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CHAPTER 2

Truth Serum: Coming Clean About the Serotonin Myth

How You’ve Been Misled, Misdiagnosed, and Mistreated

There’s no such thing as an antidepressant.

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The chemical imbalance theory of depression is heavily promoted but remains unfounded.

Do you take antidepressants? Do you know someone who does? Maybe you even have friends and family members who swear they have been lifesaving. Antidepressants might seem like a reasonable option, particularly if things are dire. But do you know the whole story?

At the risk of sounding extreme, let me give you an example from my own case files that sets the tone for this chapter. Kate had never been on an antidepressant and never suffered from depression, but she felt overwhelmed and frazzled after the birth of her first baby. At her six-week postpartum follow-up appointment, her obstetrician prescribed Zoloft. Within one week of starting it, she had written a suicide note and was planning to jump off of her fifteenth-floor Manhattan balcony. She said to me, “It just made sense at the time. And I felt really detached about it, like it was nothing.”

Kate’s experience is not an outlier. She is among millions of women who are reflexively prescribed medication for symptoms of distress. She’s also among those who have serious side effects that may seem like part of the depression—­not a result of the drugs. Rather than examining the sources of her postpartum plight, Kate found herself in dangerously unfamiliar territory in the name of treatment. If only she had known the whole story before deciding to fill that prescription.

The ease with which these medications are dispensed is partly why so many take them: 11 percent of all Americans, 25 percent of whom are women in their forties and fifties. The use of antidepressants has increased almost 400 percent from 1998 to 2008, making them the third most commonly prescribed drugs across all ages. The sharp increase does not necessarily signify a depression epidemic. Through the early 2000s pharmaceutical companies aggressively tested antidepressants for a variety of disorders, which led to an explosion of FDA-approved uses, from depression to premature ejaculation.¹ Believe it or not, we are spending more on antidepressants than the gross national product of more than half of the world’s countries. Sixty percent of ­people on antidepressants stay on them for more than two years, and 14 percent do so for more than a decade. By a conservative estimate, 15 percent of pregnant women take psychiatric medication today, a rate that has tripled in just the last ­couple of years.

The medical industry isn’t selling a cure. They are selling sickness.

SELLING SICKNESS²

Is there a connection between the profligate use of antidepressants and increasing rates of disability? Before antidepressants became so widely used, the National Institute of Mental Health (NIMH) ­assured ­people that recovering from a depressive episode was common and that experiencing a second episode was uncommon.³ But then how do we explain soaring rates of disability and ­escalating prescriptions?

Robert Whitaker, a notable critic of modern psychiatry and author of Anatomy of an Epidemic and Mad in America, has compiled and analyzed data showing that days of work lost are not decreased by medication treatment.⁴ Much to the contrary, they are increased by drug treatment, and so is long-term disability. He also has reported on studies showing that ­people treated for the illness are three times more likely than the untreated individuals to suffer a “cessation” of their “principal social role,” meaning that they function less optimally. And they were nearly seven times more likely to become “incapacitated.” Moreover, 85 percent of unmedicated patients recover in a year, with 67 percent doing so by six months.⁵ From my perspective, that’s an enviable statistic.

What’s going on here? In the past half century, the Diagnostic and Statistical Manual—­the DSM, the bible of diagnosable disorders in psychiatry—­has lengthened to more than three hundred diagnoses in its fifth edition. In 1952 the DSM was a slim 130 pages and outlined 106 illnesses. Today’s version is a colossal 886 pages and includes 374 diagnoses. It encompasses a general consensus by a committee consisting of practitioners with profound conflicts of interest and pharmaceutical enmeshments.⁶ As Dr. Allen Frances of Columbia University and author of Saving Normal states: “Wholesale imperial medicalization of normality that will trivialize mental disorder and lead to a deluge of unneeded medication treatment—­a bonanza for the pharmaceutical industry but at a huge cost to the new false positive patients caught in the excessively wide DSM-V net.”⁷ Dr. Frances is the psychiatrist who chaired the task force that produced the fourth edition of the DSM and has been critical of the latest tome. In 2013, Frances rightfully said that “psychiatric diagnosis still relies exclusively on fallible subjective judgments rather than objective biological tests.”⁸

