Two Conditions, One Nervous System

Before comparing anxiety and depression, it helps to be precise about what each one is. Neither is a single thing, and neither is a mood. They are patterns of symptoms that cluster together, persist over time, and interfere with a person's life.

Anxiety is not the same as being anxious

Fear is a normal and useful response. It turns attention toward a threat, speeds up the heart, tenses the muscles, and narrows thinking toward escape. Anxiety is what happens when that system runs ahead of reality, anticipating threats that have not arrived yet. In its ordinary form, anxiety is the knot in the stomach before a job interview. It is proportionate, it fades, and it does not stop you.

An anxiety disorder is different in degree and in kind. The fear or worry is out of proportion to the situation; it persists, and it leads a person to organize their life around avoiding it. The National Institute of Mental Health groups the anxiety disorders to include generalized anxiety disorder, panic disorder, social anxiety disorder, specific phobias, agoraphobia, and separation anxiety disorder, each with its own characteristic focus of fear.¹

The main anxiety disorders at a glance

ConditionCore experienceTypical avoidanceGeneralized anxiety disorderChronic, hard to control worry across many areas of life, with restlessness, muscle tension, and poor sleepReassurance seeking, over-preparing, procrastinationPanic disorderRecurrent unexpected panic attacks and persistent fear of the next oneAvoiding places or situations where escape would be hardSocial anxiety disorderIntense fear of scrutiny, embarrassment, or negative judgmentAvoiding speaking, eating, or performing in front of othersSpecific phobiaMarked fear of a particular object or situation, such as heights or needlesAvoiding the object itselfAgoraphobiaFear of situations that might be difficult to leave or where help may not comePublic transport, crowds, open spaces, being outside alone

What these share is a threat detection system that is doing its job too well. The person is not irrational. Their body is responding to a danger signal that never fully turns off.

Depression is not the same as being sad

Sadness is a normal response to loss, and it usually moves. Depression, by contrast, is a sustained episode. The World Health Organization describes a depressive episode as a depressed mood, or a loss of interest and pleasure, lasting most of the day, nearly every day, for at least two weeks, alongside changes in sleep, appetite, energy, concentration, and self-worth.²

The most useful contrast is this. Anxiety is overactivation of a threat system. Depression is underactivation of a drive and reward system. The things that normally pull a person forward, curiosity, appetite, connection, ambition, play, tend to stop generating any pull at all.

The two core symptoms of a major depressive episode

Clinical criteria for major depressive disorder require at least one of the following two symptoms, present for two weeks or more: depressed mood for most of the day, nearly every day, or markedly diminished interest or pleasure in almost all activities. The remaining criteria cover sleep, appetite, energy, movement, concentration, worthlessness or guilt, and thoughts of death. A clinician looks for five or more symptoms overall, and for impairment in functioning.²

How common are they?

These are not rare conditions. They are among the most common health conditions of any kind.

Several patterns repeat across the data. Anxiety disorders are more common in women than in men, with past year prevalence in the United States at roughly 23 percent for women and 14 percent for men.¹ Depression is about 1.5 times more common among women than among men.² Both are more common in younger adults than in adults over 60, though they affect every age group.¹

The burden is not measured only in symptom counts. Among adults with any anxiety disorder in the past year, about 22.8 percent reported serious impairment and 33.7 percent reported moderate impairment on a standard disability scale.¹ Depression is a leading cause of years lived with disability worldwide, and it is strongly associated with suicide risk.²

Why the categories are blurrier than they look

Diagnostic manuals present anxiety disorders and depressive disorders as distinct categories, and that is useful for communication, research, and insurance. But the categories are cut across a continuous landscape of distress. Researchers have long observed that the same person can meet criteria for several anxiety disorders at once, that symptoms shift over time, and that the boundary between a severe anxiety presentation and a depressive presentation is often a matter of which symptom currently dominates.

This is not a flaw in the person. It is a reflection of how the underlying systems are wired. The threat system and the reward system are not separate machines in separate rooms. They share circuitry, they influence each other, and the stress response touches both. That is the subject of parts 2 and 3.

Anxiety and depression are best understood less as two diseases and more as two ways the same emotion regulation machinery can fail.

