part of the brain that plays a vital role in decision-making and reward-related behavior such as addiction and learning (Brookshire, 2021). Therefore, it is crucial to identify any potential disruptions in the neural circuitry that may be causing this symptom. It is important to remember that anhedonia encompasses complex reward-related deficits seen in MDD or other neuropsychiatric disorders, such as disruption of the anticipation, motivation, and decision-making processes involved in obtaining a reward (Der-Avakian & Markou, 2012).

Anhedonia has been connected to issues with the dopamine and reward systems in general (Wise, 2008). The dopamine system affects motivational arousal, reactivity to conditioned incentive cues and reward prediction. Dopamine is also required to attribute incentive salience to motivational stimuli, turning the perception of liking a reward into a wanted incentive. This idea aligns with the disruptions of the motivation to seek pleasurable experiences described in people with MDD. (Bromberg-Martin et al., 2010). Reduced activity in the ventral striatum, a part of the brain involved in the reward system, is one of the anatomical causes of anhedonia. The nucleus accumbens, known as the "pleasure center," is housed in the striatum.

The prefrontal cortex, which is involved in planning and personality expression, may exhibit an abnormal increase in activity in addition to the loss of activity in the ventral striatum in anhedonia. Both the insula, which is assumed to play a key role in consciousness and self-awareness, and the amygdala, which processes emotions and is involved in decision making, are other areas of the brain that are dysregulated in anhedonia (Corral-Frías et al., 2015).

Many interventions have been tried and reviewed over the years; a few of the most popular and successful ones include:

1.Cognitive Behavioral Therapy (CBT)

One biological aspect that has lately been investigated as a potential cause of depression is the altered activity of specialized brain nerve cells called serotonin receptors, which are at decreased levels in depressed individuals.

Serotonin is a hormone that is known to affect mood naturally, and depression treatments that try to raise serotonin levels are crucial to improve symptoms. Serotonin levels in the brain may be increased, and depressive symptoms may improve with cognitive behavioral therapy (CBT), which teaches techniques to change attitudes and behaviors that contribute to depression (, 2008). The foundation of CBT is that your thoughts, feelings, bodily sensations, and behaviors are interconnected and that having unfavorable ideas and feelings can keep you stuck in unfavorable patterns. By dividing up significant problems into smaller ones, cognitive behavioral therapy (CBT) seeks to help you cope with them more constructively. You are shown how to alter these unfavorable tendencies to feel better. CBT addresses your current difficulties rather than concentrating on problems from the past, in contrast to specific other talking treatments, and searches for doable strategies to elevate your mood (Kaur, 2022).

2. Exercise

Exercise triggers a biochemical chain of events with various positive health effects, including decreasing blood pressure, preventing diabetes and heart disease, and enhancing sleep. Endorphins, the body's feel-good chemicals, are released during high-intensity exercise, giving rise to the "runner's high" that joggers claim. However, sustained low-intensity exercise has the greatest benefits for most people. Such activity triggers the production of proteins called neurotrophic or growth factors, which lead to the expansion and development of new connections between nerve cells (Harvard Health, 2021). The improvement in brain function is what helps alleviate depressive symptoms. "In people who are depressed, neuroscientists have noticed that the hippocampus in the brain region that helps regulate mood is smaller. Exercise supports nerve cell growth in the hippocampus, improving nerve cell connections, which helps relieve depression," explains Dr. Miller (Harvard Health, 2021).

3. Getting Enough Sunlight

When exposed to sunlight, your brain produces more serotonin, a hormone linked to mood enhancement, relaxation, and improved concentration. On the other hand, as night falls, the absence of light causes the brain to produce melatonin, a hormone that promotes relaxation and sleep. Your serotonin levels will drop if you don't receive enough sun exposure, as in the winter, which can increase your risk of developing seasonal affective disorder (SAD), a form of depression brought on by the changing of the seasons. It improves mood by increasing serotonin levels, also known as the "happiness hormone," and makes you feel peaceful but awake (Pathways Home Health and Hospice, 2018). More melatonin is produced at night, which enhances sleep, synchronizes your biological clock, and reduces stress. The more exposure you have to the sun during the day, the less prone you are to depression and bipolar disorder.

