Despite the controversial findings in older and recent scientific studies, depression continues to be misleadingly treated as a disease, as an illness of the brain.

The old school was telling us that the brain was out of whack, mixing the wrong juices – hence the “the brain chemical imbalance” theory.

Following more than 60 years of failure to prove itself and given the rising number of depression cases, the serious adverse effects of antidepressants, added to the numerous scientific studies disproving the serotonin imbalance guesswork theory, a new theory is about to dethrone the former: the brain inflammation theory.

But let’s look at the history behind the two.




The title is perhaps as misleading as the theory itself, since the order was in reverse: the discovery by chance of antidepressants, followed by a theory meant to sustain them.

The era of antidepressants started around 1952 with isoniazid, a drug against tuberculosis, which was accidentally found to have euphoric effects in patients treated for this condition.
The secondary effects of this tuberculosis drug shortly became the hero in the treatment of “mental conditions,” paving the path for the “brain chemical imbalance” theory. Source:

Note that the science behind the serotonin imbalance theory and the multi billion dollars industry relies on a discovery by pure chance, and not on a research model based on a theory waiting to be proved or disproved.

The order of events behind the conclusion is: tuberculosis – isoniazid – side effects – mood elevation – drug prescribed for depression = theory launched to sustain the prescription of the drug for mental conditions.

In 1998, clinical psychologist Irving Kirsch, P.h.D, took a closer look at the evidence-based results obtained by both placebo and antidepressants. From all the clinical trials (38 clinical trials involving over 3000 patients suffering from depression) on which the pharmaceutical industry relied to obtain approval from the FDA, the results showed that 75% of antidepressants are no better than placebo (a neutral sugar pill). Otherwise said you are 75 times more likely to increase serotonin level and stabilise mood disorders by taking a mock sugar pill and have 0 side effects. Conversely, by taking an antidepressant, you have 75% chance to obtain the same effect as a sugar pill, with 100% ‘side’ effect risks, which in some cases are more severe than the condition for which they are prescribed.
In the light of the evidence, the so-called ‘side effects’, are not side at all, but main effects.

In conclusion, the chemical imbalance theory pretends to reinstall brain chemistry balance through the introduction of a long-term treatment that causes a massive chemical imbalance in the whole body, of which the brain is a part…?

Whose interests do you think this theory serves best?




Based on the same vested interests of its proponents (the pharmaceutical industry), and following the same unorthodox ‘scientific’ rigour, the brain inflammation theory is nothing but a desperate attempt to substitute a manifestly false hypothesis with another, while maintaining the need for a drug as an imperative.

Simply put, “the people grew smarter since 1952, and since we cannot substantiate our claims for antidepressants, we better switch gear to deflect the attention from 60 years of misuse and misrepresentation towards a promising ‘breakthrough’. And this time, we better find a physical link to ensure the undisputable need and dependence on drugs.”

Like its former star, the inflammation theory receives a suspicious round of applauses and professional support on all media channels, heralded as the new messiah before the ink has even dried on the research papers.

At a closer scrutiny of this new ‘miracle cure’ waiting for the theory to become established fact through clever lobbying and ghost-writing scientific shenanigans, we discover that this theory, too, is pulled by the hair, just as its serotonin precursor.

In one of their scientific papers regarding the new theory of inflammation being the cause of depression, Dr. Charles Raison, Department of Psychiatry and Behavioral Sciences, of the Emory Mind Body Program and director of the Behavioral Immunology Clinic, and his colleague, D. Andrew H. Miller wrote:

“…the answer to the question of whether depression is an inflammatory disorder is a resounding “no.”

Even with a nod of recognition toward the fact that all disease processes have an inherent “sloppiness” that precludes absolute one-to-one correspondences between putative causes and observed symptomatic outcomes, it is clear that inflammation is neither necessary nor sufficient to cause MDD. Desperately depressed people often have low levels of systemic inflammation, and individuals with ragingly high inflammatory activity are often—but less commonly—able to retain a good mood and hopeful stance toward their lives.”