What this means practically

• A diagnosis is a description of a pattern, not an explanation of a cause.
• Two people with the same diagnosis can have quite different biology and quite different histories.
• If you have one of these conditions, having the other one later is common rather than a personal failing.
• Treatment often targets processes that both conditions share, which is why the same therapy can help with either one.

Key takeaways

• Anxiety disorders center on a threat system that is stuck on, with fear and avoidance out of proportion to the situation.
• Depressive disorders center on a drive and reward system that has gone quiet, with low mood or loss of pleasure as a core symptom.
• Both are common, both cause real impairment, and both are treatable.
• The diagnostic categories are useful tools, but the underlying biology is shared, and the boundaries are softer than the labels suggest.

References and further reading

1. National Institute of Mental Health. Any anxiety disorder. Prevalence and impairment data from the National Comorbidity Survey Replication. nimh.nih.gov/health/statistics/any-anxiety-disorder
2. World Health Organization. Depressive disorder (depression). Fact sheet. who.int/news-room/fact-sheets/detail/depression
3. National Institute of Mental Health. Major Depression. Annual prevalence among U.S. adults. nimh.nih.gov/health/statistics/major-depression
4. National Institute of Mental Health. Anxiety Disorders. Overview and links to condition specific pages. nimh.nih.gov/health/topics/anxiety-disorders
5. National Institute of Mental Health. Statistics. Index of prevalence and treatment data. nimh.nih.gov/health/statistics

← Series overview: Anxiety vs. Depression: A Six Part Series Next Part 2: Why They Travel Together →

Anxiety vs. Depression is an educational series. It is not medical advice, and it cannot replace an evaluation by a qualified clinician.

Why They Travel Together

If you have ever wondered why the same person so often reports both anxiety and depression, the answer is not bad luck. Co-occurrence between these conditions is one of the most reliably replicated findings in mental health research.

The headline numbers

A systematic review and meta-analysis of the comorbidity between mood and anxiety disorders pooled data across a large body of studies and found strikingly high overlap. Cumulatively, about 72 percent of lifetime anxiety cases had a history of depression, and about 48 percent of lifetime depression cases had an anxiety disorder, with odds ratios between 4.7 and 5.5.¹

For current, rather than lifetime, co-occurrence, the picture is similar. In a large clinical sample, 45 to 67 percent of people diagnosed with a unipolar depressive disorder met criteria for at least one concurrent anxiety disorder, and 30 to 63 percent of people diagnosed with an anxiety disorder met criteria for concurrent unipolar depression.² In primary care the overlap is even denser. One review reported that more than 75 percent of patients diagnosed with depression in a primary care setting also had a current anxiety disorder.³

Some pairings are tighter than others

Not every combination is equally strong, and the numbers are worth looking at closely because they shape how clinicians think about assessment. In the meta-analysis, the association between broadly defined depressive disorder and generalized anxiety disorder was the strongest pairing, with a crude odds ratio of 13.8 (95 percent confidence interval 9.9 to 19.3) and an adjusted odds ratio of 11.7 (95 percent confidence interval 5.2 to 26.3) for period prevalence.¹

At the other end of the range, the association between depression and specific phobia was weaker, with an adjusted odds ratio of 2.9. Social phobia sat in the middle.¹

Why the depression and generalized anxiety pairing is so tight

Generalized anxiety disorder is defined by chronic, diffuse, difficult-to-control worry, and it comes with restlessness, fatigue, difficulty concentrating, irritability, muscle tension, and disturbed sleep. Depression is defined by low mood, loss of interest, fatigue, difficulty concentrating, and disturbed sleep. Four symptoms overlap in the criteria themselves. It should not be surprising that the two conditions find each other.

The mixed anxiety and depression category

Clinicians have long recognized a presentation that sits in the space between the two diagnoses, where a person has symptoms of both but does not clearly meet full criteria for either. Surveys of patients in primary care have reported the prevalence of this mixed anxiety and depression presentation to be in the range of 1 to 5 percent.³

This matters because people in that middle zone often get less attention than people who neatly fit one category, even though their distress and impairment can be comparable. If your experience feels like a blend rather than a match, that is a recognized clinical pattern, not a sign that you are describing it wrong.

