Depression has been around since the first days of humankind. For centuries, if not millennia, doctors and physicians treated “melancholia” as simply a depressed mood, one that would surely be treatable with a variety of off-the-cuff cures.
But with the 1900s came advancements in psychology and our understanding of how the brain works. It was finally clear that depression wasn’t simply a temporary sad mood or case of the blues, but an affliction that could last for days, weeks, or even years if not treated.
Surprisingly, in the 1950s scientists were experimenting with cheap, leftover rocket fuel from WWII. Their mission? To discover a cure for the age-old disease of tuberculosis. Some of these experiments ended up using two chemicals called iproniazid and isoniazid.
While they didn’t end up curing tuberculosis, their experiments came to a surprising result—many patients reported feeling happier after ingesting the chemicals.
The First Generation of Antidepressants
These efforts led to the very first antidepressants — monoamine oxidase inhibitors, or MAOIs, which hit U.S. markets in the 1950s. Early formulations like MAOIs and tricyclics were known to have numerous side effects and patients could easily overdose on the substances. Side effects could be brutal; constipation, dry mouth, hypertension, and even death. As such, they were prescribed carefully and with strict monitoring regimens.1
By the 1960s, scientists started believing that low neurotransmitter levels were the true cause of depression in individuals.2,3 The basic idea was that depression was caused by a lack of serotonin and other specific neurotransmitters. And since antidepressant medication increased the availability of mood-altering neurotransmitters in people, the medical industry assumed the drugs would help cure depression.
A simple cause-and-effect connection, right?
Unfortunately, as with many aspects of the human body, it’s more complicated. But one thing was for sure, the concept of depression being a simple disorder with a basic cause and solution in the brain’s chemistry proved to be a highly marketable idea.
Pharmaceutical companies, in their never-ending search for expanding profit, were more than willing to advertise their medications as “cures” for neurotransmitter deficits.
However, as the progress of research continued, it became increasingly clear that the full causes of depression were far more complex than a simple lack of a few brain chemicals.4
The Start of the Prozac Revolution
Scientists, doctors, and patients still weren’t satisfied with this first generation of antidepressants. MAOIs were far too dangerous to liberally prescribe to the general public and the millions of people who were suffering from depression in silence.
Something was needed that was just as effective, if not more, but without all of the dangerous side effects.
That’s why researchers began focusing on serotonin itself, and spent years finding a way to specifically increase the amount of this neurotransmitter in the brains of patients.
Eventually, Prozac hit the market in 1988 amid a wave of hype and promising clinical trial statistics, which sparked a huge change in popular opinion and medical standards. Not only was Prozac effective, said the drug manufacturers, but it was also safe, with a range of potential applications that extended beyond the treatment of clinical depression.
It wasn’t long before Prozac was advertised as a way to adjust and even alter desirable aspects of the human personality:
- “Are you too shy? Prozac can help.”
- “Do you need more ambition to reach that job promotion? Try Prozac to boost your motivation.”
In no time at all, Prozac became a household term synonymous with a magic-bullet cure for personal failings. With the need for a legitimate therapeutic solution for depression as high as ever, and the lines between a much-needed medicine and a personality upgrade beginning to blur, Prozac was touted as nothing less than a wonder pill.5
Psychiatry needed a miracle cure to revolutionize depression treatment, and Prozac seemed to be just that: an easy-to-take, hassle-free pill to finally become happy.
The notion of a wonder pill appealed to far more than just people dealing with depression. After all, if a single capsule could “wash away the blues” and give one’s personality a bit of targeted improvement, there was no reason to question anything else. Seemingly everyone who wanted to be happier in their day-to-day lives lined up at their doctor’s office to get their hands on the drug.
Demand for antidepressant medications skyrocketed, and the long-term side effects and emerging withdrawal symptoms of Prozac and similar drugs went unrecognized — or completely ignored.
Pharmaceutical Companies and SSRI Marketing
While cultural hype played a role in Prozac’s meteoric rise to fame and popularity, the direct actions of the drug manufacturers were equally as significant. Pharmaceutical companies heavily promoted their research when they introduced new antidepressants to the market in the late 1980s and 1990s.
