Fraud and Dogma — 2 Sides of a Coin
Fraud in the Largest Antidepressant Study - Part 2
This post is Part 2 on the April 29, 2024 session of the IPAK-EDU Director’s Science Webinar featuring the research and journalism of Robert Whitaker.
Part 1 is HERE.
Junk Science?
Several commentators have criticized the science on antidepressants and SSRIs naming it ‘junk science’.
The word ‘junk’ connotes several things. Poor or garbage-like quality (as in a ‘junk yard’), or unwanted (as in ‘junk mail’), and lacking substance (as in ‘junk food’). Combining these connotations with the word ‘science’, while sometimes appropriate, is imprecise.
‘Junk science’ has been used as a pejorative in many contexts; indeed, everything from describing the work of non-scientists, or those perceived as ‘outsiders’, to dismissal of research into such subjects as ESP or the Bermuda Triangle. Whatever the motivation, the label is a dismissal.
What is revealed by Robert Whitaker’s research and writing, on the other hand, is much more pointed than a backhanded colloquialism. What Whitaker describes, in the case of the STAR*D Study and the role of the NIMH, is a publicly-funded fraud, and there’s a tremendous difference.
Whereas ‘junk science’ may be frivolous or lack rigor, the term itself is simply a dismissive insult, whereas fraud is a criminal act of deception. It is, without equivocation, an intentional misrepresentation and perversion of evidence; and in the case of STAR*D, a crime in the context of one of the most influential studies on mental health paid for by an unsuspecting public.
Let us be clear: fraud is fundamentally a betrayal of trust.
And further, when mainstream media provides cover, while simultaneously propagating and compounding the fraud, they are acting as enablers and abetting the fraud.
Watch.
The Serotonin Hypothesis
At the root of the fraud here is a mythology, a set of beliefs so widely disseminated that it has taken on the luster of truth.
The popular version of how SSRIs work is a cartoon that holds that depression is a result of serotonin deficiency. Thus, by monkey-wrenching and inhibiting the serotonin reuptake cycle, the drug increases serotonin activity. But the truth of the matter is that even the experts don’t know precisely how these drugs work.
For context, Joanna Moncrieff and colleagues recently published a systematic umbrella review in Molecular Psychiatry (a Springer Nature journal) on the evidence concerning the serotonin theory of depression.1
The idea that depression is the result of abnormalities in brain chemicals, particularly serotonin (5-hydroxytryptamine or 5-HT), has been influential for decades, and provides an important justification for the use of antidepressants. A link between lowered serotonin and depression was first suggested in the 1960s and widely publicised from the 1990s with the advent of the Selective Serotonin Reuptake Inhibitor (SSRI) antidepressants. Although it has been questioned more recently, the serotonin theory of depression remains influential, with principal English language textbooks still giving it qualified support, leading researchers endorsing it, and much empirical research based on it. Surveys suggest that 80% or more of the general public now believe it is established that depression is caused by a ‘chemical imbalance’. Many general practitioners also subscribe to this view and popular websites commonly cite the theory.
The public has been indoctrinated to hold a general perception, mirrored by practitioners, prominent researchers, textbooks, popular websites, news media coverage, and social media. Like a self-serving house of mirrors, the mythology surrounding serotonin persists because it has been seeded everywhere, and sound criticism and those willing to give it voice, are suppressed.
The Serotonin Hypothesis is literally, dogma.
dogma (noun) : a principle or statement of ideas, or a group of such principles or statements, especially when considered to be authoritative or accepted uncritically.
-The American Heritage Dictionary
In the Discussion section of their systematic review of the scientific literature, Moncrieff et. al. state rather emphatically (emphases added):
Our comprehensive review of the major strands of research on serotonin shows there is no convincing evidence that depression is associated with, or caused by, lower serotonin concentrations or activity.
They continue:
The chemical imbalance theory of depression is still put forward by professionals, and the serotonin theory, in particular, has formed the basis of a considerable research effort over the last few decades. The general public widely believes that depression has been convincingly demonstrated to be the result of serotonin or other chemical abnormalities, and this belief shapes how people understand their moods, leading to a pessimistic outlook on the outcome of depression and negative expectancies about the possibility of self-regulation of mood. The idea that depression is the result of a chemical imbalance also influences decisions about whether to take or continue antidepressant medication and may discourage people from discontinuing treatment, potentially leading to lifelong dependence on these drugs.
