What Truly Occurs When You Begin—and Attempt to Cease—Antidepressants
The following information is based on information originally published by A Midwestern Doctor. Key details have been streamlined and editorialized for clarity and impact. Read the original reports here and here.
Mikhaila Peterson says she went through “two years of pure hell” when she decided to stop taking SSRIs.
She didn’t need the drugs anymore. Her paleo/keto diet had put her depression into remission.
The first few days off the medication, she felt “on top of the world.”
But once week two hit, her life “turned upside down.”
For years, she blamed her “intolerable symptoms” on what she ate.
Little did she know… she was actually experiencing severe antidepressant withdrawal.
One of the symptoms Mikhaila experienced during her own SSRI withdrawal is the same condition her dad is suffering from right now: akathisia.
Akathisia is an extremely distressing neurological condition that makes you feel an unbearable inner restlessness and agitation.
This condition, she describes as “the worst thing I’ve ever seen anyone go through…”
When Mikhaila experienced it, she described it as being “overwhelmed with a sense of impending doom that was stronger than anything you can naturally feel.”
“It felt like I was falling into a volcano while being chased by a bear,” she said.
Mikhaila’s gut-wrenching anti-depressant story is available to read in full here: https://prescribed-harm.com/stories/story-001.html
But as bad as her experience was, her dad is currently going through a form of akathisia that’s even worse.
Last week, Mikhaila shared an emotional update on her father, Jordan Peterson’s health.
He is dealing with a recurrence of akathisia stemming from an old psych med–induced neurological injury.
Mikhaila explained that this is a flare-up of a neurological injury caused by benzodiazepines, primarily clonazepam, that he took around 2019–2020. He has been completely off all psychiatric medications since January 2020.
The recent symptoms intensified last summer after he was diagnosed with Chronic Inflammatory Response Syndrome (CIRS) from mold exposure. About a month later, he developed pneumonia and sepsis, which further worsened the condition and triggered the akathisia.
“Dad’s been suffering from an old neurological injury that’s more recently been causing akathisia,” Mikhaila said.
“Akathisia is the worst thing I’ve ever seen anyone go through… it’s catastrophic.”
She stresses that this is a neurological injury from past psychiatric medication use, not from any current medications. Her dad has been psych med-free for six years.
But for the past 8–9 months, akathisia has taken over his life without warning or relief, making this an extremely difficult time for the entire family.
For decades, the medical establishment told us that depression was caused by a “chemical imbalance” in the brain, specifically a lack of serotonin.
This simple idea was repeated by doctors, psychiatrists, and pharmaceutical companies as established scientific fact.
It gave patients a clear explanation, doctors a straightforward framework, and the pharmaceutical system a powerful way to communicate value.
Depression became something measurable, correctable, and treatable with a targeted intervention.
But simplicity can also obscure complexity.
Because the brain isn’t a system governed by a single chemical variable, it’s a dynamic network of interacting pathways, feedback loops, and adaptive responses that change over time.
And when you try to reduce that system to one variable, you risk misunderstanding what your intervention is actually doing.
If depression were primarily caused by a serotonin deficiency, we would expect a few things to be consistently true:
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Restoring serotonin should produce predictable improvements.
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Higher serotonin activity should correlate with better outcomes.
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And long-term treatment should stabilize patients in a lasting way.
But when researchers began looking more closely at long-term data, those patterns didn’t hold.
Some patients improved. Many plateaued. Others experienced outcomes that didn’t align with the original model at all.
And that’s where the problem begins.
This information comes from the work of medical researcher A Midwestern Doctor. For all the sources and details, read the full report on antidepressants.
For more sources and details on anxiety, read the full report from A Midwestern Doctor.
In real-world settings, patients often describe a more complicated trajectory than the one outlined in clinical messaging.
Initial changes can occur—sometimes subtle, sometimes noticeable—but over time, the experience can shift. Emotional blunting, reduced responsiveness, or a sense that something fundamental has changed about them.
These effects are not universal, but they are common enough to raise important questions about how these drugs are interacting with the underlying system.
Because when a treatment alters perception, motivation, and emotional range, it’s doing more than correcting a deficit—it’s reshaping function.
This is where the conversation usually narrows.
Side effects are acknowledged, but often framed as manageable trade-offs. Variability in response is attributed to individual differences. And when outcomes fall short, the default assumption is that the condition itself is the problem—not the model guiding treatment.
But that framing limits deeper investigation.
Because if the underlying theory is incomplete, then the way we interpret both success and failure may also be incomplete.
And that means some of the most important signals—especially those that don’t fit expectations—can be overlooked.
To understand what’s really happening, you have to look beyond the simplified explanation and into the actual biological effects of these drugs.