Corporate strategies and advertising campaigns were planned and executed attempting to increase the drug’s use and shape popular opinion as to the safety, utility, and “life-changing” benefits of antidepressant therapy.
This approach was wildly successful.
By 1990 Prozac was the country’s most prescribed antidepressant, with annual sales exceeding 1 billion dollars.5 But the good news didn’t last forever, as cracks began to emerge in Prozac’s carefully crafted image.
Previously stable individuals reported thoughts of violence and fantasies of killing themselves after starting the drug. Other people started appearing on talk shows describing themselves as “Prozac survivors,” a term never heard in society previously.5
Other people even noted — correctly — that antidepressants were being prescribed far too often, especially when considering science still lacked a complete understanding as to how the drugs — let alone the biology of depression itself — actually worked.
More importantly, psychiatrists began to hear from patients that tried reducing their antidepressant dosage produced withdrawal symptoms that were often debilitating and prolonged.
Patients who tried stopping Prozac and related medicine outright reported dizziness, lightheadedness, burning or tingling in the extremities, anxiety, gastrointestinal problems, a lack of coordination, headaches, insomnia, irritability, nausea, and tremors.
These symptoms bear a marked similarity to the withdrawal symptoms observed with benzodiazepine discontinuation.6
What is Depression?
Fast forward to today, and neurotransmitters — particularly serotonin — are still presumed to play key roles in the development of depressive disorders. But with decades of more research, we now know the number of underlying causes of depression is simply huge.
Among them, genetic, epigenetic, metabolic, and biochemical components have been implicated.7 External factors have also been identified as influencing depression risk, meaning it’s not simply genetic, but the environment we’re raised and live in can affect us, too.8-13
We are all humans, after all.
Brain imaging and genetic assay technologies have evolved the biological model of depression at breakneck speed. You’d think with all the tremendous advancements in medical knowledge, we would’ve updated how we treat the disorder by now. And yet, when it comes to depression, the gap between understanding and practice has widened substantially.
Depression is still treated very much the same way it was fifty years ago!
How Depression is Treated Today
To treat depression in the modern age, most doctors will simply prescribe certain drugs to target specific neurotransmitters in a patient’s brain. Of course, new antidepressants have become available, and older formulations refined, but the methodology has largely remained the same.
And all of this is despite the fact we are in the middle of a global mental health crisis. It’s estimated that more than 264 million individuals worldwide currently struggle with depressive disorders.14 Depression is also a leading cause of global disability and is on the rise, having jumped 14.3% between the years 2007 and 2017.15,16
So, how did the psychiatry industry fix this problem?
By prescribing even more pills, of course.
From 2000 to 2011, most of the wealthiest nations in the world saw a doubling in public usage of antidepressant medications.17 The number of Americans taking antidepressant medications is simply staggering: 40 million Americans — one in eight individuals — filled a prescription for antidepressants in 2017 alone.18 Of these 40 million, 25% have been on an antidepressant for a decade or longer.
These are astounding numbers, and they are climbing, especially with the advent of COVID and the associated lock-downs and isolation.
In the middle of the greatest pandemic in a century, with people stressed, afraid, and worried about the virus, more people than ever before turned to doctors for help with depression. And with the solution usually being a highly addictive pill, more Americans than ever will experience antidepressant withdrawal in the coming years.
Do You Want to Stop Taking Antidepressants?
With so many Americans and patients all around the world regularly taking antidepressant medications, a large number of them wish to stop due to the wide array of negative side effects. The problem is, there isn’t an industry-agreed-upon method to help wean patients off of the highly addictive medications.
Fortunately, there is a solution.
I’ve spent decades treating patients for depression with an approach called Integrative Psychiatry—a practice that takes into account an individual’s personal lifestyle and needs to treat afflictions like depression.