When you look at the impossibly long list of symptoms and maladies for which antidepressants can be prescribed, it’s practically farcical. These drugs are indicated for classic signs of depression as well as all of the following: premenstrual syndrome, anxiety, obsessive-compulsive disorder (OCD), bipolar disorder, anorexia and binge eating, pain, irritable bowel, and explosive disorders fit for anger management 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 can describe. To be clear, SSRIs block the removal of serotonin from the junctions between nerve cells (synapses) in the brain so there’s increased firing of serotonin nerves. But when serotonergic nerves are overstimulated, they become less sensitive in a bid to establish equilibrium again. In science speak this is called downregulation. And such downregulation doesn’t return to normal after the drug is stopped. We in the scientific community still don’t know if the downregulation can become permanent, but a cadre of my colleagues and I believe this poses a serious risk to the brain. It’s no surprise to me that in the first twelve years after its initial marketing blitz, Prozac was named in more than 40,000 reports of adverse effects submitted to the FDA.²⁵ No other drug comes close to such a history.

Even if we accepted the proposition that these drugs are helpful for some ­people, extrapolating a medical cause from this observation would be akin to saying that shyness is caused by a deficiency of alcohol, or that headaches are caused by a lack of codeine. And what about a genetic vulnerability? Is there such thing as a depression gene? In 2003, a study published in Science suggested that those with genetic variation in their serotonin transporter were three times more likely to be depressed.²⁶ But six years later this idea was wiped out by a meta-analysis of 14,000 patients published in the Journal of the American Medical Association that denied such an association.²⁷ Dr. Thomas Insel, director of the National Institute of Mental Health, commented with the following: “Despite high expectations, neither genomics nor imaging has yet impacted the diagnosis or treatment of the 45 million Americans with serious or moderate mental illness each year.”²⁸ Dr. Carlat speaks the truth in his own words: “And where there is a scientific vacuum, drug companies are happy to insert a marketing message and call it science. As a result, psychiatry has become a proving ground for outrageous manipulations of science in the ser­vice of profit.”²⁹

Suffice it to say the data has poked so many holes in the serotonin theory that even the field of psychiatry itself is putting down its sword. In a 2005 essay for PLOS Medicine by Drs. Jeffrey R. Lacasse and Jonathan Leo, the authors gathered sentiments from influential thinkers in the field, including conventional clinicians and researchers who have expressed doubt on the entirety of what psychiatry has to offer around antidepressants (see tables on the following pages).³⁰

The medical-pharmaceutical complex has constructed quite a few houses of cards, and far too many of its treatments—­very profitable treatments—­are offered without solid evidence to support doing so. In fact, only two studies are required for FDA licensure of most pharmaceuticals, essentially leaving the population to participate in a post-marketing experiment in which adverse effects—­causalities—­are monitored passively. It’s a fabrication of science to think these drugs have a place in medicine, what is meant to be the art of healing. It could be argued that antidepressants are the new tobacco, and, like the tobacco industry, Big Pharma can wield a lot of power through clever marketing to seduce and influence us in stealthy, seemingly benign ways that are anything but.

DIRECT-TO-CONSUMER ADVERTISING

Sadly, direct-to-consumer advertising (DTCA) in America has allowed pharmaceutical companies to “teach” the public about brain chemical imbalances and serotonin deficiencies via sound bites and cleverly worded taglines that escape FDA policing. I have patients who come in believing that the solution is in a pill—­what they’ve learned essentially from commercials. It’s been calculated that DTCA advertising is responsible for nearly half (49 percent) of requests for drugs.³¹ And fully seven out of ten times doctors prescribe based on appeals made by patients who learned through their computers and televisions that they have an “imbalance” that must be fixed with a pill.³²

“Antidepressants and the Chemical Imbalance Theory of Depression: A Reflection and Update on the Discourse,” Behavior Therapist 38, no. 7 (October 2015): 206–213. Reprinted with permission.