To the question of whether the inflammatory process contributes to most or just to some cases of depression, Raison & Miller elaborate:

“If depression is not an inflammatory disorder in the sense that RA and other autoimmune conditions are inflammatory disorders, how should we best understand the growing database (which now includes three meta-analyses [5–7]) indicating that depression is associated with increased inflammation? Three points are most important here.
First, what studies actually report is that on average, the mean value for an array of inflammatory mediators tends to be higher in depressed groups than in groups of nondepressed individuals. In many studies, this increase in the mean is independent of other factors associated with increased inflammation, such as body mass index and sex. In other studies, the difference between depressed and nondepressed groups goes away when these types of factors (many of which are overrepresented in depression) are taken into account [2].
Second, the elevations in proinflammatory cytokines and other inflammatory elements observed in groups of depressed individuals are far more modest than increases typically observed in autoimmune or infectious diseases, with mean values in depression typically not exceeding two to three times the values found in healthy control groups [5]. Consistent with these modest differences, mean values for inflammatory markers in groups of depressed individuals are typically in the “normal” range when such norms have been established [8•, 9–13], as is the case with CRP [14].

When put this way, the connection between depression and increased inflammation seems underwhelming, and one might be tempted to dismiss it as physiologically irrelevant.  As it turns out, depression is far from alone in being a condition characterized by reliable—but often only mildly increased— inflammatory activity. Other modern illnesses with evidence of moderately increased inflammatory signaling include cardiovascular disease, stroke, cancer, diabetes, and dementia. Conversely, even minor increases in inflammation—such as are observed in depression—are enough to strongly predict the development over time of many of these modern disease states [15–20].
Finally, we come to a third point that is vital for understanding the nature of the association between inflammation and depression: the values for any given inflammatory marker always overlap between groups of depressed and nondepressed individuals, regardless of how much higher the marker’s mean value may be in the depressed group. Thus, it is not unheard of for the highest value in any particular study to be in the nondepressed group and the lowest value to be in the depressed group. More importantly, it also means that a large proportion of the depressed group in any given study will have values similar to those in the nondepressed group, which—at least on first blush—makes it hard to envision these people as suffering from a disease state caused by increased inflammation. On the other hand, even though values tend to be fairly evenly distributed across the whole range in both depressed and nondepressed populations, typically about one-third or so of the depressed group have values that are clearly higher than the majority of nondepressed comparison individuals. These are the people responsible for the finding that depression is associated with increased inflammation.

It is a dirty little secret of sorts that they have been pulling all their noninflamed depressed colleagues along with them in publication after publication, giving the world a slightly misguided sense that depression—as a whole—is driven by increased inflammation.”

(emphasis added,

The theory behind the theory has somewhat vague and mysterious origins. It started with a five years study (no longer present on the internet, strangely!) on mice and rats exposed to tests causing chronic pain to understand its effects.
In a nutshell, the results were that chronic pain stimulates the production of cytokines, which, in their turn cause inflammation, and that these poor mice and rats suffering from such ordeals were also depressed (what a surprise!)

Once again, we have a theory born from thin air, following an ambitious reasoning equilibristic. Whatever happened to the original papers, the chronic pain has been conveniently left out of the new scientific pro-drugs articles.

The scientific reasoning, when reduced to evidence, follows a precarious order: depressed people (1/3 of cases) have shown high markers of cytokines – cytokines cause inflammation = depression is caused by inflammation.

In another article in the BMC Medicine Journal, a group of scientists tackle the common sense missing link of this theory, under the self-explanatory title:

“So depression is an inflammatory disease, but where does the inflammation come from?”