4. Behavior Therapy

Contrary to CBT, behavior therapy does not attempt to alter attitudes and beliefs. Behavior therapy strongly emphasizes promoting rewarding, enjoyable, or fulfilling behaviors. It seeks to break the cycles of avoidance, disengagement, and inactivity that exacerbate depression (Schimelpfening, 2022). 

When investigating strategies to treat or alleviate the symptoms of depression, the nature vs. nurture argument always seems to spark a grand debate. However, it is neither nature nor nurture alone. The specifics of how much each element contributes to the final result are still up for debate. To better understand depression, Gerald Haeffel and colleagues at the University of Notre Dame looked at both genes and the environment. Dopamine has long been speculated to be a factor in depression. A specific gene has been discovered that codes for a dopamine transporter, which eliminates excess dopamine from the synaptic cleft—the area between connecting neurons—and has been linked to depression (Haeffel et al., 2008). 177 male teenagers from a Russian juvenile detention center were the subject of Haeffel's study. They were checked for the particular dopamine transporter gene previously linked to depression, given a depression assessment, and given a questionnaire to ascertain their mother's parenting style. The findings indicated that neither the dopamine transporter gene alone nor harsh parenting styles might predict depression. However, a person was more likely to have depression and suicidal thoughts if they had both of these factors (Haeffel et al., 2008). In addition to being the first to substantiate the idea that a dopamine transporter gene contributes to sadness, this work is revolutionary because it advances our understanding of how nature and nurture interact (Dingman, 2008.).

Sleep Disturbances

An association exists between depression and having problems sleeping. In other words, having depression increases the likelihood that a person may have sleep issues, and not getting proper rest may contribute to the development of depression. It can be difficult to determine whether sleep problems or depression began initially because of their intricate relationship (Newson & Dimitriu, 2023).

We also need to take into consideration the effect that dopamine has on both sleep and mood, as they can intersect.

Dopamine has the ability to block the actions of norepinephrine, a neurotransmitter involved in the production and release of melatonin, in the pineal gland. The pineal gland produces and releases less melatonin under the effect of dopamine, leading the person to become more alert (González et al., 2012). Norepinephrine and dopamine's roles in depression are intricately linked to one another and to the ways antidepressants work. 

Over the past 50 years, various aspects of these neurotransmitters' functions have been studied (Nutt, 2002). Animal studies, human biology and postmortem studies, and inferences from pharmacological activities seen in antidepressant trials are among the methods used to understand their roles in depression (Slattery et al., 2004). Few conclusive findings from biological and postmortem studies have been obtained, but some give hints about the function of particular metabolites. Studies on cerebrospinal fluid metabolites, including the homovanillic acid metabolite of dopamine in depression, show low levels in various types of the condition. Using PET and SPECT tracers sensitive to synaptic dopamine levels, multiple groups have discovered evidence for lower synaptic dopamine, demonstrating the rapid advancement of brain imaging to research dopamine's role in depression (Slattery et al., 2004). Making assumptions about dopamine and norepinephrine in depression based on a patient's reaction to antidepressant medication is yet another approach that has been used. For instance, it is generally known that amphetamine-induced mania is likely caused by an increase in dopamine release, either alone or in combination with norepinephrine. It has also been demonstrated that other stimulants that release dopamine, particularly cocaine, can cause mania. Reserpine, an antihypertensive, was utilized in research to simulate human depression (Coupland et al., 1992). Depression can also be brought on by clonidine, another antihypertensive drug that lowers norepinephrine through a different method.

Substantial research has also shown that several antidepressants, particularly tricyclic antidepressants (TCAs) and some of their derivatives, impact norepinephrine and, to a lesser extent, dopamine (Nutt D.J.,2006). Norepinephrine is thought to influence the body's stress response, which also controls blood pressure, sleep, and alertness. Dopamine is a crucial component of movement and influences motivation, reality perception, and the capacity for enjoyment. Because their mode of action differs from that of the other known antidepressant classes, these drugs are sometimes referred to as atypical antidepressants. Major depressive disorder can be treated with Norepinephrine-Dopamine Reuptake Inhibitors (NDRIS), especially in those who do not respond well to SSRIs or who are unable to endure their adverse effects (Wagener, 2022). NDRIs are a class of drugs used primarily for the treatment of depression. NDRIs are antidepressant medications that block the action of specific transporter proteins, increasing the amount of active norepinephrine and dopamine neurotransmitters throughout the brain (Wagener, 2022). Norepinephrine and dopamine cannot be transported by NDRIs back into the brain cells that released them. As a result, the brain has access to more active neurotransmitters, which may eventually result in modifications that lessen depressive symptoms  (Wagener, 2022). Sleep deprivation reduces the availability of specific dopamine receptor subtypes (Volkow et al., 2008). Because there are fewer receptors, dopamine lacks receptors to connect to, making it harder to stay awake.