In the ten-year period between 1999 and 2008, DTCA tripled, from $1.3 to $4.8 billion, their efforts at educating patients about their need for psychiatric medication. The modern drug business has been built on “brain” medicines. Valium was the first blockbuster, selling 2 billion tablets in 1978. Then in the 1990s came Prozac, which defined the industry. The pharmaceutical industry spent $4.53 billion on direct-to-consumer advertising in the United States alone in 2014, up 18 percent from the previous year.³³

The flagrant disconnect between the advertisements and scientific literature has been written about for more than a decade now, but you probably haven’t read about it. It was clearly stated by Drs. Lacasse and Leo in their 2005 paper: “These advertisements present a seductive concept, and the fact that patients are now presenting with a self-described ‘chemical imbalance’ shows that the [advertising] is having its intended effect: the medical marketplace is being shaped in a way that is advantageous to the pharmaceutical companies.”³⁴ As far back as 1998, at the dawn of consumer advertising of SSRIs, Professor Emeritus of Psychology and Neuroscience Elliot Valenstein of the University of Michigan summarized the scientific data by concluding, “What physicians and the public are reading about mental illness is by no means a neutral reflection of all the information that is available.”³⁵

The United States and New Zealand are the only countries in the world that allow advertisement on television for prescription drugs. In 1997, a change to an FDA regulation opened the floodgates on direct-to-consumer advertising, allowing drug makers to promote their wares on television. This also paved the way for celebrities, athletes, models, and aging baby boomers to dominate those ads.

Given these forces, along with the number of symptoms listed under antidepressant use, it’s really no surprise that more than $11 billion is spent each year on these medications.³⁶ Pharmaceutical companies have more than six hundred lobbyists, and they finance more than 70 percent of FDA trials.³⁷ They court physicians, toss them copious free samples, pay consultants to speak at scientific meetings, advertise in medical journals, fund medical education, and ghostwrite, selectively choosing and redundantly submitting data for publication. Psychiatric studies funded by Big Pharma are four times more likely to be published if they report positive results. Only 18 percent of psychiatrists disclose their conflicts of interest when they publish data.³⁸ Their studies allow for all kinds of indiscretions, such as removing ­people who are likely to respond to placebo before the study to strengthen the perceived benefit and using sedative medications with the study’s medications, thereby skewing results in favor of the drug (more on this shortly).

A now famous 2008 study in the New England Journal of Medicine led by Dr. Erick Turner at Portland VA Medical Centers sought to expose the extent of data manipulation.³⁹ Through valiant efforts to uncover unpublished data, he and his team determined that from 1987 to 2004, twelve antidepressants were approved based on seventy-four studies; thirty-eight were positive, and thirty-seven of these were published. Thirty-six were negative (showing no benefit), and three of these were published as such, while eleven were published with a positive spin (always read the data, not the author’s conclusion!), and twenty-two were unpublished.

The FDA requires only two studies for drug approval, so you can see how these companies are tossing the coin over and over again until heads comes up and hoping no one is looking when it’s tails. To get a sense of just how misleading the pharmaceutical industry can be, consider the largest study to date funded by the National Institute of Mental Health, conducted at the University of Texas in 2006.⁴⁰ It cost the public $35 million for researchers to follow more than four thousand patients who were treated with Celexa over twelve months. This was not a double-blind placebo controlled study, so the ­people knew what they were getting. Half of them reportedly improved at eight weeks. Those who didn’t were switched to Wellbutrin, Effexor, or Zoloft or “augmented” with Buspar or Wellbutrin. Guess what? It didn’t matter who took what, because the same percentage of the group allegedly improved (18 to 30 percent) no matter what drug they were on. Only 3 percent of patients were supposedly in remission at twelve months. Now here’s where the story gets interesting.

In February 2012, a suit was filed against Celexa’s maker, Forest Pharmaceuticals, alleging that the company paid a bribe to the principal investigator of this particular study to fix the results in favor of Celexa.⁴¹ The suit was settled out of court, and it came on the heels of the company having to pay a criminal fine of $150 million and forfeit assets of $14 million for suppressing and misrepresenting data on the negative effects of using their drug to treat adolescents. Celexa was only approved to treat adults, but in pursuit of selling more drugs and increasing profits, the company targeted doctors who treated children and teens.⁴²

It’s a foregone conclusion: these practices sabotage the accuracy of data and convey information that corrupts a doctor’s delivery of care and endangers patients. The tragic cost of this data manipulation is the loss of true informed consent. Physicians cannot adequately share with their patients the risks and benefits if the benefits are fabricated and the risks are not uncovered or are unacknowledged. What’s more, these drugs are no more effective than a placebo. As far back as 1984, the National Institute of Mental Health was quoted as saying: “Elevations or decrements in the functioning of serotonergic systems per se are not likely to be associated with depression.” The good old placebo effect likely explains any perceived short-term effects from the antidepressants.

