Discover how modern psychiatry was built on myths and why restoring the body’s energy and natural balance could transform our understanding of depression.

Introduction

For more than half a century, modern psychiatry has consolidated its power around two master ideas:

The supposed existence of individual genetic defects as the origin of mental disorders, and
The theory of a chemical imbalance in the brain, especially a serotonin deficiency, claimed to explain depression, anxiety, PTSD, and even schizophrenia.

These two hypotheses, never actually demonstrated, have underpinned a multibillion-dollar industry.
They justified the explosion of prescriptions for antidepressants, anxiolytics, antipsychotics, and a dominant pharmaceutical psychiatry.

Today, the foundations of this paradigm are collapsing under the weight of extensive scientific evidence.
Major publications, including Psychiatry Research (2019), Molecular Psychiatry (2022), and Nature (2024), have exposed the emptiness of the serotonin-deficit theory and the lack of solid evidence for an identifiable genetic basis for depression (Moncrieff et al., 2022; Border et al., 2019).

As Joanna Moncrieff emphasizes in a letter published in Molecular Psychiatry:

“Difficult lives explain depression better than broken brains.” (Moncrieff et al., 2024)

These results force a radical reassessment of psychological suffering.
Far from being isolated biological errors, mental disorders appear to be natural responses to an increasingly hostile, stressful, and energy-depleting environment.

The true origin of mental disorders: chronic stress and energetic collapse

Recent clinical and experimental data converge on a simple conclusion:

Chronic stress is the central etiological factor in depression, PTSD, anxiety, and associated cognitive disturbances.
Mitochondrial collapse and bioenergetic dysfunction explain the persistence of these pathological states.

Thus, depression is not a “brain disease” caused by a mysterious neurotransmitter deficit.
It is a systemic disease, rooted in the chronic wear-and-tear of living systems.

In the face of this reality, institutional psychiatry—too often guided by financial interests and outdated dogmas—persists with a destructive chemical approach: artificially increasing serotonin, denying the impact of stress, medicalizing human suffering.

It’s time to demystify psychiatry, recognize the real causes of psychic suffering, and explore authentic paths to healing grounded in the restoration of vital energy.

1. Modern psychiatry: a diagnostic and biological sleight of hand

1.1 The mirage of psychiatric diagnosis

Since the adoption of DSM-III in 1980, psychiatry has claimed to classify psychological suffering into distinct diagnostic entities, analogous to classic organic diseases. Each mental disorder would have precise criteria, a predictable natural course, and a dedicated treatment.

However, recent critical work reveals the total absence of biological foundations for these categories.
A landmark study in Psychiatry Research (Allsopp et al., 2019) concludes that:

Psychiatric diagnoses rely on arbitrary criteria,
They show massive symptom overlap between different disorders (e.g., anxiety, depression, bipolar disorder),
They systematically conceal the role of life events and trauma in the emergence of psychological suffering.

The authors go so far as to call the current diagnostic system a:

“Fallacious categorical system devoid of scientific validity.”

Professor Peter Kinderman, co-author of the study, notes:

“Diagnoses create the illusion of an explanation. In reality, they provide no genuine understanding of human distress.”

The implications are profound: the majority of current psychiatric practice rests not on science but on a social and commercial construction.

1.2 The collapse of the genetic model

In parallel, the hypothesis of a strong genetic basis for depression, anxiety, or schizophrenia has unraveled over the last decade.

The largest genetic study ever conducted on depression (Border et al., American Journal of Psychiatry, 2019), with more than 620,000 participants, showed:

No single gene has a significant effect,
The genetic “associations” reported in the 1990s–2000s were artifacts of small samples,
Even combining thousands of markers, the overall effect remains tiny and biologically insignificant.

As Science put it in a 2019 analysis:

“There is no gene for depression. The prior literature is statistical noise.”

This unequivocal disavowal signals the failure of a psychiatry built on the promise of DNA-based “precision psychiatry.”

The genetic dream collapses because it rests on a mistaken premise: psychic suffering is primarily an adaptive response to a deleterious environment, not an intrinsic biological anomaly.

