🧠 Overview — What is it?
Steroid-Induced Depressive Disorder is a depressive condition that arises directly as a result of medications in the steroid group (corticosteroids), especially systemic forms that must be taken orally or injected into the body, such as prednisone, prednisolone, dexamethasone, methylprednisolone, etc. It is not considered a “primary” depressive disorder that arises on its own from genetics, hormones, or life experiences, but rather a Depressive Disorder with a clearly identifiable medication-related cause, and it is categorized under Substance/Medication-Induced Depressive Disorder in DSM-5-TR, which refers to a state of sadness, loss of drive, and hopelessness that can be systematically traced back to the effect of a drug.
Steroid medications play a crucial role in medicine because they reduce inflammation and suppress immune function, allowing them to treat a wide variety of conditions—from allergies and asthma, rheumatoid arthritis, autoimmune diseases, all the way to certain skin diseases, and even in critical cases such as severe acute immune reactions or diseases that require strong suppression of inflammation. The problem is: “the drug that can save lives” also has another side that can heavily affect the brain and mood.
Many studies report that when systemic steroids are used at moderate to high doses, about 20–30% of patients may develop some form of mood or behavioral disturbance, such as anxiety, irritability, insomnia, abnormally elevated mood like hypomania, or even psychotic symptoms. Among these, roughly 5–6% develop a clear depressive state, which is by no means a small number—especially in those who must use high doses continuously for several weeks or months.
The pattern of risk is also clearly related to dose and duration:
- If high dose for a short period, it is more common to see abnormally elevated mood, euphoria/hypomania.
- If steroids are used for many months to years, mood tends to gradually decline and eventually form a full depressive picture, especially in those taking around 20–40 mg/day of prednisone or in cases that require repeated pulse doses.
Even though the depressive symptoms in this context may “look like” Major Depressive Disorder (sadness, low energy, cognitive slowing, negative thinking), in reality it has a distinct signature: a temporal relationship with the medication—symptoms usually start after a dose increase or prolonged use beyond the individual’s vulnerability threshold, and if the steroid can be reduced or discontinued correctly under medical supervision, symptoms will gradually improve over the following 1–4 weeks after dose reduction. Some cases may take months to return to their previous baseline.
Therefore, diagnosing Steroid-Induced Depressive Disorder is not about labeling it as “just ordinary depression,” but about clearly identifying that the primary driver is the medication. The importance of this diagnosis lies in the fact that:
- Physicians must plan together around the underlying physical disease that requires steroid therapy
- Balance the benefits vs. mental side effects
- And monitor emotional symptoms from the early phase of treatment
Overall, this disorder communicates that “this is not the patient’s fault at all”, but rather an effect on the nervous system, hormones, and brain caused by medications that are necessary for their physical illness—effects that can be managed, adjusted, and treated in parallel if recognized correctly from an early stage.
🔍 Core Symptoms — Main Symptoms Commonly Seen
Overall, the symptoms closely resemble typical Major Depressive Episode, but what makes this case special is that:
- It clearly starts after using or increasing the dose of steroids, and
- Some features may be mixed with over-arousal effects from the drug, such as insomnia, irritability, anxiety, etc.
Let’s break it down by category and expand each block.
1. Mood & Affect
Key point: Patients often describe it as “it feels like my heart dropped through the floor”, and they themselves may be confused about why they suddenly feel this way, when before the dose adjustment they were still relatively okay.
Persistent low mood almost all day, for many days in a row
It’s not just “a bit moody then it goes away,” but a persistent sense of gloom, sadness, and heaviness that stays with them nearly the whole day. They wake up already feeling burdened and heavy-hearted, and by evening they still don’t feel like anything has truly improved. This feeling lasts for “days to weeks,” not just hours.
Loss of interest/pleasure in previously enjoyed activities (anhedonia)
Things that used to feel rewarding—drawing, gaming, watching series, talking with friends—suddenly become “I don’t feel like it, I’m not into it at all,” as if someone pulled the plug on their brain’s enjoyment system.