SSRIs don’t simply “add serotonin” to a deficient system. They alter how serotonin is recycled, which changes signaling dynamics across multiple brain regions. Over time, the brain adapts to this altered environment—receptors can downregulate, feedback mechanisms shift, and the system recalibrates.
That adaptation is key.
Because once the brain adjusts to the presence of the drug, its baseline state is no longer the same as it was before treatment began.
Most people are told these drugs aren’t addictive—but that’s not the same as saying they don’t create dependence.
Dependence means the brain adapts to the presence of the drug. And once that adaptation happens, removing it is no longer neutral—it becomes a physiological stressor.
This process—often referred to as neuroadaptation—is not inherently harmful. The brain is designed to adapt.
But adaptation has consequences.
When signaling pathways are persistently altered, the system reorganizes around that new state. What was once “normal” becomes something different, and the longer the intervention continues, the more entrenched that new equilibrium can become.
That means the drug isn’t just influencing mood in the moment—it’s participating in a longer-term restructuring of how the system operates.
And that distinction becomes critical later.
The full breakdown of these mechanisms, including how receptor sensitivity and feedback loops evolve over time, is explored in A Midwestern Doctor’s article on antidepressants.
It’s one of those areas where the deeper you look, the less the simple model holds up—and the more important it becomes to understand what’s actually driving patient outcomes.
The deeper you go into the science behind these drugs, the less the “chemical imbalance” story holds up.
Because once you move beyond the simplified theory, the variability in outcomes starts to make more sense.
If you’re altering a complex adaptive system, you’re not going to get uniform results. You’re going to see a spectrum—some patients benefit, others don’t, and some experience effects that weren’t part of the original expectation.
And importantly, those outcomes can evolve over time.
What feels helpful in the short term doesn’t always translate into long-term stability, especially if the underlying system continues to adapt in ways that aren’t fully understood.
That raises a difficult but necessary question:
Are we evaluating these medications based on short-term symptom changes… or long-term system behavior?
Because those are not the same thing.
Short-term studies often focus on symptom reduction over weeks or months. And in that window, measurable improvements can occur.
But long-term data introduces more complexity. Patients may remain on medication for years, during which time the brain continues to adapt and new patterns of function emerge.
Those longer timelines are harder to study, harder to standardize, and often less emphasized in public messaging.
But they’re where many of the most important outcomes actually unfold.
And when you look at those longer timelines, a different picture can begin to emerge.
Some patients maintain stability. Others find that benefits diminish, requiring dose adjustments or additional medications. And some experience new challenges that weren’t present before treatment began.
None of this fits neatly into a single narrative.
Which suggests the original framework may be too narrow to capture what’s really happening.
And in some cases, patients don’t just plateau—they deteriorate in ways they don’t understand at the time.
That’s the part that makes this so difficult to recognize in real time.
A medication can feel like it works—and still contribute to deeper problems later.
Mikhaila describes how, at first, Celexa made her feel like she could breathe again. The panic stopped. Suicidal thoughts eased. It felt like relief.
But over time, things didn’t stabilize.
They escalated.
She describes becoming “more and more mentally ill,” developing new symptoms, new diagnoses, and side effects she didn’t realize were connected to the medication.
That doesn’t happen to everyone.
But it happens often enough to raise a serious question about what’s really driving long-term outcomes.
And the changes patients notice aren’t always dramatic at first.
Most patients are prepared for the idea that a medication might not work perfectly.
Fewer are prepared for the possibility that it might change how they experience themselves in ways that are difficult to describe—subtle shifts in emotional range, motivation, or sense of connection that don’t always register as “side effects,” but still matter.
Those kinds of changes are harder to quantify, but they play a significant role in how people evaluate their overall well-being.
And they often don’t show up clearly in standard outcome measures.
Then there are reactions that go far beyond emotional blunting or reduced motivation.
This is where the human side of the story becomes impossible to ignore, because some patients describe symptoms that don’t feel like depression, anxiety, or ordinary distress. They describe something neurological, physical, and almost impossible to explain to people who haven’t experienced it.
Mikhaila calls akathisia “intolerable discomfort” that makes people feel like they want to crawl out of their skin.
Because for many patients, the real problem doesn’t begin when they start the medication—it begins when they try to come off of it.
What’s often described as a simple “discontinuation” process can turn into something far more complex. People report waves of anxiety, insomnia, agitation, dizziness, and even physical symptoms they never experienced before starting the drug.
And this is where things become deeply confusing:
Those symptoms are frequently interpreted as a return of the original condition—rather than a physiological response to the drug being removed.
That distinction changes everything. Because if withdrawal is mistaken for relapse, the response is almost always more medication.