1.3 The serotonin myth, debunked

Finally, belief in a “serotonin deficit” as the cause of depression has also crumbled under independent research.

In Psychology Today (2022), Professor Steven Hollon summarizes recent data:

“Depressed patients have higher-than-normal brain serotonin levels, not lower.”

Work such as Gjerris et al. (1987) and Sullivan et al. (2006) had already observed that:

Levels of serotonergic metabolites (like 5-HIAA) are elevated in depressed patients,
Serotonin functions not as a ‘happiness hormone’ but as an energetic brake, inducing passivity, social withdrawal, and behavioral inhibition.

The meteoric rise in SSRI prescriptions is therefore based on a fundamental misunderstanding.

Worse, many studies show that artificially increasing extracellular serotonin via SSRIs:

Initially heightens anxiety and suicide risk,
Induces lasting emotional blunting,
Impairs the capacity to feel joy, guilt, attachment.

In other words: psychiatry has built its empire on a complete inversion of biological reality.

2. Chronic stress: the real engine of depression, anxiety, and PTSD

2.1 Stress: the ignored origin

While official psychiatry continues to hunt for genetic causes and hypothetical biochemical anomalies, clinical data increasingly converge on a simple fact:
Chronic stress is the principal cause of mental disorders.

According to WebMD (Stress and Depression, 2022):

“Around 90% of major depressive episodes are preceded by a stressful life event.”

World-renowned neuroendocrinologist Robert Sapolsky writes in Why Zebras Don’t Get Ulcers:

“Chronic stress is a major risk factor for virtually all human mental illnesses.”

Divorce, economic precarity, social isolation, abuse, early trauma—these events can durably alter brain function with no genetic predisposition required.

Yet, despite this clinical reality, stress is systematically underestimated (or denied) in contemporary psychiatric practice.

2.2 Cortisol: the brain’s silent destroyer

Cortisol is the body’s main stress hormone, produced by the adrenals via HPA-axis activation. It is vital for short-term survival.

When stress becomes chronic, however, cortisol stops being protective and becomes destructive:

It atrophies the hippocampus, critical for memory, learning, and emotional regulation,
It inhibits neurogenesis,
It impairs mitochondrial function, leading to a progressive collapse in cellular energy production.

A Science study (Liston et al., 2019) shows that chronic cortisol administration in animals leads to:

Massive synapse loss in the prefrontal cortex,
Marked reductions in exploratory and social behaviors,
A progressive onset of symptoms akin to clinical depression.

A crucial fact: in labs around the world, depression does not appear spontaneously in animals it is induced experimentally via chronic unpredictable stress, social defeat, or separation. No gene or inherited vulnerability is necessary. Apply intense, repeated, inescapable stress and you see human-like outcomes: inhibition, withdrawal, disordered sleep, loss of motivation, reduced exploration.

In other words, chronic cortisol exposure reproduces experimentally the major features of human depressive disorders.

2.3 PTSD: the experience of extreme trauma

Post-traumatic stress disorder (PTSD) powerfully demonstrates the role of stress in the genesis of mental disorders.

Contrary to the official narrative implying underlying genetic vulnerability, declassified military documents (Amnesty International, 2014; ACLU, 2015) reveal that:

“The goal of so-called ‘enhanced interrogation’ techniques was to induce a state of depression and total passivity (learned helplessness) by prolonged exposure to inescapable stress.”

In PTSD:

The HPA axis is dysregulated,
Serotonin (5-HT) and norepinephrine (NE) remain abnormally elevated during sleep,
Emotional circuits fail to extinguish traumatic memories.

A recent study (Vijayan et al., Journal of Neuroscience, 2023) shows that chronically elevated serotonin and norepinephrine during sleep inhibit fear-extinction circuits, thereby maintaining trauma re-experiencing and recurrent nightmares.

Crucially, several clinical trials (e.g., Neylan et al., 1998) have shown that blocking serotonin with antagonists like cyproheptadine effectively abolishes PTSD-related nightmares, restoring normal sleep.