This is different from normal laziness because even if they force themselves to do it, they still don’t feel better, as if there is no emotional reward in return.
Feelings of despair, hopelessness, or a sense that “there is no future”
Patients may say things like:
“Even if this illness gets cured, I don’t know if anything in my life will actually get better.”
Or
“I don’t see any future for myself. It’s like everything is just dark.”
This is not just a passing thought during stress; it becomes a persistent narrative in their mind.
Excessive guilt or constant self-blame
For example, feeling like they are a burden because they have to take medications and need others to care for them.
Or taking small incidents and magnifying them, such as: “Yesterday I snapped at my child/partner” → automatically interpreted as “I’m a terrible person, I’m awful, I don’t deserve anyone’s love.”
The key point is that the weight of guilt in their mind is disproportionate to the actual situation.
Most of the time, if you listen carefully, you’ll see a pattern:
Before using steroids (or before the dose increase), the patient could still manage their emotions and daily life, but after the dose adjustment for a while, their mood feels like it “fell off a cliff,” without any major external life event that sufficiently explains it.
2. Energy & Function
This overlaps with all three: effects of the physical illness itself + effects of steroids + depression, which means we need to look at it carefully.
Severe fatigue, easily exhausted even without strenuous activity
Depressive fatigue is not just “physically tired,” but more like:
“Just thinking about having to get up and take a shower already makes me feel drained.”
It’s exhaustion of both body and mind at the same time. Long-term steroid use can also cause muscle weakness, which further reinforces the feeling of being incapable or “useless.”
Reduced concentration, difficulty making decisions, even small tasks feel heavy
Patients might complain: “Nothing sinks in when I read, I can’t think, I’m slow at deciding anything.”
Tasks that used to be easy—replying to chats, managing documents, cooking—now demand a lot of mental energy and feel full of friction.
In brain terms, this reflects a drop in executive function due to mood changes + neurobiological disruption from steroids.
Clear impairment in work/study/household functioning
Changes that people around them can clearly observe usually include a drop in productivity:
- Used to always show up on time for work → now starts coming late, taking more sick leaves
- Used to do house chores → starts letting the room pile up with mess, laundry remains undone
- Used to submit work on time → starts submitting late, procrastinating
The critical sign is that this is a change from their usual self, not just a continuation of a previously lazy pattern.
Social withdrawal — not wanting to talk or see people
Someone who used to chat, joke, or message friends gradually becomes silent, stops replying, and declines social invitations.
They may feel:
- “I have nothing to say.”
- “I don’t want anyone to see me like this.”
- “It’s easier to just be alone.”
Interestingly, some began steroids because of physical illness, which already forced them to cut down many activities, and once the mood drops as a result, they end up shutting themselves off even more.
3. Sleep & Appetite
Steroids and sleep are already a legendary duo for disrupting balance, and when combined with depression, the situation becomes even more chaotic.
Insomnia, fragmented sleep, or frequent nocturnal awakenings
Mechanism: glucocorticoids interfere with circadian rhythm + arousal systems → patients complain that:
- They have trouble falling asleep, even though their body feels physically tired
- They fall asleep but wake up frequently, as if their brain refuses to rest
- In the morning, they still feel like they “didn’t really rest”
This kind of insomnia is both a direct drug side effect and a potent amplifier of depression.
Some patients sleep excessively but still wake unrefreshed
On the opposite end: hypersomnia—sleeping a lot, but still waking up feeling gloomy, heavy-headed, and numb.
This is not “restorative sleep,” but often a way of escaping the world / escaping their thoughts, which feel too stressful and depressing to face awake.
Poor appetite, weight loss, or in some cases overeating—especially sweets and carbs
- Some patients don’t want to eat anything, feeling that food has no taste or that there is no point in eating.
- Some eat more, especially sweets, carbohydrate-rich foods, and fried food because they serve as temporary comfort food that stimulates brief bursts of dopamine/serotonin.