Social Withdrawal 

Neurotransmitters like dopamine and endorphins and neuropeptides like oxytocin and vasopressin play a key role in fostering affiliative and social behavior (Vitale & Smith, 2022). Additionally, social rejection and isolation raise the levels of stress-related neuropeptides such as glucocorticoids and corticotropin-releasing hormone, which can cause anxiety and depressive-like behaviors as well as other sociality-altering effects. 

According to a study, receiving a social snub results in a chain reaction of emotional and cognitive effects. Anger, anxiety, despair, envy, and grief are all worsened by social rejection. According to DeWall in a review (DeWall & Bushman, 2011), it decreases performance on demanding intellectual tasks and can also lead to violence and poor impulse control. Rejection also affects one physically. Persons frequently feel excluded have lower sleep quality and less effective immune systems than those with strong social relationships (Weir, 2012).

The neurotransmitter dopamine, produced in the midbrain ventral tegmental area and released into the ventral striatum and higher-order cortical regions, drives social interaction neurobiologically. Forming and maintaining social interactions is satisfying and beneficial due to this process and its interaction with the neuropeptides oxytocin and vasopressin released during social contact and intimacy (Baskerville & Douglas, 2010). 

However, loneliness can make people more sensitive to social isolation, affecting how they feel about it and how they perceive others (National Academies Press- US, 2020). People with a history of trauma are correlated with those who have a history of social isolation as self-protection strategies. Therefore, the sense of isolation might result from functional adjustments in the parts of the brain responsible for receiving social information, managing and expressing emotion, and valuing social relationships (Vitale & Smith, 2022).

Nevertheless, research shows that people who live alone have poorer health outcomes and shorter life longevity than those who live with others. Regardless of compensatory neural pathways (social isolation in the case of traumas), it could be that social interaction aids a healthier regulatory neurotransmitter balance in the brain, expressed first and foremost through human communication and vice versa. As is the case of pet presence’s benefits in the life of people who live alone (Martinez-Caja et al., 2022).


Substance Abuse

People who are recovering from substance use disorders and experiencing post-acute withdrawal syndrome have lower levels of dopamine (PAWS). Because the brain cannot produce dopamine on its own, it must rely on external sources (Meghan, 2022). When a substance is used repeatedly over an extended period, the brain's dopamine receptor count decreases to compensate for the system's increasing dopamine levels (US Department of Health and Human Services, 2016). Addiction is affected in two different ways by this decrease in dopamine receptors. First, there is a link between impulsive behavior and decreased dopamine receptors in the substantia nigra, which is a component of the brain's reward system along with the nucleus accumbens and ventral tegmental area (Adinoff, 2004). Impulsive behavior has been linked in laboratory studies to increasing compulsive drug self-administration (Kozak et al., 2018).

Anhedonia is a side effect of decreased dopamine receptors. When a user experiences depressive symptoms of anhedonia, particularly when they lack self-control, they may react by using drugs to feel pleasure once more (Hatzigiakoumis et al., 2011). In the case of substance use, this happens, as well as in the absence of it.

As the harmful effects of long-term drug use start to erode prefrontal cortex grey matter, users' capacity to logically weigh consequences is compromised due to impaired executive function (Connolly et al., 2013), and the prefrontal cortex's function in controlling the brain's reward system is also diminished (Goldstein & Volkow, 2011).


Similar to how drugs and alcohol produce dopamine, sugar causes the body to generate a lot of it before levels crash temporarily. Drug-like damage to the receptors caused by the instability impairs the body's ability to control dopamine levels (Rada et al., 2005). Blood sugar, often known as glucose, is the most basic type of carbohydrate. Additionally, it is necessary for human survival. Every cell in the body uses glucose as its primary energy source, including the brain. The brain maintains a balanced state by an even supply of glucose (Rada et al., 2005).