SHORT-TERM EFFICACY: THE POWER OF THE PLACEBO EFFECT

Despite Big Pharma’s efforts, the truth about these brain bombs is emerging. In 1998, the year direct-to-consumer advertising took off, Harvard psychologist and researcher Dr. Irving Kirsch, an established and respected expert on the placebo effect, published a landmark meta-analysis of nearly three thousand patients who were treated with antidepressants, psychotherapy, placebo, or no treatment.⁴³ The results of the study became front-page news and received widespread attention—­and criticism. Kirsch found that placebo duplicated 75 percent of the drug’s effect, that non-antidepressant medications had the same effect as antidepressants, and that the remaining 25 percent of the apparent drug effect was attributable to what’s called the “active placebo effect.”

Kirsch uses this term to refer to the effect of the mere belief in antidepressants—­a belief that is triggered by the experience of side effects such as nausea, headache, and dry mouth. What happens in a trial is that subjects are put in either the placebo group or the medication group without knowing which group they were assigned to. Because the placebo is without side effects (an inactive placebo), when they develop side effects, all of those commercial-inspired beliefs about their brain’s chemical correction are kicked into high gear, and at least a quarter of these ­people begin feeling better because of it.

So how much can we thank the placebo effect when we experience fewer symptoms while taking an antidepressant? The backlash to Kirsch’s study inspired him to continue exploring the power of the placebo. By 2008 he’d published another compelling meta-analysis study that further stirred up an incendiary response from critics.⁴⁴ This time he leveraged the Freedom of Information Act to access unpublished studies and found that when these unpublished studies were included, antidepressants outperformed placebo in only twenty of forty-six trials. That’s less than half! What’s more, the overall difference between drugs and placebos was 1.7 points on the 52-point Hamilton Rating Scale for Depression, used to rate depression in clinical research. Put simply, this small increment is clinically insignificant, and likely accounted for by minor side effects (such as activation and sedation).

The response to this publication led Kirsch to come out with another paper that clearly laid out the facts, counterchallenged his critics, and further demonstrated the power of the placebo.⁴⁵ In his concluding thoughts, he writes: “Without accurate knowledge, patients and physicians cannot make informed treatment decisions, researchers will be asking the wrong questions, and policymakers will be implementing misinformed policies. If the antidepressant effect is largely a placebo effect, it is important that we know this. It means that improvement can be obtained without reliance on addictive drugs with potentially serious side effects.”

When Kirsch’s book The Emperor’s New Drugs: Exploding the Antidepressant Myth came out in 2010 with proof that antidepressants do not have a clinically meaningful advantage over placebo, his analysis was acknowledged by researchers as a valid albeit provocative contribution to medical literature. But it didn’t change clinical psychiatry or the number of antidepressants prescribed, and it continued to incur the criticism and even rage of prescribing psychiatrists desperate to pick apart his findings to defend their now baseless practices. It’s hard to blame them—­they put a lot of time, money, and effort into learning mistruths around antidepressants! The irony in Kirsch’s findings is that the results came from studies that were underwritten and designed by the drug companies themselves. These studies were conducted in a way that would give the drugs an advantage, yet they still didn’t outperform the placebo.⁴⁶

In order for a drug to be approved, it must be shown to be superior to placebo. As you can imagine, drug companies despise placebo effects. They will do everything in their power to minimize the impact of placebo in their studies. That the FDA allows them to use these techniques is wrong, another example of Big Pharma’s shameless misconduct.

Because the FDA database contains all of the data from initial trials, both published and unpublished, analyzing its data is exceptionally useful. Keep in mind that drug companies normally don’t publish negative results. They prefer to file away those studies in a drawer where they will never be found; hence the “file drawer” phenomenon.

A fascinating 2014 study published in the Journal of Clinical Psychiatry, one of my field’s most respected journals, explored—­and exposed—­the real power of belief in psychiatric treatment. A group of researchers at Columbia University analyzed data from two large, multicenter discontinuation trials encompassing 673 ­people diagnosed with major depressive disorder and who were taking fluoxetine (generic Prozac) for twelve weeks.⁴⁷ After those three months, they were told that they’d be randomized to either a placebo or continued fluoxetine. So while they all knew they were taking the antidepressant in the first three months, they didn’t know if what they were given afterward was an active antidepressant or a sugar pill. The results spoke for themselves: both groups—­the ones still taking the fluoxetine and those on the placebo—experienced a worsening of depressive symptoms. This outcome suggests two significant interpretations: (1) the initial effect during the first three months was attributable to placebo, as all patients knew they were receiving treatment; and (2) the worsening of symptoms upon the mere possibility of getting just a placebo is indicative of the undoing of the placebo effect, what’s sometimes called the nocebo effect.