To make it more complex: steroids themselves can increase appetite and cause weight gain, and when combined with low mood, some patients feel even worse about their body image.
4. Negative Cognitions & Suicidality
This is where safety becomes the primary concern.
Repetitive thoughts like “I’m worthless, a burden, and completely useless”
Patients may go very hard on themselves with overgeneralized thinking:
“I can’t do anything. I just sit here taking pills and making everyone work to take care of me.”
“There is no way I can ever go back to how I used to be.”
This is more than self-pity; it is a narrative that they should not exist or that they are worthless to the world.
Suicidal ideation or feeling that “everyone would be better off if I disappeared”
It often starts as a passive wish, like:
“It would be nice if I fell asleep and never woke up.”
Or
“If an accident happened and I died, that would be better, so no one has to struggle.”
Even if there is no clear plan yet, this already counts as high risk, because it means the patient is starting to see “disappearing from the world” as a valid option.
In severe cases, plans for self-harm or suicide attempts emerge
For example, thinking:
- “What would happen if I took a large amount of pills at once?”
- Starting to hoard medications or sharp objects
- Searching for methods of suicide on the internet, etc.
At this stage, it is a psychiatric emergency, regardless of whether it is triggered by medication or underlying psychiatric illness. Safety must be addressed first; diagnostic fine-tuning can wait.
5. Other Associated Symptoms (Mixed Symptoms & Atypical Features)
Because steroids affect hormonal systems, stress circuits, emotion processing, and sleep, it’s often not “just depression,” but a strange cocktail.
Irritability and easy anger
Some patients don’t look purely depressed but rather “sometimes okay, sometimes suddenly explode.”
They get angry easily, feel attacked by minor comments, and even get furious at themselves when things don’t go their way—as if the entire emotion regulation system has collapsed.
Severe anxiety, palpitations, and hypervigilance
When the HPA axis is heavily triggered by steroids, the brain feels like it’s constantly in “fight-or-flight” mode:
- Rapid heart rate and trembling hands
- Overthinking and mental rumination on the same issues
- A sense that everything is threatening
This picture can sometimes overshadow the depression and make the person look like they are just “extremely stressed,” but if you zoom in, you’ll see a core depressive mood underneath.
Severe insomnia → further worsening of depression
This is the loop:
Steroids → insomnia → brain fatigue → worse mood → more stress → even worse insomnia → deeper depression
If sleep disturbance is never addressed, the depressive symptoms often become more stubborn and chronic.
Some patients develop psychotic symptoms
For instance, auditory hallucinations (hearing voices insulting or commanding them) or nihilistic / guilt-based delusions, such as:
“I’ve destroyed this world; everyone will die because of me.”
This often forms the theme of depressive psychosis.
Once psychotic features appear, suicide risk rises sharply, and management usually has to be more aggressive, often requiring antipsychotic medications or even ECT.
In short, for the Core Symptoms section:
It is not “just feeling a bit low because of illness,” but rather a full depressive syndrome that happens to occur at a time when steroids are running through the bloodstream and heavily disrupting brain and hormonal systems.
📋 Diagnostic Criteria — Conceptual Framework of Diagnosis
This is essentially explaining the logic behind DSM-5-TR criteria—why each point must be checked, rather than just lazily labeling everything as “drug-induced.”
1. Presence of a Clinically Significant Depressive Episode
It’s not just “feeling down” or “irritable because of illness,” but must rise to the level of a “depressive syndrome” that truly impairs functioning.
At least two core axes must be present:
- Depressed mood, or
- Loss of interest/pleasure (anhedonia)
Plus other accompanying symptoms, such as:
- Poor appetite / refusal to eat or significantly altered eating patterns
- Disrupted sleep patterns/poor sleep quality
- Easy fatigue, lack of energy
- Impaired concentration, feelings of worthlessness
- Thoughts about death
This criterion exists to exclude cases where mild mood changes due to general stress of illness would not qualify as a disorder. To apply the label “disorder”, severity must reach a level that genuinely disrupts life function.