PTSD is not a “mysterious illness”:
It is a living scar left by extreme emotional stress, consolidated by hormonal and neurochemical imbalances.

2.4 Serotonin: the hidden engine of stress

Contrary to popular belief, serotonin does not soothe the organism.
On the contrary, in chronic-stress conditions it acts as an amplifier of stress.

The 5-HT2C receptor, in particular, plays a critical role:

Its activation stimulates ACTH secretion, triggering increased cortisol production,
It promotes anxiety, conditioned fear, and social passivity.

Mouse studies with genetic deletion of 5-HT2C (Heisler et al., 2007; Spoida et al., 2022) show:

Much faster fear extinction,
Marked resistance to experimentally induced anxiety.

This confirms a disquieting observation:
Serotonin is a biological messenger of danger, inhibition, and giving up, not of well-being.

The mass promotion of serotonin by pharmaceutical psychiatry, notably through SSRIs, is therefore an inversion of biological reality.

3. Bioenergetics and mental health: restore energy to heal

3.1 Mitochondria: the forgotten key to mental health

Mitochondria, the cell’s “power plants,” are fundamental to psychological balance.
The brain is only ~2% of body weight yet consumes ~25% of total energy.

When mitochondrial function is impaired, ATP production drops sharply.
This energy shortage has dramatic consequences:

Reduced emotional adaptability,
Lowered neuronal plasticity,
Disrupted reward and motivation circuits,
Increased vulnerability to stress.

A recent study in The American Journal of Geriatric Psychiatry (Mastrobattista et al., 2022) showed:

“Older patients with major depression exhibit impaired mitochondria marked by elevated GDF-15, a signal of accelerated aging and degraded energetic function.”

The worse the mitochondrial dysfunction, the faster the biological aging and the more severe the depressive symptoms.

3.2 Energetic collapse under stress

Chronic stress triggers multiple harmful mechanisms:

Elevated cortisol and sustained serotonin directly disrupt mitochondrial activity,
Reduced oxidative phosphorylation (OXPHOS), the main ATP-producing pathway,
Activation of anaerobic glycolysis even in the presence of oxygen (a “cerebral Warburg effect”),
Accumulation of free radicals and glycation products, accelerating cellular damage.

The result is a bioenergetic collapse, in which brain cells:

Run on low power,
Lose adaptive capacity,
Enter self-degrading cycles.

This energetic collapse explains why depression, severe anxiety, or PTSD often become chronic states resistant to symptomatic treatments.

3.3 Restoring energy: a neglected yet effective strategy

Restoring mitochondrial function is a major therapeutic approach still largely ignored by conventional psychiatry.

Several natural agents have shown the capacity to support cellular bioenergy:

Niacinamide (vitamin B3): direct precursor of NAD+, essential for mitochondrial enzymes,
Thiamine (vitamin B1): indispensable cofactor for glucose entry into the Krebs cycle,
Magnesium: stabilizer of respiratory-chain enzyme complexes,
Flavonoids (quercetin, apigenin): potent antioxidants that support mitochondrial biogenesis,
Progesterone and pregnenolone: natural steroid hormones with direct protective effects on neuronal mitochondria.

For example, an animal study (eNeuro, 2018) showed that niacinamide administration led to:

Rapid restoration of brain ATP after stress,
Regression of anxiety and passivity behaviors,
Improved resilience to new stressors.

Restoring the brain’s energetic capacity is not a secondary luxury; it is the core of authentic psychological healing.

By strengthening mitochondria, we do more than treat a symptom:
We return to living systems their fundamental capacity to repair, adapt, and regain vital momentum.

4. Massive medical errors: SSRIs and the promotion of serotonin

4.1 SSRIs: an illusory solution with harmful consequences

Selective serotonin reuptake inhibitors (SSRIs) were marketed in the 1980s as a revolutionary advance against depression, supposedly “correcting” a chemical deficit by boosting extracellular serotonin.

Decades of clinical observation and research radically challenge this approach.