They conclude:
This review suggests that the huge research effort based on the serotonin hypothesis has not produced convincing evidence of a biochemical basis to depression. This is consistent with research on many other biological markers. We suggest it is time to acknowledge that the serotonin theory of depression is not empirically substantiated.
Serotonin: Ancient and Fundamental
The cartoon model of ‘serotonin deficiency’ flies in the face of well-supported, diverse biological evidence.
The deficiency model is overly simplistic, like a see-saw, which contends that tipping the balance of serotonin one way or the other is a reasonable strategy for treating depression. That dogmatic model, of course, serves the goal of selling pharmaceuticals, but is poorly aligned with what is empirically known.
Serotonin is an evolutionarily ancient molecule. It is found throughout life: in plants, animals, fungi, and single-cell organisms, like protozoa. It is found in mammals, worms, lobster, crawfish, mollusks, and all insects—the list goes on and on. Some estimates locate its entry in the evolutionary tree, as an intracellular signaling molecule, at over 2 billlion years ago.2
It is simultaneously a signaling molecule, a hormone, a growth regulator, and a neurotransmitter. It has been found to be fundamentally involved in a wide range of functions at the cellular level, even in the absence of a neuronal network: cell maturation, proliferation, differentiation, and migration. It has even been connected to gene expression, cellular pigmentation, and organism plasticity.
It’s important to note that much of this complexity was already recognized by the late 1990’s.3
Like many aspects of science, the deep story of serotonin is extraordinarily complex, and what we think we know is perhaps just a few patterns of threads woven in the incredibly complex intertwined tapestry of life.
Fraud and Dogma
If fraud is a betrayal of trust, then dogma is ever close at hand; likewise, when dogma is well-established, then fraud is almost inevitable, especially when extraordinary profit is to be made. They are two sides of a coin.
In the case of antidepressants, the dogma of the Serotonin Hypothesis frames the rationale for drug treatment. It is the reason undergirding research and the pursuit of new and ‘better’ SSRIs, the gravity that drives more prescriptions.
The fraud of STAR*D, in the end, is no more than an attempt to rationalize giving escalating levels of pharmaceuticals to patients who don’t respond to treatment, ensuring more prescriptions. And when the data doesn’t support the desired conclusion (the dogma), the data is simply twisted and manipulated so that it does. Fraud in the service of dogma.
That is one way of looking at it.
One might also consider that this was not a study performed to answer a scientific question, it was a performance in and of itself. A performance with the intent of framing a possibility space where only antidepressants can address depression. A performance where ‘remission’ is valued above ‘stay-well’, and where meeting a metric that reinforces the dogma is valued over real healing.
You can’t sell prescriptions to people who get well, after all; but escalating cost tiers for any type of product is a tried and true sales model. And if the drugs being proffered have the potential for long-term use (or even addiction), all the better for the bottom line, and the industry as a whole, no?
Whatever conclusion one comes to, it is clear that dogma can serve as a foundation for fraud, just as fraud can sustain dogma. It runs both ways, like a self-sustaining recursive loop.
In the case of STAR*D, what is documented and can be shown is that:
The conflicts of interest in the STAR*D study are abundant.
Fraud has been clearly demonstrated (go to Mad In America to dig deeper).
The fraud is built on dogma unsubstantiated by empirical evidence.
The cycle goes on, because the loudest voices with the largest reach continue the charade, reifying the dogma and compounding the fraud.
All of this may give the impression of hopelessness; but now you know, and you can inform others.
After all, dogma can only claim authority when it is accepted uncritically.
#questioneverything
Follow Robert Whitaker at Mad In America.
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Moncrieff, J., Cooper, R.E., Stockmann, T. et al. The serotonin theory of depression: a systematic umbrella review of the evidence. Mol Psychiatry 28, 3243–3256 (2023). https://doi.org/10.1038/s41380-022-01661-0
Turlejski, K. Evolutionary ancient roles of serotonin: long-lasting regulation of activity and development. Acta Neurobiologiae Experimentalis Vol 56, No. 2 (1996). https://doi.org/10.55782/ane-1996-1167
Ibid.