Identifying a tremendous placebo effect has been further echoed by other meta-analyses. The power of belief and the expectation of healing cannot be dismissed when medical treatments appear to work. In my opinion, the use of medications associated with serious short- and long-term side effects and which primarily ride the placebo effect represents an ethically questionable practice.

I work with the placebo effect every day in my office because I aim to inspire a different set of beliefs. Even ­people who claim to be suicidal can experience the placebo effect under my care. The decision to consider taking your own life is not a trait that would have been selected for over the millennia of human evolution. It’s more logical to assume it has roots in physiological imbalances, which is where I like to spend my time searching for solutions with my patients. I look for problems like nutrient deficiencies, endocrine disruption, and autoimmunity. The first and most important thing I like to convey to patients is that they are in charge. They have agency. This sensibility can go a long way, because they’re coming to me thinking I have what they don’t have—­a quick fix. A quick fix is a lovely idea, and if one existed, it could be great. Unfortunately, the weight of the data suggests that it doesn’t and that we may be doing more harm than good by collectively pretending it does. The challenge is that it’s human nature to feel better after doing something we think will make us feel better. But sometimes inaction is the best medicine.

LONG-TERM SIDE EFFECTS: MORE MEDS, MORE DEPRESSION, MORE DISABILITY . . . AND DEATH?

But you might ask, “What if these drugs are in fact working some of the time for some ­people?” They still wouldn’t be worth the consequences for the placebo effect, particularly given their side effects, which are notoriously hidden from the lay public. I find it outrageous that drug companies can use any number of tactics to establish efficacy, including the suppression of data, and then use those tactics to legitimize long-term prescribing with no thought or attention to the real side effects over time.

When I lecture on the futility and perils of antidepressants, I like to employ the following analogy courtesy of Dr. David Healy, an internationally respected psychiatrist based in the UK: Let’s say you’re somebody who experiences a lot of social anxiety. You have a ­couple glasses of wine at a party as a preemptive strike. A sense of calmness washes over you and your symptoms evaporate. Through deductive reasoning, you could say, “Well, I must have an alcohol deficiency, so I should continue to consume alcohol every time I have this symptom, and I might want to drink regularly to prevent it altogether.” This analogy is emblematic of the practice of dishing out antidepressants without any consideration of their long-term consequences.⁴⁸

We’ve arrived at a place in psychiatry’s abuse of antidepressants where we have a half-baked theory in a vacuum of science that the pharmaceutical industry raced to fill. We have the illusion of short-term efficacy and assumptions about long-term safety. The potential emerging side effects are nothing short of horrifying, from suppressed libido and sexual dysfunction, abnormal bleeding, insomnia, migraine, weight gain, and blood sugar imbalances to risk of violent, irrational behavior and suicide. Before I get to the ugliest of side effects and withdrawal complications, let’s focus on how your ability to function long ­term in the world with depression is significantly sabotaged by treating that first episode of depression with medication. This too has been expertly explored by Robert Whitaker, whose website (www.madinamerica.com) is a virtual library of published data and thoughtful reviews of multiple long-term studies that have followed large groups of ­people taking antidepressants. Time and time again these studies demonstrate poor functional outcomes for ­people treated with antidepressants relative to those with minimal to no medication treatment.⁴⁹ They are at greater risk for all the acute side effects I’ve already listed, as well as increased risk of relapse, cognitive impairment, secondary diagnosis and medication treatments (first a depression diagnosis followed by a bipolar one), and recurrent hospitalization.

A breathtaking 60 percent of patients are still diagnosed with depression one year into treatment, despite temporary improvement within the first three months.⁵⁰ Two prospective studies in particular support a worse outcome in those prescribed medication. In one such British study, an unmedicated group experienced a 62 percent improvement by six months, whereas the drug-treated patients experienced only a 33 percent reduction in symptoms.⁵¹ And in another study of depressed patients conducted by the World Health Organization (WHO) in fifteen cities across the UK, it was found that at the end of one year, those who weren’t exposed to psychotropic medications enjoyed much better “general health,” their depressive symptoms were much “milder,” and they were less likely to still be “mentally ill”!⁵²