Consuming too much-added sugar may cause irritability to increase as well as energy peaks and valleys. Although eating sugar may feel good initially, it will lower blood glucose levels. This is what has such a profound impact on the body and psyche. However, sugar can be incredibly addictive for some people. The mesolimbic dopamine pathway in the brain provides a reward when sugar is consumed, increasing mood. When pleasure is about to hit, the dopamine system kicks in (Bell, 2020). Because they are added sugars, the body cannot in any way benefit from them. Chemical alterations in the body will result in a large intake of them. These take place to avoid overstimulation, so the body might crave more sugar in the future to maintain the same elevated mood (Bell, 2020).

The neurotransmitter dopamine regulates reward signaling in the brain and is associated with feelings of pleasure. Any dysfunction in its signaling may result in a depressive state, resulting from a down-regulation of dopamine production and/or activity (Belujon & Grace, 2017). Sugar is one of many compounds that stimulate the production of dopamine in the brain. However, animal research has demonstrated that chronic sugar consumption results in a down-regulation of the dopamine response and may lead to depressive symptoms (Levy et al., 2015).


Foods high in saturated fat, such as palm oil and animal fat, can desensitize dopamine receptors and are associated with a reduced reward response, which results in a lack of drive and desire (McCabe, 2021). Both caffeine and alcohol in excess can result in abnormally high dopamine levels, which can result in the downregulation of dopamine receptors (Volkow et al., 2015).

(Image Source: Pinch an Inch)

It is recommended that caffeine intake for healthy persons not to exceed 400 mg per day. That is comparable to 10 cans of cola or four 8-ounce cups of brewed coffee. Teenagers should keep their daily caffeine intake to under 100 mg (approximately two cans of cola or one 8-ounce cup of coffee). The following groups of people should avoid caffeine entirely: children, individuals who take anti-anxiety medications, women who are nursing or pregnant, people with high blood pressure or heart disease (Hortonj, 2022). 

People under the age of 18, pregnant people, and breastfeeding people should not consume any alcohol to avoid harm to themselves and/or their unborn children (Australian Government Department of Health and Aged Care, 2022). Healthy men and women should consume no more than ten standard drinks per week and no more than 4 standard drinks on any given day to limit the risk of harm from alcohol-related disease or injury. (How Alcohol Affects Your Health, 2023). Your risk of alcohol-related harm decreases as you consume less alcohol. 

Additionally, high consumption of fruits, vegetables, whole grains, fish, olive oil, low-fat dairy products, and antioxidants, along with a reduced intake of animal products, was found to be connected with a lower incidence of depression (Tello, 2020).

High Cortisol Levels

Cortisol is a hormone that the body produces in response to stress. Even though the body needs cortisol to survive, a high concentration can wreak havoc on neurotransmitter receptors. In other words, it prevents them from getting the dopamine-based messages (Thau, 2022). The body uses cortisol as a temporary remedy when dopamine levels are low. It gives the metabolism the energy it needs. However, if the body doesn't reduce the cortisol it produces, it becomes reliant on it and produces less dopamine. Although the alternative is a safety precaution, it has harmful side effects such as weight gain, high blood pressure, and other ailments (Baik, 2020). 

A stress response is triggered by any physical or psychological factors that disturb equilibrium. It is the result of physiological and behavioral changes brought on by exposure to stressors, which are referred to as stressors. The sympathetic-adreno-medullar (SAM) axis, the hypothalamus-pituitary-adrenal (HPA) axis, and the immune system are all activated during a stress response, which is regulated by a complex interaction of neurological, endocrine, and immunological systems (Chu, 2022). The body's physiological reactions to trauma and invasive surgery, for example, serve to prevent additional tissue damage. The stress response is initially adaptive, preparing the body to face the obstacles given by an internal or external environmental challenge (stressor). However, the stress response becomes maladaptive and harmful to physiology if the exposure to a stressor is actually or perceived as intense, repetitive (repeated acute stress), or prolonged (chronic stress). For instance, exposure to chronic stressors can result in maladaptive reactions such as depression, anxiety, cognitive impairment, and heart disease (Ketchesin et al., 2017).