First, SSRIs often worsen symptoms in the first weeks:

Numerous studies show a clear rise in suicide risk during the initial phase, especially in young adults (FDA black-box warning, 2004).

Second, where improvement exists, it is often:

Small (less than 2 points on the Hamilton Depression Scale),
Below the threshold of clinical relevance,
Comparable to a placebo effect amplified by patient expectations (Kirsch et al., 2008).

False winners? The “active-placebo” problem

Most SSRI trials compare the drug to inert placebos. Yet SSRIs commonly produce noticeable side effects (dry mouth, nausea, agitation, sexual dysfunction). This often unblinds participants and clinicians, inflating apparent efficacy by boosting placebo response among those who sense side effects and infer they’re on the real drug.

A 2024 paper in Brain (How side effects can improve treatment efficacy: a randomized trial) showed:

“Mild side effects can serve as a signal of an effective treatment, thereby influencing expectations and outcomes.”

Participants receiving an active placebo (producing mild side effects) reported significantly greater improvements than those receiving an inert placebo. In short, feeling a side effect can increase the subjective therapeutic response.

Third, prolonged SSRI use induces deleterious neuropsychological effects:

Emotional blunting,
Reduced empathy (Schreiter et al., 2021),
Lasting sexual and emotional dysfunction (post-SSRI syndrome),
Entrenchment of depressive states via secondary brain changes (5-HT2C up-regulation, reduced plasticity).

Steven Hollon writes in Psychology Today (2022):

“SSRIs don’t restore impaired brain function; they force a compensatory adaptation to abnormally high serotonin levels.”

Far from being curative, SSRIs impose a biochemical stress to which the brain must painfully adapt.

4.2 The ignored alternative: blocking serotonin to heal

A growing body of data suggests that reducing serotonergic activity, rather than increasing it, may be a much more effective approach for stress-related disorders and depression.

Agents with beneficial effects via serotonergic antagonism include:

Cyproheptadine: 5-HT2A/5-HT2C antagonist, used successfully to abolish PTSD-related nightmares (Neylan et al., 1998).
Metergoline: non-selective serotonin inhibitor with demonstrated anxiolytic and antidepressant properties.
Diphenhydramine at low doses (50–100 mg): blocks several 5-HT receptors without acting as an SSRI.

Animal studies confirm this approach.
In Neuropsychopharmacology (2011), 5-HT7 antagonism showed:

Faster extinction of conditioned fear,
Significant reductions in depressive and anxious behaviors,
Quicker restoration of synaptic plasticity.

Even more strikingly, in Spoida et al. (2022):

“Mice lacking the 5-HT2C receptor exhibited accelerated fear extinction and exceptional resistance to experimentally induced anxiety.”

It becomes clear that stimulating serotonin is not only ineffective but potentially harmful, whereas antagonizing it offers a powerful route to restore emotional resilience.

5. Natural solutions: restoring hormonal and energetic balance

5.1 Rebalancing stress hormones: a therapeutic priority

Chronic stress, traumatic, psychological, or environmental deeply disrupts endocrine balance.
Two major imbalances are consistently observed in people with depression, PTSD, or generalized anxiety:

Pathologically elevated cortisol, the catabolic stress hormone,
A marked drop in protective steroid hormones such as testosterone, DHEA, progesterone, and pregnenolone.

In men, a high cortisol/testosterone ratio correlates with increased PTSD vulnerability (Josephs et al., 2017).
In women, the cortisol/DHEA ratio appears to predict depressive and anxiety severity (Goodyer et al., 2001).

Several of these steroids have powerful neuroprotective and anxiolytic effects:

Pregnenolone enhances synaptic plasticity and dampens HPA activation.
Progesterone and its metabolite allopregnanolone positively modulate GABA-A receptors, yielding a profound calming effect.
DHEA regulates reward circuits and lowers cortisol production.
Testosterone improves emotional resilience and cognitive function.

A recent paper in Biological Psychiatry (2023) showed that allopregnanolone supplementation:

“Completely reversed stress-induced depressive symptoms by locally restoring neurosteroid biosynthesis in the amygdala.”