Their findings regarding the cause of depression and brain inflammation are:

“A range of factors appear to increase the risk for the development of depression, and seem to be associated with systemic inflammation; these include psychosocial stressors, poor diet, physical inactivity, obesity, smoking, altered gut permeability, atopy, dental cares, sleep and vitamin D deficiency.”

In examining further the increased risks of inflammation and depression, they enlist amongst causal factors: childhood or adult psychological traumas and environmental stressors. These, in their turn, lead to oxidative and nitrosative stress, found in chronic fatigue, somatization and psychosomatic conditions – all causing intracellular inflammation. Source

Their findings are salutary since their main accent is on prevention and natural cure instead on a drug treatment as a primary course of action. From psychotherapy, counselling and meditation, to diet, exercise, sleep and vitamin D, the natural treatment proves the healthier solution.

“In terms of behavioral strategies, recent research suggests that interventions known to benefit depression—such as physical exercise or psychotherapy—also reduce peripheral inflammatory biomarkers [85–88], although the degree to which this effect is essential for antidepressant efficacy is an open question. Other more experimental interventions for depression, such as meditation, also have been reported to reduce peripheral inflammatory responses to psychosocial stress [89, 90].”

The authors conclude on the same plea I have been making for years, insisting on the urgent need of education of the population in preventive care, rather than relying exclusively on treatment. Which is a fancy way of saying, “rather than waiting until is too late”.

“Psychiatry largely lacks an integrated model for conceptualizing modifiable risk factors for depression. It has, therefore, lacked conceptually and pragmatically coherent primary prevention strategies, prioritizing the treatment of established disorders. Yet the rationale, targets and imperative to focus on prevention of depression at a population level is clear.”


So nothing’s new under the sun!

Psychosocial stress (poverty, wars, extreme competition, job insecurity, poisoned food and air, lack of proper education, etc.) is behind all kinds of conditions, which may or may not cause brain inflammation, but which could and do cause depression and a long list of other serious illnesses, including premature death.

What is the solution?

Prevention through a proper public and professional holistic education, of course! However, since we are a bit late for that, we should start with a good education of the person suffering from any condition, including depression.

I say education and not therapy first, since, in my view, no therapy in the world could effectively address any issue if the individual is not educated into its own functioning to ensure that the old habits (mental, emotional or physical) are not repeated, leading to further issues or “relapses”.

Therapy is secondary in importance. I found that a thorough education of my clients, which lead them to heightened self-awareness regarding their self-destructive patterns and to a better life hygiene, had a profound transformative effect in itself. Put it simply: ignorance causes illness, knowledge heals!

When it comes to depression, I recommend that people work only with coaches and therapists who have suffered themselves from this condition and have proven to have successfully come out of it naturally. Only those who have beaten the invisible path of this labyrinth called depression could successfully guide those in the dark.

I have, and so have all my clients.
I have proven time and time again that depression can be cured in 8 – 12 weeks naturally, with a total discontinuation of antidepressants from the beginning, without any withdrawal symptoms and with no relapse.

However, I have to give credit to the pharmaceutical industry when it comes to cases of poor education, low level of intellect individuals. There is no nicer way to put it either than simple-minded people would take ages to catch up on the learning abilities and level of cognition. Their beliefs systems are deeply rooted in religion, pseudoscience, superstition, and all kinds of mixed new-age nonsense, making it almost impossible to make them accept responsibility for their health, mental states and life in general. For this type of individuals (and unfortunately that is an overwhelming majority), their condition (whether physical, mental or social) must be attributed to external factors than themselves. And as such, only an external intervention will ‘cut it’ (being drug-based medicine, a miracle healer, angels, extraterrestrials or God.
For these cases, the mainstream treatment, as disputable as it may be, is the only hope, besides a miracle or a sudden epiphany.

To enrol on my email mentoring programmes for depression, anxiety, burn out and stress-related conditions:


Copyright Gratiela M. Rosu,

Founder of CWS Coaching*, Author, Therapist, Preventive Health Educator


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