What she describes next doesn’t feel like anxiety—or even severe anxiety.
It feels like something entirely different.
If withdrawal is mistaken for relapse, the clinical response is predictable.
The medication is restarted, the dose may be increased, or additional drugs are introduced to manage the symptoms.
From the outside, it looks like the condition is chronic and requires ongoing treatment.
But from another perspective, it can look like the system is reacting to the removal of a substance it has adapted to.
And those two interpretations lead to very different conclusions.
Withdrawal is one of the most important—and least understood—parts of the conversation.
Because once you recognize how withdrawal can present, it becomes much easier to see how patients can get caught in a cycle that’s difficult to exit.
For some people, this isn’t temporary—it reflects deeper neurological disruption that doesn’t resolve quickly, and sometimes doesn’t fully resolve at all.
Severe insomnia, sensory sensitivity, and dysregulation of core systems like GABA and glutamate have all been reported—symptoms that go far beyond the original condition being treated.
This dynamic is explored extensively in A Midwestern Doctor’s full article on antidepressants.
It reframes many of the experiences patients report—not as isolated incidents, but as part of a broader pattern that deserves closer attention.
At this point, the system often introduces another solution—something meant to calm the symptoms that are now emerging.
A second medication is added to stabilize sleep, reduce agitation, or control anxiety.
And that’s where benzodiazepines enter the picture.
Benzodiazepines can be effective in the short term, particularly for acute anxiety.
But their mechanism—enhancing inhibitory signaling through GABA pathways—comes with its own set of adaptive consequences.
Over time, tolerance can develop, meaning higher doses are needed to achieve the same effect. And dependence can form, making discontinuation challenging in ways that parallel, and sometimes exceed, what is seen with SSRIs.
What starts as one medication becomes two. Then sometimes three.
Each one addressing the side effects of the last.
And over time, the system becomes harder—not easier—to stabilize.
One medication alters serotonin signaling and induces adaptation. Another modulates inhibitory pathways to manage the resulting symptoms.
Individually, each intervention has a rationale.
But together, they can create a system that becomes increasingly complex—and increasingly difficult to unwind.
There’s another layer to this that rarely gets discussed—and for many patients, it’s one of the most devastating.
Some effects don’t resolve when the medication is stopped. They persist. In some cases, they appear after discontinuation and never fully go away.
We’re no longer talking about temporary side effects. We’re talking about long-lasting changes in emotional range, physical sensation, and basic neurological function that can fundamentally alter how someone experiences their life.
And because these outcomes are poorly recognized and rarely explained beforehand, many people don’t even realize what’s happening to them—only that something feels permanently different.
And when patients try to explain what’s happening, they often run into another problem.
Their experience doesn’t fit the expected model.
So it gets dismissed.
Symptoms are minimized. Stories are misinterpreted. And in many cases, patients are told what they’re experiencing isn’t real, or is simply a return of their underlying condition.
But when large numbers of people describe the same patterns—severe reactions, prolonged withdrawal, and symptoms that don’t match the original diagnosis—it raises a different possibility:
That something is being consistently overlooked.
Learn more: https://prescribed-harm.com/
A lot of what we call “anxiety” doesn’t behave the way we think it does.
A Midwestern Doctor explains why.
And even after stopping the medication, the story doesn’t necessarily end.
For some patients, the system doesn’t simply return to baseline. It remains altered—sensitive, reactive, and in some cases vulnerable to being triggered again by stress, illness, or environmental factors.
That means symptoms can reappear months or even years later, not because the original condition has returned, but because the underlying system has been destabilized.
This is one of the least discussed aspects of these medications—and one of the most difficult for patients to navigate.
If you want to understand why people get stuck in these cycles, this full article from A Midwestern Doctor is worth reading.
This doesn’t mean these medications have no place in treatment.
Some patients do benefit—in specific contexts.
But the larger question is whether the framework guiding their use is complete enough to account for what patients actually experience over time.
Because if the model is incomplete, then the outcomes we’re seeing may not be surprising—they may be the natural result of a system that doesn’t fully understand what it’s intervening in.
And if patients aren’t being fully informed about the risks, that’s not just a gap in knowledge.
It’s a failure of the system itself.
Thanks for reading! This information was based on a report originally published by A Midwestern Doctor. Key details were streamlined and editorialized for clarity and impact. Read the original reports:
For more sources and details on anxiety, read the full report from A Midwestern Doctor.
For a deeper dive into what modern medicine has overlooked—or intentionally buried—check out these other eye-opening reports by A Midwestern Doctor:
The Forgotten Cancer Cure Hiding in Plain Sight
What They Don’t Tell You About C-Sections
What’s The Healthiest Water To Drink?
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