A Mind of Your Own: The Truth About Depression and How Women Can Heal Their Bodies to Reclaim Their Lives. Dr Brogan Kelly
class. Some doctors prescribe them for arthritis, hot flashes, migraine, irritable bowel syndrome, and panic disorder. The fact that antidepressants can be prescribed to treat arthritis, an inflammatory disease of the joints, undermines any beliefs about their ability to precisely correct a chemical imbalance at the root of everything from phobias to bulimia and melancholic depression. The condemning 2015 paper by researchers at Johns Hopkins Bloomberg School of Public Health that I discussed in the previous chapter clearly states that antidepressants are used willy-nilly.9 In their study, the authors conclude that most people who take antidepressants never meet the medical criteria for a bona fide diagnosis of major depression, and many who are given antidepressants for conditions like OCD, panic disorder, social phobia, and anxiety don’t actually have these conditions.
Let’s not forget the use of these medications in young children. And they are prescribed not only for depression but behavioral issues such as inattention, temper tantrums, tics, autism, and impaired thinking. How did we ever come to think that this could be a safe and effective treatment for two-year-olds still in diapers who don’t even speak in full sentences yet? For starters, consider Study 329, which cost GlaxoSmithKlein $3 billion for their efforts to promote antidepressants to youngsters.10 This drug company manipulated data that hid signs of increased risk of suicide. The company also falsely represented Paxil as outperforming a placebo.11
Among the most celebrated and respected thought leaders in my field is Joanna Moncrieff. She is a senior lecturer in psychiatry at University College London and co-chair of the Critical Psychiatry Network, a group of psychiatrists who dispute the generally accepted model of depression and seek alternative approaches to psychiatry. In a seminal 2006 paper, “Do Antidepressants Cure or Create Abnormal Brain States?” Moncrieff and her coauthor write: “Our analysis indicates that there are no specific antidepressant drugs, that most of the short-term effects of antidepressants are shared by many other drugs, and that long-term drug treatment with antidepressants or any other drugs has not been shown to lead to long-term elevation of mood. We suggest that the term ‘antidepressant’ should be abandoned.”12
At this point, you might be wondering: Where did antidepressants come from and how did they get so popular?
A MEME IS BORN13
The predominant theory behind modern antidepressants (SSRIs, or selective serotonin reuptake inhibitors) is that they work by increasing the availability of serotonin, a neurotransmitter famously associated with mood, in the gaps between cells of the brain. In fact, if you were to quiz someone on the street about the biology of depression, they would likely parrot “chemical imbalance” in the brain and go so far as to say a “serotonin deficiency.” This hypothesis, referred to as the monoamine hypothesis, grew primarily out of two main observations made in the 1950s and ’60s.14 One was seen in patients being treated for tuberculosis who experienced mood-related side effects from the antitubercular drug iproniazid, which can change the levels of serotonin in the brain. Another was the claim that reserpine, a medication introduced for seizures and high blood pressure, depleted these chemicals and caused depression—that is, until there was a fifty-four person study that demonstrated that it resolved depression.15
From these preliminary and largely inconsistent observations a theory was born, crystallized by the work and writings of the late Dr. Joseph Schildkraut, who threw fairy dust into the field in 1965 with his speculative manifesto “The Catecholamine Hypothesis of Affective Disorders.”16 Dr. Schildkraut was a prominent psychiatrist at Harvard who studied catecholamines, a class of naturally occurring compounds that act as chemical messengers, or neurotransmitters, within the brain. He looked at one neurochemical in particular, norepinephrine, in people before and during treatment with antidepressants and found that depression suppressed its effectiveness as a chemical messenger. Based on his findings, he theorized broadly about the biochemical underpinnings of mental illnesses. In a field struggling to establish legitimacy (beyond the therapeutic lobotomy!), psychiatry was desperate for a rebranding, and the pharmaceutical industry was all too happy to partner in the effort.
This idea that these medications correct an imbalance that has something to do with a brain chemical has been so universally accepted that no one bothers to question it or even research it using modern rigors of science. According to Dr. Joanna Moncrieff, we have been led to believe that these medications have disease-based effects—that they’re actually fixing, curing, correcting a real disease in human physiology. Six decades of study, however, have revealed conflicting, confusing, and inconclusive data.17 That’s right: there has never been a human study that successfully links low serotonin levels and depression. Imaging studies, blood and urine tests, postmortem suicide assessments, and even animal research have never validated the link between neurotransmitter levels and depression.18 In other words, the serotonin theory of depression is a total myth that has been unjustly supported by the manipulation of data. Much to the contrary, high serotonin levels have been linked to a range of problems, including schizophrenia and autism.19
Paul Andrews, an assistant professor of psychology, neuroscience, and behavior at McMaster University in Canada, is among the vocal experts challenging the traditional depression model. In a 2015 review, he declares that the science behind antidepressant medications appears to be backward: serotonin is a downer, not an upper.20 He argues that serotonin is almost like a first responder to stress. When our bodies are under duress, serotonin helps to reallocate resources at a cellular level. This further shows that we really have no idea what’s going on when it comes to looking at one simple chemical. Andrews brings up a good point in a recent review: we can’t measure serotonin in a living human brain yet, so it’s impossible to know exactly how the brain is releasing and using serotonin. What scientists must do instead is rely on evidence about levels of serotonin that the brain has already metabolized, and by studying seratonin in animal models. To date, the best available evidence indicates that more serotonin—not less—is released and used during depressive episodes. This natural surge of serotonin helps the brain adapt to depression; it forces the body to spend more energy on conscious thought than to areas such as growth, development, reproduction, immune function, and the stress response.21
Andrews also happens to be an evolutionary psychologist, and has asserted in previous research that antidepressants leave individuals worse off after they stop taking them. He agrees that even though depression can be a painful, troubling experience, most forms of depression are normal adaptations to stress. According to Andrews, when patients on SSRI medication improve, it appears that their brains are actually overcoming the effects of antidepressants, rather than being helped by them. The drugs are interfering with the brain’s own mechanisms of recovery. This is an important point, because time and time again people ask me how antidepressants appear to be helpful in the short term. Perhaps, in the rare instance that their effects are adaptive, it is by virtue of the brain’s own powers trying to combat the assault of the antidepressants—not the other way around. But over time, as the assault continues, the brain is functionally compromised under the constant force of the incoming drugs.
One critical review of the serotonin hypothesis concludes: “ . . . there is no direct evidence of serotonin or norepinephrine deficiency despite thousands of studies that have attempted to validate this notion.”22 And in a scathing review on major depression published in the New England Journal of Medicine in 2008, the researchers write: “. . . numerous studies of norepinephrine and serotonin metabolites in plasma, urine, and cerebrospinal fluid as well as postmortem studies of the brains of patients with depression, have yet to identify the purported deficiency reliably.”23
In the cogent words of Dr. Daniel Carlat, author of Unhinged, “We have convinced ourselves that we have developed cures for mental illnesses . . . when in fact we know so little about the underlying neurobiology of their causes that our treatments are often a series of trials and errors.”24 Indeed, the brain orchestrates a delicate interplay among some one hundred neurotransmitters, including fourteen different types of serotonin receptors. To think we can cherry-pick one brain chemical and cure all and every behavioral disturbance is a gross oversimplification and downright absurd.
The brain is much more complex than the serotonin model