2. Temporal Association with Steroid Use
This is the heart of the word “induced.”
In simple terms, the clinician will ask:
“What were they like before starting the medication or increasing the dose?”
“After how many days/weeks on the drug did the symptoms appear?”
The practical rules:
- Symptoms usually start within a few days to a few weeks after beginning steroids or increasing to a high dose.
- In those on long-term therapy, depressive symptoms may begin after crossing a certain threshold—for instance, several months on moderate–high doses.
- When steroids are reduced or discontinued appropriately, symptoms often gradually improve within weeks to months (not instantly, but with a clearly improving trajectory).
If the timeline doesn’t fit—e.g., severe depression existed long before steroid use, or worsened before the drug was started—then we start suspecting that this is more likely a primary depressive disorder that coincidentally encountered steroid treatment, rather than something “triggered by the drug.”
3. Reasonable Confidence That Steroids Are the Most Likely Cause
There is no such thing as 100% certainty in clinical practice, but physicians roughly estimate:
“If I had to pick one main cause that explains why the mood is collapsing now, what would it be?”
They check by:
History of prior depressive disorders
- If there has never been MDD/PDD/Bipolar/etc., and suddenly there is severe depression after starting steroids → probability is high that it is medication-related.
- If there is a pre-existing depressive disorder → then we have to ask:
- Is this episode more severe than their usual pattern?
- Can we clearly map the timing: did the crash occur after steroid adjustment?
Other life stressors at that time
- Were there any major events, such as bereavement, job loss, breakup, etc.?
If there are no significant life factors, but mood suddenly crashes right after starting/injecting steroids, the scale tips even more toward the drug.
Response after medication adjustment
- If after safely tapering the steroid dose, symptoms start improving without major changes in other factors → this is further evidence that the drug plays an important role.
- But if tapering steroids does not improve the mood, and depression persists for a long period, we begin considering the possibility that the depression has become independent of the drug, or that there is a co-existing primary depressive disorder.
This criterion helps prevent us from “blaming the drug for everything” in a lazy way and instead forces a careful examination of the entire clinical context: patient, disease, and concomitant medications.
4. Not Occurring Exclusively During Delirium
In severely ill patients using steroids together with other medications or conditions such as sepsis, hypoxia, etc., delirium can occur (confusion, disorientation, fluctuating consciousness, visual hallucinations, etc.).
The question becomes:
Are we truly seeing “depression,” or just part of a delirium picture?
- If there is confusion, severely disrupted sleep-wake cycles, incoherent speech, inability to remember what was said, etc. → this is primarily delirium.
- The depressive state we diagnose under mood disorders should:
- Have a coherent symptom structure
- Allow the patient to communicate
- Let them describe their thoughts and emotions to some extent
- Not be just fluctuating confusion like in delirium
Why does this need to be separated?
Because management of delirium vs. depressive disorder is completely different—misdiagnosis means going down the wrong treatment path.
5. Clinically Significant Distress or Impairment
DSM has a classic phrase:
“Symptoms must cause clinically significant distress or impairment.”
In this context, that means:
- The patient is truly suffering, feeling like they are drowning in emotions they cannot handle,
- Or work/self-care/relationships are clearly falling apart,
- Or there is significant risk, such as suicidal ideation or planning self-harm.
If the patient only has slightly lower mood, becomes a bit more irritable, but is still functioning normally at work and in relationships → that would count as emotional side effects, but not yet as a disorder.
This criterion prevents clinicians from over-pathologizing every emotional shift caused by medication.
6. Classified Under “Substance/Medication-Induced Depressive Disorder,” with Corticosteroids as the Culprit
Once points 1–5 are met, clinicians categorize the condition under the proper DSM section in order to:
- Document the diagnosis systematically
- Plan treatment (for both physical disease and emotional state)
- Track the condition long term (if an episode like this has occurred once, future steroid use requires extra caution)
In this case, the substance/medication responsible is corticosteroids, regardless of whether it’s prednisone, dexamethasone, or any brand name exerting systemic glucocorticoid effects.