Each one raises the risk of the other

The relationship is not just simultaneous. It is directional across time. A meta-analysis of 66 longitudinal studies covering 88,336 people examined how anxiety and depression predict each other prospectively and found several clear results.⁴

• Anxiety symptoms predicted later depressive symptoms, with a correlation of about 0.34.
• Depressive symptoms predicted later anxiety symptoms, with a correlation of about 0.31.
• Having any diagnosed anxiety disorder predicted later depressive disorders, with an odds ratio of 2.77.
• Having any depressive disorder predicted later anxiety disorders, with an odds ratio of 2.73.

In other words, the risk runs both ways and the strength is close to symmetric. The authors concluded that for most anxiety and depressive disorders, the relationship is genuinely bidirectional, with one exception worth noting. Depressive disorders predicted later social anxiety disorder and specific phobia more strongly than the reverse, which led the authors to suggest that depression may sometimes act as a precursor for those particular anxiety conditions.⁴

A separate analysis of community surveys from 27 countries found that among people with major depression, the risk of developing generalized anxiety disorder remained roughly seven times higher even after 15 years, with a hazard ratio of 6.6 (95 percent confidence interval 5.7 to 7.7).¹

Anxiety and depression are not competitors for the same diagnosis. Having one meaningfully raises your odds of the other, in both directions, over years.

Four explanations that are probably all partly right

1. Shared symptoms inflate the overlap

Some of the co-occurrence is built into the definitions. Fatigue, concentration problems, and sleep disturbance appear in the criteria for both. When two checklists share items, people will score on both more often than chance alone would predict. This is a real effect, but it cannot account for the full picture, because the longitudinal associations remain after researchers account for overlapping items.

2. A shared underlying vulnerability

The tripartite model of anxiety and depression, proposed by Clark and Watson, argues that the two conditions share a common factor usually labeled negative affectivity, and differ mainly in two other respects. Anxiety is distinguished by physiological hyperarousal. Depression is distinguished by low positive affect, meaning an absence of pleasure, interest, and energy.⁵

That framework explains a great deal. Two people can both score very high on general distress and still look quite different, because one is flooded with arousal and the other is flat and withdrawn. It also explains why treatments that target negative affectivity broadly tend to help with both conditions, which is the subject of part 5.

3. Behavioral cascade

Avoidance links the two conditions in a very concrete way. Anxiety drives a person to avoid the thing they fear. Avoidance brings short term relief but shrinks their world. Over time, the loss of activities, relationships, and accomplishments that follow from that shrinking world removes the very sources of reward that protect against depression. Research has shown that avoidance mediates the relationship between anxiety and depression over periods as long as a decade.⁴

The reverse cascade also happens. Depression saps energy and motivation, which makes it harder to face feared situations, so anxiety gets worse. Rumination, the repetitive and unproductive replaying of worries and regrets, is common to both and can act as a hinge between them.

4. Shared biology

The stress response system, the same circuitry that governs fear learning, and overlapping genetic vulnerabilities all cut across the diagnostic boundary. Part 3 covers this in detail.

Why comorbidity matters clinically

Overlap is not a technicality. It changes outcomes. Research on anxiety disorders has found that comorbid depression, rather than comorbid anxiety, predicts poorer outcomes in people being treated for an anxiety disorder.⁶ People with both conditions tend to have more severe symptoms, more functional impairment, a more chronic course, and a higher risk of relapse than people with either condition alone.

There is a practical consequence too. When only the more visible condition is treated, the other one often undermines the treatment. A person treated for panic disorder who is also depressed may struggle to complete exposure exercises because they lack the energy and hope to try. A person treated for depression who is also anxious may not improve because relentless worry prevents them from engaging with the work.

What to do with this information

• Describe all of your symptoms, not just the ones that seem most serious. Clinicians work from the full picture.
• If you are being treated for one condition and the other is present, say so explicitly.
• Do not read a second diagnosis as a worse prognosis. It signals that treatment should cover more ground, not that it will fail.
• If a treatment seems to be stalling, the presence of the other condition is one of the first things a good clinician will reassess.

Key takeaways

• Around half to three quarters of people with one of these conditions also have the other at some point, depending on the sample and time frame.
• The association is strongest between depression and generalized anxiety disorder.
• Each condition raises the risk of the other across years, and the effect runs in both directions.
• Shared symptoms, a common vulnerability, avoidance cascades, and shared biology all contribute to the overlap.
• Comorbidity predicts worse outcomes, which is a strong argument for treating both when both are present.