Over time, sustained stress can produce an excess of stress hormones, which can cause dangerous bodily imbalances. Increased levels of stress hormones have been associated with memory loss, impaired immune systems, high blood pressure, and heart disease. Furthermore, when adrenaline constantly pumps, blood vessels may constrict, impairing vision and hearing (Ketchesin et al., 2017).

The brain's capacity to control the amount of stress hormones declines with age. This causes hormonal imbalances and higher stress levels in older persons, in addition to contributing to hormonal abnormalities. Chronic stress increases a person's propensity to lead an unhealthy lifestyle, which leads to more health issues. Put it another way, stress speeds up aging, and aging speeds up stress (Yaribeygi et al., 2017).

Stress has a biological impact on the body as well. Over time, telomeres, which serve as protective "caps" on the ends of DNA chromosomes, will inevitably wear out. However, scientists have discovered that when the body is under stress, the process might quicken. Telomeres that are too short no longer provide sufficient protection for the cells. Parkinson's disease, diabetes, cardiovascular disease, and cancer have all been associated with shortened telomeres (Rizvi et al., 2015).

Immune System and Inflammation

Depression may be exacerbated by the symptoms of chronic pain, being confined to the house or bed, being unable to engage in our favorite activities, and ongoing concerns about one’s sickness. Researchers discovered that poor sleep, a lack of energy, and physical inactivity can result in mood swings and depression. The results contradict the widely held belief that depression promotes inactivity and suggest that the converse may be true ( Wein, 2019). Regular exercise may reduce anxiety and depression by releasing feel-good endorphins, endogenous cannabinoids, and other naturally occurring brain chemicals that can improve your sense of well-being. One can also try putting anxieties aside to break the cycle of pessimistic thinking that feeds depression and anxiety.

Certain medical disorders can also cause depression. These consist of degenerative neurological disorders, cardiovascular diseases, epilepsy, brain tumor, metabolic conditions such as vitamin B12 and folate deficiency, endocrine disorders (such as thyroid problems, diabetes), and some forms of cancer (e.g. pancreatic and lung cancer).

Other experts are investigating the potential link between your immune system, inflammation, and depression (Toups, 2018). Pathways of interaction are symbiotic. For instance, a Taiwanese study found that those with allergies and asthma were more likely than people without allergies to experience a mental disease like depression (Tseng et al., 2018). Carmine Pariante, professor of biological psychiatry at King's College in London and the study's principal investigator, said that roughly one-third of persons with depression may be affected by an immune system that has been activated by long-term stress (King’s College London, 2023). The new theory of depression and Alzheimer’s says that such conditions are manifestations of a compromised immune system in the brain. “Most of the time in modern society, stress wounds you psychologically, but the [immune] mechanism is still there, so you have … chronic psychosocial stress that activates your immune system,” Pariante previously said. “Then the immune system that’s chronically activated affects the brain and imbues a change in emotions and behavior that resembles depressive symptoms” (King’s College London, 2007).

There is strong evidence demonstrating that stress and depression have a significant negative impact on people's well-being, primarily by impairing the immune system's normal function and causing low-chronic inflammation, which favors the development of infections, metabolic diseases, and even cancer (Cañas-González et al., 2020). The host defense hypothesis suggests that depression is a component of "sickness behavior" or one part of a more comprehensive coordinated adaptive response to infection or tissue injury (Shattuck & Muehlenbein, 2015). Pro-inflammatory cytokines are produced by innate immune cells, which then influence the brain through the endocrine, circulatory, and neurological systems to encourage disease behaviors (such as anorexia). It is believed that depression is brought on by illness or injury and that depression promotes energy management and conservation to aid innate or adaptive immune activation in response. Additional benefits include the reduction in risk of infection transmission to loved ones and kin through social withdrawal and the reduction in risk of infection or injury during times of higher immune activation through risk aversion (Shattuck & Muehlenbein, 2015).