This hormonal approach is not blind substitution but a careful restoration of physiological ratios to rebuild the organism’s adaptive capacity to stress.

5.2 Supporting bioenergy through diet and micronutrients

Beyond hormones, bioenergetic reconstruction also requires targeted nutritional inputs.
Key nutrients involved in ATP production, neuronal protection, and oxidative-stress modulation include:

Thiamine (B1): crucial for glucose metabolism and pyruvate dehydrogenase function,
Niacinamide (B3): NAD+ precursor, vital for mitochondrial function,
Magnesium: necessary for 300+ enzymatic reactions, including ATP synthesis,
Zinc and selenium: cofactors for antioxidant and detox enzymes,
Natural flavonoids (quercetin, apigenin, luteolin): potent modulators of inflammation and mitochondrial stress.

Complementary dietary approaches can support energetic rebalancing:

Reducing tryptophan intake (serotonin precursor) via protein/gelatin balance,
→ Animal studies show excess tryptophan favors neuroinflammation and HPA activation.
High glycine intake via gelatin or hydrolyzed collagen,
→ Glycine supports deep sleep, improves gut barrier function, and favorably modulates neurotransmission.
Moderate restriction of polyunsaturated fatty acids (PUFAs), which oxidize mitochondria and promote chronic inflammation.

Lifestyle factors are also crucial:

Regular natural light exposure to synchronize circadian rhythms and support steroidogenesis,
Gentle but consistent physical activity to stimulate mitochondrial biogenesis,
Adequate deep sleep, a sine qua non for neuronal restoration.

5.3 An integrative, systemic, and resolutely non-psychiatric approach

All these hormonal, nutritional, micronutritional, and environmental strategies share a fundamental principle:

They do not treat “depression” as an abstract entity but as the tangible reflection of a multifactorial biological imbalance caused by stress, energy deficit, and environment.

They target root causes, not mere symptoms.
They restore the body’s capacity to self-regulate, rather than forcing it to adapt to an artificial, chemically imposed state.

Given the evident failure of medication-centric psychiatry, this restorative approach offers a coherent, biological, humane—and above all effective—alternative.

Conclusion

For decades, modern psychiatry has imposed a biomedical reading of mental distress based on two pillars: the faulty gene and the deficient neurotransmitter. This deeply reductionist vision has medicalized human suffering, turning adaptive, reactive states into chronic diagnoses, and millions into lifelong patients.

Yet, as an ever-growing literature shows, this paradigm is not only scientifically unfounded but actively harmful.

Depression, anxiety, PTSD, and related disorders are not brain defects.
They are intelligible, predictable, adaptive, albeit painful, responses to a world that has become toxic to the organism.

At the root:

Chronic stress, psychological, social, nutritional, metabolic,
Bioenergetic dysfunction, particularly mitochondrial,
The progressive collapse of hormonal and emotional regulation systems.

Rather than recognizing this, institutional psychiatry persists:

Denying the central role of stress,
Promoting chemical treatments that worsen imbalances (SSRIs, antipsychotics),
Pathologizing normal suffering for profit.

The facts are increasingly clear:

SSRIs do not produce durable improvement in depression.
Serotonin is a mediator of stress, not well-being.
The “depressed brain” is not “sick”: it is exhausted, overloaded, desynchronized.

In response, one path stands out:

Restore cellular energy,
Rebalance stress hormones,
Favor nutrients that support neuroplasticity and metabolism,
And above all, reclaim the human meaning of suffering.

Depression is not a defect to be silenced.
It is a vital signal that the system is overloaded, that the environment has become incompatible with equilibrium.

The task is not to mute it chemically.
It is to listen, understand, and repair the living system where it has been wounded.

As long as we treat depression as a brain anomaly, we will keep manufacturing millions of patients.
The day we recognize it as a healthy response to a sick world, we can finally begin to heal.

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Demystifying Psychiatry and the Betrayal of Mental-Health Medicine