References and further reading

1. Co-morbidity between mood and anxiety disorders: A systematic review and meta-analysis. Systematic review with pooled prevalence and odds ratios, plus the 27 country community survey finding (hazard ratio 6.6). Full text: pmc.ncbi.nlm.nih.gov/articles/PMC7984258
2. Investigating the nature of co-occurring depression and anxiety: Comparing diagnostic and dimensional research approaches. Source of the 45 to 67 percent and 30 to 63 percent concurrent comorbidity ranges. Full text: pmc.ncbi.nlm.nih.gov/articles/PMC5308464
3. The Comorbidity of Major Depression and Anxiety Disorders: Recognition and Management in Primary Care. Source of the primary care figures, including the more than 75 percent overlap and the 1 to 5 percent mixed anxiety and depression range. Full text: pmc.ncbi.nlm.nih.gov/articles/PMC181193
4. Jacobson NC, Newman MG. Anxiety and depression as bidirectional risk factors for one another: A meta-analysis of longitudinal studies. Psychological Bulletin, 2017, 143(11), 1155-1200. pubmed.ncbi.nlm.nih.gov/28805400
5. Clark LA, Watson D. Tripartite model of anxiety and depression, as described in the adolescent Unified Protocol trial protocol. pmc.ncbi.nlm.nih.gov/articles/PMC11815469
6. van Balkom AJLM et al. Comorbid depression, but not comorbid anxiety disorders, predicts poor outcome in anxiety disorders. Depression and Anxiety, 2008, 25, 408-415. doi.org/10.1002/da.20386

← Previous Part 1: Two Conditions, One Nervous System Next Part 3: Inside the Brain and Body →

Anxiety vs. Depression is an educational series. It is not medical advice, and it cannot replace an evaluation by a qualified clinician.

In an emergency in the United States, call or text 988 to reach the Suicide

Inside the Brain and Body

Anxiety and depression are not inventions of the mind separate from the body. They involve measurable changes in brain circuits, stress hormones, immune signaling, and gene regulation. The biology is real, and it is more complicated than any single molecule.

First, an important correction

The idea that depression is caused by low serotonin, or that anxiety is caused by a shortage of a calming chemical, is a simplification that has been repeated so often it sounds like established fact. A systematic umbrella review of the evidence published in Molecular Psychiatry found no consistent evidence of a relationship between serotonin levels or activity and depression, and concluded that the serotonin theory is not supported by the data.¹ That review has itself been contested by other researchers, and the debate is ongoing.²

The takeaway is not that biology is irrelevant. It is that the biology does not reduce to one chemical being too high or too low. The National Institute of Mental Health describes depression as involving a combination of genetic, biological, environmental, and psychological factors.³ That is a much wider and more accurate frame.

The threat circuit

The central piece of machinery in anxiety is a network centered on the amygdala, a pair of almond shaped structures deep in the temporal lobes. The amygdala is not a fear center exactly. It is a salience and threat detection system that rapidly evaluates whether something in the environment deserves attention and alarm.⁴

Two of its subregions do related but different jobs. The basolateral complex receives sensory input and is heavily involved in learning which cues predict danger, which is the basis of fear conditioning. The central nucleus of the amygdala has extensive connections to brainstem and hypothalamic regions and acts as the output hub, triggering the physical signs of fear: rapid heart rate, sweating, muscle tension, and the release of stress hormones.⁴

Imaging studies of people with generalized anxiety disorder have repeatedly shown elevated amygdala and insula activation during the processing of negative emotional information.⁴ The insula is worth mentioning separately. It is involved in interoception, the sense of what is happening inside your own body, and overactivity there fits with the way anxiety so often shows up as physical sensation before it shows up as a thought.

The brakes that are supposed to work

The prefrontal cortex sits at the front of the brain and handles what researchers call executive function: planning, weighing consequences, inhibiting impulses, and deliberately reframing a situation. In emotional terms, it provides top down regulation. It is the part of the system that can tell the amygdala that the noise was a branch, not a burglar.⁴

Research has shown that the amygdala and the ventromedial prefrontal cortex tend to be inversely coupled during the successful regulation of negative emotion. When one is up, the other tends to be down. That inverse relationship also tracks with the daily rhythm of cortisol secretion.⁵ In plain language, the capacity to calm yourself is not just a matter of will. It depends on a specific circuit working, and that circuit can be strengthened or weakened.