Now let’s consider the more serious possible side effects of violent behavior, relapse, and crippling withdrawal among those who try to escape their grip. Antidepressants have a well-established history of causing violent side effects, including suicide and homicide. In fact, five of the top ten most violence-inducing drugs have been found to be antidepressants.⁵³ Over the past three decades there have been hundreds of mass shootings, murders, and other violent episodes that have been committed by individuals on psychiatric drugs. Big Pharma spends around $2.4 billion a year on their direct-to-consumer television advertising for drugs like Zoloft, Prozac, and Paxil. The networks can’t afford to run negative stories about prescription drugs, as they would lose tens of millions of dollars in ad revenue (no wonder the connection is habitually downplayed or ignored entirely). The Russian roulette of patients vulnerable to these “side effects” is only beginning to be known and may have something to do with how their bodies (and actions of their unique genetic code) metabolize these chemicals and preexisting allostatic (stress) load. Dr. Healy has worked tirelessly to expose data implicating antidepressants in risk of suicide and violence, maintaining a database for reporting, writing, and lecturing about cases of medication-induced death that could make your soul wince. And what about our most vulnerable: new mothers of helpless infants? I have countless patients like Kate in my practice who report never-before thoughts of suicide within weeks of starting an antidepressant for postpartum depression.

In a population where only a few randomized trials have examined the use of antidepressants for postpartum depression, I have grave concerns for women who are treated with drugs before more benign and effective interventions such as dietary modification, thyroid treatment, and addressing their sleep habits during this period when sleep deprivation runs high are explored. We already know that “low mood” is likely to resolve on its own within three months without any treatment, and upward of 70 percent of ­people will be free of depression without any medication whatsoever within a year.⁵⁴ Yet we reflexively turn to these drugs and their unpredictable effects that can rob us of the ability to find permanent relief through the body’s own powerful systems, even though, by their own claims, they take six to eight weeks to “take effect.”

In 2004, the U.S. Food and Drug Administration (FDA) revised the labeling requirements for antidepressant medications with a warning that: “Antidepressants increased the risk compared to placebo of suicidal thinking and behavior (suicidality) in children, adolescents, and young adults in short-term studies of major depressive disorder (MDD) and other psychiatric disorders.”⁵⁵ The FDA was pushed to revise the labeling following a bevy of lawsuits in which pharmaceutical companies were forced to reveal previously undisclosed drug data.

You’d think such labeling would give ­people—­and parents—­pause. But since 2004, antidepressant use has only increased among both children and adults. I am routinely helping women who want to have a baby either avoid or taper from antidepressants, despite having been “specially trained” to prescribe for this population. For many of them, the first step is simply accepting the fact that they’ve been lied to about the value of antidepressants and their alleged benefits. Meanwhile, their downsides are not only downplayed but actively concealed.

All you have to do is spend a few minutes on SurvivingAntidepressants.org, BeyondMeds.com, or SSRIstories.org to appreciate that we have created a monster. Millions of men, women, and children the world over are suffering side effects, including complicated withdrawal routinely dismissed by their prescribing clinicians. Contrary to what Big Pharma would have you believe, weaning off antidepressants is extremely difficult, so choosing to take them could be signing up for a lifetime of medication use that creates and sustains abnormal states in the brain and entire nervous system. As a clinician who once believed in these medications, I have been humbled by what they are capable of. In fact, even when I have tapered women off of Celexa at extremely low increments of .001 mg a month, it can be hard to imagine another class of substances on earth so potentially complicated to discontinue.

I first became aware of the habit-forming nature of these medications when I worked with a patient who wanted to become pregnant in the coming year to taper off of Zoloft. She experienced about six months of protracted withdrawal that began at about two months after her last dose. My training did nothing to prepare me to deal with that.

The truth is that we have very little idea about what these medications are actually doing! At the same time, though, we need to acknowledge that the complexity of neurophysiology is overwhelming. Although the appeal is to think that we’ve cracked the code on human behavior and all of its intricate physiology, we’re far from it. For example, ten years ago we didn’t even know that the brain had an immune system, and two years ago we didn’t know it had lymphatics—­basic anatomy. We used to think that immune activity in the brain only happened under certain pathological circumstances. But now we’ve identified microglia—­billions of cells that play a specific role in managing inflammatory responses in the brain based on perceived threats from the rest of the body.⁵⁶ And it’s not just about tinkering with chemical levels in the brain or the body for that matter.