Summary of a Physician’s Thought Process When Encountering Such a Case (As a Flow)
When a psychiatrist or medical doctor starts to suspect “this might be Steroid-Induced Depressive Disorder,” they roughly think through:
- Does the patient have a full depressive syndrome, not just mild grumpiness?
- When did symptoms begin? Before or after starting/increasing the steroid dose?
- Is there pre-existing depression? If so, is this episode different from usual?
- Are there any major life events that better explain the symptoms than the drug?
- Is there any delirium or severe confusion right now? If yes → treat delirium first.
- How much are symptoms impairing life / posing risk? Is hospitalization needed?
Then plan:
- How much can the steroid be adjusted (after discussing with the treating physician for the physical disease)?
- Are antidepressants or adjunctive psychotropic drugs needed?
- How urgently does safety around self-harm need to be addressed?
- How to explain to the patient and family that “this is the effect of medication + brain,” not a personal failure.
🧩 Subtypes or Specifiers — Commonly Discussed Patterns
In DSM itself, there aren’t separate specifiers dedicated solely to steroids, but in clinical practice and research, people tend to think in patterns like these:
1. Classification by Duration of Steroid Use
Acute high-dose steroid depression / mood change
- Occurs during the period of starting high-dose therapy (e.g., prednisone ≥ 40 mg/day)
- Usually begins within the first 3–14 days
- Some patients start with euphoria/hypomania and later crash into depression
Chronic steroid therapy depression
- Long-term use of moderate to high doses over months to years
- Mood gradually declines, forming a pattern of “chronic low mood – burnout – persistent fatigue.”
2. Classification by Mood Profile
Pure Depressive Form
- Dominated by sadness, lack of energy, and loss of drive
- No clear manic/hypomanic features
Mixed Affective Form
- Includes depression plus agitation, irritability, insomnia, and periods of racing thoughts
- Resembles “steroid-induced mood disorder, mixed” (as often described in clinical reports and ScienceDirect+1)
3. Classification by Severity and Associated Features
- With Psychotic Features – presence of hallucinations and/or delusions (e.g., depressive psychosis–type themes)
- With Prominent Anxiety – marked tension, panic-like symptoms, and over-arousal
- With Cognitive Impairment – significantly impaired attention, memory, and executive functioning compared to baseline
🧬 Brain & Neurobiology — How Do Steroids Hit the Brain?
The impact of steroids on the nervous system is not minor, and it does not manifest equally in everyone. The crucial point is that glucocorticoids mimic cortisol, a hormone deeply involved in the body’s stress system. Using steroids at high doses or for prolonged periods is therefore like “switching the brain into a permanent stress mode,” causing disturbances at multiple levels: hormones, neural circuits, brain chemistry, and even brain structure over time.
Let’s expand each point systematically:
1) Dysregulation of the HPA Axis (Hypothalamic–Pituitary–Adrenal Axis)
The HPA axis is the central stress hormone control system, starting from the hypothalamus → pituitary → adrenal gland, which secretes cortisol in response to stress.
But when steroids are administered from outside:
- The body receives “fake cortisol” in high amounts → the brain shuts down its feedback loop.
- The hypothalamus and pituitary are suppressed, disrupting the entire cortisol regulatory circuit.
- The brain interprets the state as “sustained high stress”, even when there is no actual external stressor.
As a result:
- The brain’s internal alarm system (amygdala) is left switched on
- The reasoning and executive center (prefrontal cortex) functions less effectively
- Reward and pleasure circuits become impaired
Altogether, this leads to depression, anxiety, and irritability at the same time.
This explains why many patients say:
“I don’t feel like myself. It’s like my brain is spinning all the time,”
even when their external environment is not particularly stressful.