Anxiety is not a failure of character. It is a threat detection system with a regulatory system that is not keeping up.

The stress hormone system

The hypothalamic pituitary adrenal axis, usually shortened to HPA axis, is the body's main stress response pathway. It works in three steps. The hypothalamus releases corticotropin releasing hormone. That signals the pituitary gland to release adrenocorticotropic hormone. That in turn signals the adrenal glands to release cortisol, the primary stress steroid in humans.⁶

In a healthy system, cortisol then feeds back and shuts the response down. The hippocampus suppresses HPA axis activation, while the amygdala enhances it.⁴ When that feedback loop is impaired, the stress response runs longer and harder than it should.

HPA axis dysregulation has been documented in major depressive disorder, anxiety disorders, and post traumatic stress disorder.⁵ One hypothesis is glucocorticoid resistance, in which the negative feedback signal becomes less effective, so the system keeps releasing stress hormones even when levels are already high.⁵ Post mortem studies have found higher levels of corticotropin releasing hormone in prefrontal regions of people who died by suicide with depression.⁵

Cortisol also affects thinking. In one study of people with major depression, cortisol levels accounted for between 5 and 16 percent of the variance across several cognitive domains, with the strongest effects on memory tests.⁶ This helps explain why trouble concentrating is such a common complaint in both conditions.

The hippocampus and the cost of chronic stress

The hippocampus is central to memory and to the contextual processing that lets you distinguish a genuinely dangerous situation from a safe one that merely resembles one. It is also one of the most stress sensitive regions in the brain, because it is dense with receptors for glucocorticoids.

Chronic stress is associated with structural and functional changes in the hippocampus, and depressed patients have shown decreased expression of mineralocorticoid receptors in the hippocampus and prefrontal cortex.⁶ Researchers increasingly describe this as a problem of impaired neuroplasticity rather than simple cell death, which is an important distinction because it means the changes are potentially reversible.

Inflammation and the immune system

One of the more interesting developments in the field is the finding that the immune system is involved. Post mortem studies of people with depression have found activation of microglia and astroglia, the brain's resident immune cells, in multiple regions including the frontal cortex, anterior cingulate cortex, and thalamus.⁵

In animal models, repeated stress produces a pro inflammatory state, increases amygdala neuronal and microglial activation, and causes anxiety like behavior.⁵ This line of research is promising because it links mental health to physical health conditions with an inflammatory component, and it may one day point to treatments for the subset of people whose symptoms have an immune signature.

Why this matters for understanding depression and physical illness

Depression is consistently associated with worse outcomes in cardiovascular disease, diabetes, and other chronic conditions, and the relationship runs in both directions. Inflammation is one proposed mechanism linking the two. It is a reminder that treating mental health as separate from physical health is a false split.

Neurotransmitters, accurately described

Serotonin, norepinephrine, and dopamine are genuinely involved in these conditions, and medications that act on them help many people. But their role is better understood as modulating circuits rather than supplying a missing ingredient. The same transmitter system participates in sleep, appetite, attention, pain processing, and motivation, which is exactly why drugs that change it have effects well beyond mood, and why side effects are so common.

Gamma aminobutyric acid, or GABA, is the main inhibitory transmitter in the brain and is central to the calming side of the equation. Glutamate is the main excitatory transmitter. Emerging work has found dysfunctional glutamatergic and GABAergic activity in the prefrontal cortex in animal models of chronic stress.⁵

Genetics and environment, tangled together

Both conditions run in families, and twin studies indicate a meaningful heritable component. But the genetics are highly polygenic, meaning hundreds or thousands of genetic variants each contribute a small amount of risk rather than a single gene determining the outcome. Genome wide studies have identified multiple risk regions, and notably, some of the genetic signal overlaps across different mental illnesses.⁷

A key insight is that the candidate genes and biological pathways appear to be largely the same across diagnoses. One review of the neurobiology of anxiety disorders noted that genetic contributors tend to be genes whose products regulate the HPA axis and monoaminergic signaling, regardless of which specific diagnosis a person has.⁴ This is direct biological evidence for the shared vulnerability discussed in part 2.