If you or a family member is looking to stop taking antidepressant medication, please check out my easy-to-read ebook guide on what to expect, effective ways to approach it, and how to deal with any problems on the journey.
If you are a physician and looking for more information on an Integrative Psychiatry approach to dealing with antidepressant withdrawal, please check out our course on Managing Medication Side Effects, and my book, Functional Medicine for Antidepressant Withdrawal.
- Pletscher A. The discovery of antidepressants: a winding path. Experientia. 1991;47(1):4-8.
- Coppen A. The biochemistry of affective disorders. Br J Psychiatry. 1967;113(504):1237-1264.
- Schildkraut JJ. The catecholamine hypothesis of affective disorders: a review of supporting evidence. Am J Psychiatry. 1965;122(5):509-522.
- Cowen PJ. Serotonin and depression: pathophysiological mechanism or marketing myth? Trends Pharmacol Sci. 2008;29(9):433-436.
- Fitzpatrick L. A brief history of antidepressants. Time. http://content.time.com/time/health/article/0,8599,1952143,00.html. Published January 7, 2010. Accessed March 23, 2021.
- Nielsen M, Hansen EH, Gotzsche PC. What is the difference between dependence and withdrawal reactions? A comparison of benzodiazepines and selective serotonin reuptake inhibitors. Addiction. 2012;107(5):900-908.
- Albert PR, Benkelfat C, Descarries L. The neurobiology of depression–revisiting the serotonin hypothesis. I. Cellular and molecular mechanisms. Philos Trans R Soc Lond B Biol Sci. 2012;367(1601):2378-2381.
- Ettman CK, Abdalla SM, Cohen GH, Sampson L, Vivier PM, Galea S. Prevalence of depression symptoms in US adults before and during the COVID-19 pandemic. JAMA Netw Open. 2020;3(9):e2019686.
- Wright R. How loneliness from coronavirus isolation takes its own toll. The New Yorker. https://www.newyorker.com/news/our-columnists/how-loneliness-fromcoronavirus-isolation-takes-its-own-toll. Published March 23, 2020.
- Marchant A, Hawton K, Stewart A, et al. A systematic review of the relationship between internet use, self-harm and suicidal behaviour in young people: the good, the bad and the unknown [published correction appears in PLoS One. 2018 Mar 1;13(3):e0193937]. PLoS One. 2017;12(8):e0181722.
- Zatti C, Rosa V, Barros A, et al. Childhood trauma and suicide attempt: a meta-analysis of longitudinal studies from the last decade. Psychiatry Res. 2017;256:353-358.
- Fuller-Thomson E, Baker TM, Brennenstuhl S. Evidence supporting an independent association between childhood physical abuse and lifetime suicidal ideation. Suicide Life Threat Behav. 2012;42(3):279-291.
- Danese A, Moffitt TE, Harrington H, et al. Adverse childhood experiences and adult risk factors for age-related disease: depression, inflammation, and clustering of metabolic risk markers. Arch Pediatr Adolesc Med. 2009;163(12):1135-1143.
- World Health Organization. Depression: fact sheet. WHO.int. https://www.who.int/news-room/fact-sheets/detail/depression. Published January 30, 2020. Accessed June 16, 2020.
- GBD 2017 Disease and Injury Incidence and Prevalence Collaborators. Global, regional, and national incidence, prevalence, and years lived with disability for 354 diseases and injuries for 195 countries and territories, 1990-2017: a systematic analysis for the Global Burden of Disease Study 2017 [published correction appears in Lancet. 2019 Jun 22;393(10190):e44]. Lancet. 2018;392(10159):1789-1858.
- Friedrich MJ. Depression is the leading cause of disability around the world. JAMA. 2017;317(15):1517.
- McCarthy M. Antidepressant use has doubled in rich nations in past 10 years. BMJ. 2013;347:f726.262 263 James Greenblatt Functional Medicine for Antidepressant Withdrawal
- Pratt LA, Brody DJ, Gu Q. Antidepressant use among persons aged 12 and over: United States, 2011-2014. NCHS Data Brief. 2017;(283):1-8.