2) Effects on the Hippocampus — Memory, Mood, and Stress Regulation
The hippocampus has two key roles:
- Controlling memory
- Regulating stress via negative feedback
Studies show that prolonged high levels of glucocorticoids cause multiple adverse effects:
- Reduced neurogenesis (formation of new neurons)
- Dendritic shrinkage → fewer neural connections
- Structural shrinkage of the hippocampus (hippocampal atrophy)
- Impaired emotional regulation and memory
The same patterns have been observed in major depression and PTSD. Therefore, steroid-induced depression shares similar biological markers with chronic forms of depression.
In real life, this translates into:
- Forgetfulness
- Confusion
- Slower thinking
- A tendency to interpret situations more negatively
- Inability to “switch off” stress
This aligns with many patients’ complaints, such as:
“My thinking’s slower. My brain feels foggy and not as sharp as before I started steroids.”
3) Amygdala Dysregulation — Fear and Anxiety
The amygdala is the central hub for fear, panic, and threat detection.
When glucocorticoid levels remain persistently high:
- The amygdala becomes hypersensitive to stimuli
- There is a tendency to perceive minor issues as major threats
- People become easily anxious, easily frightened, easily irritable
- Emotional regulation circuits fail → emotional flooding
Steroids affecting the amygdala often lead to:
- Panic-like symptoms
- Over-arousal
- A persistent sense of being threatened even when there is no real danger
- Acute nocturnal anxiety
- Stress-induced hallucinations in severe cases
Thus, it’s not surprising that many patients experience “depression + anxiety + insomnia” simultaneously.
4) Neurotransmitters — System-Wide Disruption of Brain Chemistry
Steroids interfere with key brain chemicals, including:
• Serotonin
Reduced serotonin receptor function
→ leads to sadness, hopelessness, and loss of motivation.
• Dopamine
Suppression of the reward pathway
→ results in loss of passion, burnout, and rapid loss of interest in activities.
• Glutamate
Chronic stress plus corticosteroids cause hyperactivity in glutamate systems
→ leads to anxiety, irritability, overthinking, and a racing mind.
In more severe cases → increased risk of psychotic symptoms.
• GABA
In some cases, GABA levels decrease
→ results in restlessness, insomnia, and physical tension.
This collapse of multiple neurotransmitter systems at once is a hallmark signature of depression triggered by steroids.
5) Neuroinflammation — Hidden Brain Inflammation
Even though steroids are anti-inflammatory, paradoxical effects can occur in the brain:
- The brain’s immune cells (microglia) can become dysregulated
- Stress sensitivity increases
- There is low-grade, chronic neuroinflammation
- This is linked to depressive symptoms, fatigue, and brain fog
Thus, patients may experience:
- Dizziness and mental clouding
- Brain fatigue
- Poor focus
- Waking up feeling drained and without energy
All of this reflects cellular-level changes in the brain, not “just imagination.”
⚠️ Causes & Risk Factors — Why Do Some People Develop It While Others Don’t?
The reasons why some people become depressed on steroids while others do not operate on many levels: medication-related, physical, psychological, and genetic.
1) Medication Factors (Dose – Duration – Type) → The Heaviest Weight
• Dose
This is the most critical factor:
- Prednisone ≥ 40 mg/day → clearly increased risk of psychiatric side effects
- Pulse doses like IV methylprednisolone → mania/psychosis are relatively common
- High-dose therapy lasting 2–6 weeks → often the “golden window” during which depressive symptoms emerge
• Duration
- Longer use → the brain is exposed to excessive glucocorticoids for extended periods
- Cortisol fluctuates abnormally throughout the day
- Risk of both depression and cognitive impairment increases
- Those on steroids for months to years gradually sink into a “chronic burnout” state
• Formulation (Type)
- Oral/injectable → highest risk for depression
- Inhaled → lower risk, but high doses can still cause issues
- Topical → very low risk, except when applied over large areas or in high amounts
2) Patient Vulnerability Factors
• Female Sex
Studies show that women have a higher risk of mood-related side effects.