It is also suggested that psychosocial stressors, many of which involve interpersonal loss or conflict, social rejection, or both, and significantly increase the risk of depression throughout life, up-regulate innate immune system components involved in inflammation because, throughout evolutionary history, these stressors consistently predicted increased risk of pathogen exposure (for example, via wounding or ostracism) (Stieglitz et al., 2015). This contributes to the explanation of host defense for the inflammatory nature of psychosocial stress (actual, predicted, or imagined). The host defense hypothesis, in contrast to the other adaptive hypotheses discussed above, makes the unique predictions that depression is linked to morbidity indicators (such as inflammation) and that depressed people have more robust immune responses to challenges than non-depressed people.

Predisposing Factors

Hereditary and genetic factors 

The involvement of genes in depression may be epigenetic, which means that while you are born with genes that increase your risk of the disorder, they only "switch on" and produce depression when you are exposed to a stressor or environmental trigger (Pember, 2017). Epidemiological studies show that hereditary factors account for 30–40% of bipolar disorder cases. Environmental factors have a more significant impact on the development of depression. Since resilience and stress resistance are common, even though some stress may be experienced during the perinatal or embryonic period, having a genetic predisposition to mental disorders does not guarantee that a mental disorder will manifest. However, a mental disorder is triggered when a person's ability to recover from stresses experienced during puberty is compromised due to a genetic predisposition to disorders (Nabeshima & Kim, 2013).

The fact that many diseases emerge when the wrong kind of epigenetic marks are introduced or are added at the wrong time or in the wrong place illustrates the significance of epigenetics in maintaining normal development and biology. Concerning epigenetics, the role of genetic and environmental factors in the development of depression was examined (Nabeshima & Kim, 2013).


The body's systems are governed and controlled by various chemicals, including hormones. Thyroid hormones and estrogen, two hormones that assist in the regulation of neurotransmitters, appear to play a significant impact in depression in some individuals (Kamran et al., 2022). For instance, studies have revealed that fluctuations in female estrogen levels (such as those that occur right after childbirth or after menopause) may raise the risk of depression. According to an additional study, men with low testosterone may also experience more depression (Sander et al., 2021). 

Changes in Brain Structure 

Scientists found structural and functional brain alterations in particular persons with clinical depression based on brain imaging investigations. This may indicate that some parts of the brain are smaller than usual or otherwise altered, including those that control how one perceives rewards and how one processes memories. But because the brain is so complicated, it is still unclear what these changes in the brain might mean in terms of depression (Zhang et al., 2018).

Sports, exercise, and other physical activities are recognized to have a variety of positive effects on both physical and mental health. Thus, regularly practicing such techniques would improve practitioners' moods while promoting emotional well-being and lowering symptoms of anxiety and depression (Philippe et al., 2021). In this regard, mindfulness meditation can improve the health of those who practice it (Smith, 2023). Physical exercise and mindfulness practices are meant to enhance various aspects of their practitioners' emotional, mental, and/or physical well-being. Studies show that even small quantities of exercise have a significant impact. Regardless of your age or fitness level, you can learn to use exercise as a potent tool to manage mental health issues, enhance your energy and attitude, and get more out of life (Robinson, 2023).


Depression is a prevalent mental illness. According to estimates, the condition affects 5% of adults worldwide. Consistent sorrow and a lack of interest in formerly fulfilling or joyful activities are its defining traits. Dopamine-containing circuits in the central nervous system play a role in regulating motivation, psychomotor speed, concentration, and the capacity for pleasure. Impairment of these functions is a hallmark of depression. This neurotransmitter's imbalance is thought to play a significant role in the onset of depression, according to researchers. A dopamine deficiency, among other neurotransmitters, can result in depression symptoms, such as apathy and hopelessness, by altering the way our brain's neural pathways are wired, how we navigate through our environment, and our relationship with ourselves. Many psychosocial factors can further influence dopamine regulation in the brain, which in turn can play a massive role in the potential development of depression in a specific individual.

Fortunately, as society continues to change and evolve, our scientific understanding of the link between dopamine and major depressive disorder evolves as well. Treatments ranging from antidepressants to something as simple as going on daily walks continue to be discovered and improved, which, despite much more work needing to be done, creates hope for a tomorrow where people will not have to fall victim to the circumstances they have been subjected to. Major depressive disorder is not a dead end. The most minor changes to one’s lifestyle can make the most significant differences in one’s overall quality of life - and it all begins from within.


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