We like to cling to simple explanations, but even the categorical name of the various antidepressants, selective serotonin reuptake inhibitors, is misleading. They are far from selective. In September 2014, an alarming new study from the Max Planck Institute in Leipzig, Germany, showed that even a single dose of an antidepressant can alter the brain’s architecture within three hours, changing the brain’s functional connectivity.⁵⁷ The study, published in the journal Current Biology, was shocking not only to the health journalists who reported on it, but also to the doctors who prescribe these drugs.

An important analysis by the former director of the NIMH and published in the American Journal of Psychiatry shows that antidepressants “create perturbations in neurotransmitter functions,” causing the body to adapt through a series of biological events that occur after “chronic administration,” leading to brains that after a few weeks function in a way that is “qualitatively as well as quantitatively different from the normal state.”⁵⁸ In other words, the brain’s natural functionality is assaulted by the medication to the point that it can become permanent. That said, everything we will explore in this book speaks to the body’s tremendous and almost unstoppable resilience when properly supported.

Dr. Paul Andrews of the Virginia Institute for Psychiatric and Behavioral Genetics demonstrated through a careful meta-analysis of forty-six studies that a patient’s risk of relapse is directly proportionate to how disruptive the medication is to the brain.⁵⁹ The more disruptive the medication, the higher the risk of relapse upon discontinuation. He and his colleagues challenge the whole notion of relapse, suggesting that when you feel terrible upon stopping an antidepressant, what you’re experiencing is withdrawal—­not a return of your mental illness. And when you choose the medication route, you’re actually extending the duration of your depression. Andrews writes: “. . . unmedicated patients have much shorter episodes, and better long-term prospects, than medicated patients . . . [T]he average duration of an untreated episode of major depression is twelve to thirteen weeks.”⁶⁰

In a retrospective ten-year study in the Netherlands, 76 percent of those with unmedicated depression recovered without relapse relative to 50 percent of those treated.⁶¹ Unlike the mess of contradictory studies around short-term effects, there are no comparable studies that show a better outcome in those prescribed antidepressants long term.

Harvard researchers have also concluded that at least 50 percent of drug-withdrawn patients relapsed within fourteen months.⁶² In the words of one team of researchers led by Dr. Rif El-Mallakh from the University of Louisville: “[L]ong-term antidepressant use may be depressogenic . . . it is possible that antidepressant agents modify the hardwiring of neuronal synapses [which] not only render antidepressants ineffective but also induce a resident, refractory depressive state.” Dr. El-Mallakh and his colleagues wrote this bold statement in a letter to the editor of the Journal of Clinical Psychiatry in 1999.⁶³ Then, in 2011, they published a new paper including eighty-five citations proving that antidepressants make things worse in the long run.⁶⁴ (So when your doctor says, “You see, look how sick you are, you shouldn’t have stopped that medication,” you should know that the data suggests that your symptoms are signs of withdrawal, not relapse.)

In Anatomy of an Epidemic, Robert Whitaker summarizes the matter succinctly:

We can now see how the antidepressant story all fits together, and why the widespread use of these drugs would contribute to a rise in the number of disabled mentally ill in the United States. Over the short term, those who take an antidepressant will likely see their symptoms lessen. They will see this as proof that the drugs work, as will their doctors. However, this short-term amelioration of symptoms is not markedly greater than what is seen in patients treated with a placebo, and this initial use also puts them onto a problematic long-term course. If they stop taking the medications, they are at high risk of relapsing. But if they stay on the drugs, they will also likely suffer recurrent episodes of depression, and this chronicity increases the risk that they will become disabled. The SSRIs, to a certain extent, act like a trap in the same way that neuroleptics [tranquilizers] do.⁶⁵

More than twenty years have passed since clinicians and researchers started collecting evidence against antidepressants. Although these drugs may offer relief in the short term thanks to the placebo effect, they lead to chronic, persistent depression that resists treatment when taken for an extended period of time. In some ­people, stopping the drug can cause a slow and gradual lightening of the mood, but this doesn’t always occur, and depression can become more or less permanent. Remember the alcohol effect.