Possible reasons include:
- Hormonal system differences
- Higher sensitivity of the HPA axis
- Different stress response patterns
• History of Mood Disorders
Patients who have had:
are at higher risk, because their emotional processing systems are already more sensitive to stress.
• Prior Adverse Reactions to Steroids
Very important!
If someone has previously experienced dizziness, depression, or abnormal mood elevation from steroids, then in the next course of steroids, there is a 50–70% chance of recurrence.
• Genetics and Personality
For example:
- People with a tendency toward overthinking
- Those with a history of trauma
- Those with high stress reactivity
are all more vulnerable.
3) Medical & Contextual Factors
• Chronic Systemic Disease
The illness itself increases the risk of depression, such as:
- Autoimmune diseases
- Cancer
- COPD
- Kidney disease
- Lupus (SLE)
- Autoimmune skin diseases
When you add steroid effects on top → it becomes a double hit to the brain.
• Stress from Illness
Having to take medications, regularly see doctors, and restrict daily activities → baseline stress is already high.
If steroid-induced dysregulation is layered on top of that → mood can drop rapidly.
• Concomitant Medications
For example:
- Immunosuppressants
- Opioid painkillers
- Hypnotics/sleeping pills
- Anticonvulsants
Some of these can increase the likelihood that steroids will severely destabilize mood.
✔️ Big Picture Summary of Both Sections
Brain & Neurobiology
→ Explains why steroids “suppress, accelerate, and disrupt” multiple brain circuits simultaneously, resulting in depression, anxiety, burnout, and insomnia.
Causes & Risk Factors
→ Explains why some individuals are hit extremely hard by these side effects while others escape relatively unaffected.
(Formula: Dose + Duration + Baseline hormones + Genetics + Stress + Chronic disease)
🩺 Treatment & Management — How Is It Managed? (Big Picture, Not Personal Medical Advice)
This section is general information for understanding, not specific treatment advice.
If anyone is currently on steroids and experiencing depression or suicidal thoughts → they must talk to their doctor immediately, and if there is any risk of self-harm, they should seek emergency care / call a mental health crisis line or emergency services in their area.
1. Adjusting Steroid Use (Under Medical Supervision Only)
Evaluate whether the dose is higher than necessary. If it can be reduced, the physician may:
- Lower the dose
- Switch to other medications (steroid-sparing agents)
- Use mainly topical / inhaled forms instead of systemic, if clinically feasible
Steroids should never be stopped abruptly without supervision, as this can cause adrenal crisis and serious deterioration in physical illness.
2. Psychiatric Treatment
Antidepressants (e.g., SSRIs)
- Used when there is clear depression that impairs life function
- Many cases in the literature respond well to SSRIs or SNRIs when used alongside careful management of steroid dosing (PubMed Central+1)
Antipsychotics / Certain Sedative Agents
- Used when there are psychotic features, marked agitation, or severe insomnia
Electroconvulsive Therapy (ECT)
- In severe cases—such as depressive psychosis, high suicidal risk, or treatment-resistant episodes—ECT has been reported to be effective in some cases of “steroid-induced depressive psychosis” (PubMed Central+2, psychiatry-psychopharmacology.com+2)
3. Psychotherapy & Psychoeducation
Psychoeducation for Patients and Families
- Clearly explain that symptoms are not due to personal weakness, but related to the effects of medication and the underlying physical illness.
- Teach family members to watch for warning signs, such as worsening insomnia, rapid mood decline, social withdrawal, not talking to anyone, or frequent mention of death.
CBT or Supportive Therapy
- Helps manage negative thinking and hopelessness
- Helps build coping skills for living with chronic illness and long-term medication use
4. Long-Term Monitoring
Those who have previously experienced steroid-induced depression should be considered a high-risk group if steroids need to be used again in the future.