Genes also do not act alone. Genetic risk interacts with environment, and research using Mendelian randomization has identified modifiable factors with apparent causal links to depression risk. In one large analysis, confiding in others appeared to have the strongest protective effect across groups, including people with genetic risk and people who had experienced early life trauma. Sleep duration was also protective, while more time spent on the computer and higher salt intake were associated with increased risk.⁸

Putting it together

SystemWhat it doesWhat goes wrongAmygdalaDetects threat, learns fear associations, triggers physical alarmOveractive, especially in generalized anxiety disorderPrefrontal cortexPlans, inhibits, reframes, provides top down controlReduced regulatory coupling with the amygdalaHippocampusContext and memory, suppresses the stress responseStress related structural and plasticity changesHPA axisReleases cortisol and shuts the stress response downImpaired negative feedback, prolonged stress responseImmune systemResponds to injury and infectionMicroglial activation and neuroinflammationGeneticsSets baseline sensitivity across many small variantsPolygenic risk shared across diagnoses, shaped by environment

None of these systems operates independently. Chronic stress changes the HPA axis, which affects the hippocampus, which weakens the contextual braking of the amygdala, which drives more anxiety, which maintains the stress. That loop is why anxiety and depression become self sustaining, and it is also why treatment can enter the loop at several different points, from therapy to medication to sleep to exercise.

What the biology does and does not tell us

• It does not mean the condition is your fault, or that you can think your way out of it.
• It does not mean there is one broken part to fix with one pill.
• It does mean these are physical conditions with measurable correlates, not moral failings.
• It does mean there are multiple entry points for effective treatment.
• It does mean that if one approach does not work, others remain available.

Key takeaways

• Anxiety centers on an overactive threat detection network involving the amygdala and insula.
• Both conditions involve impaired top down regulation by the prefrontal cortex.
• The HPA axis shows dysregulated stress hormone feedback in depression, anxiety, and PTSD.
• Inflammation and immune signaling are increasingly recognized as part of the picture.
• Genetics are polygenic, shared across diagnoses, and interact with environment.
• The chemical imbalance story is a simplification that the evidence does not support.

References and further reading

1. Moncrieff J, Cooper RE, Stockmann T, Amendola S, Hengartner MP, Horowitz MA. The serotonin theory of depression: a systematic umbrella review of the evidence. Molecular Psychiatry, 2023, 28, 3243-3256. nature.com/articles/s41380-022-01661-0
2. King's College London Institute of Psychiatry, Psychology and Neuroscience. A response to the serotonin theory of depression umbrella review. kcl.ac.uk/news
3. National Institute of Mental Health. Depression. Describes genetic, biological, environmental, and psychological factors. nimh.nih.gov/health/topics/depression
4. The Neurobiology of Anxiety Disorders: Brain Imaging, Genetics, and Psychoneuroendocrinology. Amygdala subregions, insula activation, prefrontal cortex function, HPA axis regulation, and shared genetic pathways. Full text: pmc.ncbi.nlm.nih.gov/articles/PMC3684250
5. Chronic Stress-Associated Depressive Disorders: The Impact of HPA Axis Dysregulation and Neuroinflammation on the Hippocampus. International Journal of Molecular Sciences, 2025, 26(7), 2940. pmc.ncbi.nlm.nih.gov/articles/PMC11988747
6. HPA Axis in Major Depression: Cortisol, Clinical Symptomatology, and Genetic Variation Predict Cognition. Cortisol and cognition findings, mineralocorticoid receptor expression, and amygdala prefrontal coupling. Full text: pmc.ncbi.nlm.nih.gov/articles/PMC5313380
7. National Institute of Mental Health. Tapping Crowd-Sourced Data Unearths a Trove of Depression Genes. Polygenic risk and overlap with other mental illnesses. nimh.nih.gov/news/science-updates
8. National Institutes of Health. Factors that affect depression risk. Mendelian randomization findings including confiding in others, sleep duration, and other modifiable factors. nih.gov/news-events/nih-research-matters
9. Influence of the HPA Axis on Anxiety-Related Processes. Recent review of the links between HPA axis function and anxiety. Full text: pmc.ncbi.nlm.nih.gov/articles/PMC12433346

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← Series overview Anxiety vs Depression: A Six Part Series Continue Parts 4 to 6: From Understanding to Action →

Anxiety vs Depression is an educational series. It is not medical advice, and it cannot replace an evaluation by a qualified clinician.