Not surprisingly, the powers that be in my field have not looked into this matter or launched a serious investigation. And yet the studies keep emerging. In early 2015, yet another headline hit that Big Pharma turned a blind eye to. It read “Stopping SSRI Antidepressants Can Cause Long, Intense Withdrawal Problems” and referred to the first systematic review of withdrawal problems that patients experience when trying to get off SSRI antidepressant medications.⁶⁶ A team of American and Italian researchers found that withdrawing from SSRIs was in many ways comparable to trying to quit addictive benzodiazepine sedatives and barbiturates.⁶⁷ They also discovered that withdrawal symptoms aren’t fleeting; they can last months or even years. Moreover, entirely new, persistent psychiatric disorders can surface from discontinuing SSRIs.

The authors analyzed fifteen randomized controlled studies, four open trials, four retrospective investigations, and thirty-eight case reports of SSRI withdrawal. Paroxetine (Paxil) was found to be the worst, but all the SSRI antidepressants were documented as causing a wide range of withdrawal symptoms from dizziness, electrical shock sensations, and diarrhea to anxiety, panic, agitation, insomnia, and severe depression. They write: “Symptoms typically occur within a few days from drug discontinuation and last a few weeks, also with gradual tapering. However, many variations are possible, including late onset and/or longer persistence of disturbances. Symptoms may be easily misidentified as signs of impending relapse.”

In their conclusions, they state what should be the obvious: “Clinicians need to add SSRIs to the list of drugs potentially inducing withdrawal symptoms upon discontinuation, together with benzodiazepines, barbiturates, and other psychotropic drugs.” An accompanying editorial to their paper notes that “This type of withdrawal consists of: (1) the return of the original illness at a greater intensity and/or with additional features of the illness, and/or (2) symptoms related to emerging new disorders. They persist at least six weeks after drug withdrawal and are sufficiently severe and disabling to have patients return to their previous drug treatment. When the previous drug treatment is not restarted, post-withdrawal disorders may last for several months to years.”

The editorial also states that “With SSRI withdrawal, persistent postwithdrawal disorders may appear as new psychiatric disorders, in particular disorders that can be treated successfully with SSRIs and SNRIs. Significant postwithdrawal illnesses found with SSRI use include anxiety disorders, tardive insomnia, major depression, and bipolar illness.”

This bit of news is extremely unsettling to current practices in psychiatry. According to the current American Psychological Association treatment guidelines for major depressive disorder, “During the maintenance phase, an antidepressant medication that produced symptom remission during the acute phase and maintained remission during the continuation phase should be continued at a full therapeutic dose.” Such a guideline merely promotes more drug sales, and more crippling side effects.

DON’T GO DOWN THE RABBIT HOLE

We need to break out of the spell that the pharmaceutical industry has put us under. Psychiatry’s swan song has been sung; listen for its plaintive wail. We must reject the serotonin meme and start looking at depression (and anxiety, and bipolar disorder, and schizophrenia, and OCD) for what they are: disparate expressions of a body struggling to adapt to a stressor. There are times in our evolution as a cultural species that we need to unlearn what we know and change what we think is true. We have to move out of the comfort of certainty and into the freeing light of uncertainty. It is from this space of acknowledged unknowing that we can truly grow.⁶⁸

From my vantage point, this growth will encompass a sense of wonder—­both a curiosity about what symptoms of mental illness may be telling us about our physiology and spirit and a sense of humbled awe at all that we do not yet have the tools to appreciate. For this reason, honoring our coevolution with the natural world and sending the body a signal of safety through movement, diet, meditation, and environmental detoxification represents our most primal and most powerful tool for healing. We also need to identify vulnerabilities and chemical exposures and support basic cellular function, detoxification, and immune response. This is, ultimately, personalized medicine.

To me, the worst part of the misguided mess we’ve made of mental health care is that we are missing out on the potential for true resilience and self-healing. Safe, effective alternatives to help us through these passages in life do indeed exist. Perhaps most concerning to a holistic physician is data that suggests that long-term antidepressant treatment actually compromises the benefits of exercise!⁶⁹ The effects of exercise have been shown to be comparable to Zoloft but can be diminished when combined with Zoloft; patients relapse at higher rates than they do with exercise alone. I’ll be going into much greater detail about exercise in Chapter 7, and I’ll share why I think this is the case. Exercise is an antidote to depression best used without antidepressants.

Mental health will always be grounded in whole body health. When you discover the real imbalances underlying all your symptoms—­physical and mental—­and take steps to address them, you can restore your health without resorting to problematic drug treatments and endless psychotherapy.

The next question to answer is: What kind of “imbalances” come under the veil of depression? We’ll find out in the next chapter.