Advance planning should include:
- Informing psychiatrists/primary physicians every time before starting high-dose steroids
- Establishing early mood monitoring during the initial phases of each steroid course
📝 Notes — Key Points to Distinguish and Watch Out For
Having depression + taking steroids ≠ always Steroid-Induced
- Some people already have depression and just happen to need steroid treatment.
- Others develop depression mainly because chronic illness has severely impacted their life, even without steroids.
Steroid-Induced vs. Depression from Physical Illness Itself
- Conditions like Cushing’s syndrome, hypothyroidism, SLE, chronic infections, etc., can independently cause depression.
- The physical disease context must always be considered.
In some cases, medication “switches on” an existing vulnerability
- Some studies suggest that steroids may “trigger” depression in individuals with underlying genetic or neurobiological vulnerabilities rather than “creating it from zero” (SpringerLink+1).
Informed consent before starting steroids
In an ideal world, physicians would explain from the beginning:
“This drug will help your physical illness a lot, but it can change your mood—too high, too low, even cause depression or suicidal thoughts. If anything feels off, tell us right away.”
If patients know this in advance, they are less likely to misinterpret their symptoms as “I’m going crazy” and more likely to understand that this is a brain side effect that can be addressed.
If there are suicidal thoughts or self-harm intent → this is an emergency
There is no need to waste time debating whether it is “caused by the drug” or “underlying psychiatric illness.” The key priority is safety first.
📚 References — Academic / Journal / Textbook Sources
(Reformatted for website use, but all are real sources)1) Warrington TP, Bostwick JM. Psychiatric adverse effects of corticosteroids. Mayo Clinic Proceedings.
A classic paper discussing psychiatric side effects of systemic corticosteroids across all dose ranges and mood states.
2) Lewis DA, Smith RE. Steroid-induced psychiatric syndromes. A report of 14 cases and a review of the literature. Journal of Affective Disorders.
A frequently cited early work describing depression, mania, and psychosis caused by corticosteroids.
3) Brown ES, Chandler PA. Mood and cognitive changes during systemic corticosteroid therapy. Primary Care Companion to J Clin Psychiatry.
A review on how glucocorticoids alter brain function and lead to mood and cognitive changes.
4) Brown ES. Effects of glucocorticoids on mood, memory, and hippocampal structure. Biological Psychiatry.
A deep dive into the impact of steroids on the hippocampus and neurogenesis—explaining why patients become depressed, slow-thinking, and mentally fatigued.
5) Ciriaco M et al. Corticosteroid-related central nervous system side effects. Journal of Pharmacology & Pharmacotherapeutics.
Describes psychiatric side effects of corticosteroids across the spectrum from anxiety → depression → psychosis.
6) Judd LL, Schettler PJ. The long-term sequelae of cortisol and stress-related disorders. International Journal of Neuropsychopharmacology.
Supports the idea that the severity of HPA-axis dysregulation affects the likelihood of depression related to steroids.
7) Sirois F. Steroid psychosis: a review. General Hospital Psychiatry.
Reviews steroid-induced mood and psychotic disorders along with the timeline of symptom emergence after starting steroids.
8) Nasereddin L, et al. Corticosteroid-Induced Psychiatric Disorders: Mechanisms and Clinical Implications. 2024 Review.
A recent paper that comprehensively explains neurobiology, risk factors, and clinical pathways.
9) StatPearls — Substance/Medication-Induced Depressive Disorder. NCBI Bookshelf.
Provides an overview of depressive disorders caused by medications, including corticosteroids.
10) Smith, MD. Glucocorticoids and the brain: neurochemical, neurostructural and emotional changes. Molecular Psychiatry.
Supports the mechanisms involving serotonin, dopamine, and glutamate.
11) Reus VI. The Neurobiology of Depression. In: Goodman & Gilman’s Pharmacological Basis of Therapeutics.
A standard reference detailing links between glucocorticoids and depression.
12) Lupien SJ et al. Effects of stress hormones on the brain. Nature Reviews Neuroscience.
Clearly shows how prolonged high cortisol levels affect the brain in ways similar to patients on steroids in many aspects.
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