Overmedicated America

Posted byJessica HolmesPosted inOpinionTags:, , ,

Written by Jess Holmes @realtruthcactus

“We were promised suffering. They were part of the program. We were even told, ‘Blessed are they that mourn,’ and I accept it. I’ve got nothing that I hadn’t bargained for. Of course, it is different when the thing happens to oneself, not to others, and in reality, not imagination.”

― C.S. Lewis, A Grief Observed

Modern Americans live in a psychological wasteland. Any glance at one’s fellow man would tell you so, but should you still live in doubt, just consider the horrifying statistics conveyed by our experts. Overmedicated America is the new normal.

One in five Americans suffers from a mental illness18.

Anxiety disorders are the highest reported mental health issue in the US, with 42.5 million Americans claiming to suffer from this illness10.

Mental illnesses start showing symptoms by age 1413.

Mental health crises account for 60 million visits to primary care and 6 million ER visits annually3.

Forty million Americans suffer from anxiety1.

Twenty percent of all teens suffer from depression before they reach adulthood5.

Rates of suicide have increased by 24% since 2012 (approximately 40k to 49k/year)2.

With such a bleak outlook overwhelming our nation, is it any wonder that so many are clutching, wrenching, grasping for anything that will relieve the spiraling darkness of their own thoughts? Is it any wonder that mankind has latched onto chemical imbalance theory as a harbor, a final bastion of hope, that something, anything, can take away that deep dark abyss that seems to be the torrent of the mind?

That, it seems, is what our medical experts would have us believe. But their ‘hope’ is built on a false foundation, a cornerstone of sand, and it is only recently that this reality has come to light.

New Hope for Overmedicated America

The drab walls of the Staten Island Seaview Hospital are nothing new to the sanatorium inhabitants. Rain patters against the panes of glass, and cool, sickly air wafts between bedpans and the bedridden alike. In a place such as this, hope is a rare commodity. There is no exchange rate because none can be found on an average day. The only solace is that perhaps the new day will bring brighter light rather than the never-ending rain of despair. For patients playing host to Mycobacterium tuberculosis (TB), this is the best hope they can ask for. 

Doctors want better for their patients. They see the life-weary eyes, hear the shallow, desperate gasps for breath, and want so much more for them than just the endless coughing fits and choking thoughts. In hopes of providing some relief, physicians prescribed their patients an experimental drug known as iproniazid16. Reports had shown that iproniazid demonstrated strong antibacterial action against Mycobacterium tuberculosis. Maybe, just maybe, this drug could at least ease their suffering, if nothing else.

But that is when the most extraordinary thing happened. As if invigorated by unseen spirits, the once sullen and lifeless patients leapt from their beds. They were happy, giddy even, filled with an energy heretofore unseen in those who suffer from TB. Once wan appetites were now ravenous. Patients danced in the halls, riding an inexplicable wave of euphoria that left doctors positively dumbfounded.

What on earth was going on?

How could this happen?

Around this same time, doctors were using the drug reserpine to treat patients who were suffering from high blood pressure12. Once happy, if a bit unhealthy, patients began to spiral. Notably, one 52-year-old retired police officer reported emotions of such despondency that he had lost all interest in all aspects of his life. From gardening to television to family, his once peaceful and rosy life was now overshadowed by ruminating thoughts of suicide.

This is the stage on which chemical imbalance theory began to take its shape. Physicians began prescribing iproniazid off-label for patients who demonstrated depressive symptoms. The psychiatric field began to replace phrases like ‘human experience’ with ‘chemical deficiencies.’ It was more clinical, more satisfactory. Unfortunately for the pharmaceutical company that produced iproniazid, the FDA pulled its approval in 1961 when rapid reports of serious side effects such as hypertension and liver toxicity7 began to emerge. But iproniazid and reserpine’s effects had already changed the culture of the psychiatric industry. Now, chemical companies around the country were working round the clock to create a class of drugs similar to iproniazid and reserpine – without, hopefully, the side effects – known as monoamine oxidase inhibitors, or MAOIs.

Monoamines are a class of neurotransmitters that include dopamine, epinephrine, and serotonin23. While reserpine depletes the brain’s stores of monoamines, iproniazid boosts the supply of these neurotransmitters by stymieing the enzyme that breaks them down. Dr. Dilworth Wayne Woolley was fascinated by the behavior of neurotransmitters and their interaction with MAOIs21. Woolley hypothesized that, as well as its primary function in the gut and blood platelets, serotonin’s role as a neurotransmitter was so critical that it was operationally necessary for neural development. Such claims were founded on serotonin’s similarity to the plant growth hormone auxin, which is involved in stimulating the elongation of stems. Yet, the world was not quite ready for such a claim. Even in the light of the burgeoning chemical imbalance theory, Woolley’s work was continually rejected by the prominent medical journal, the Lancet. Until he could prove his point by outright curing mental illness, his claim was nothing more than an idea on a page.

Mind of Darkness

One of the core problems with Woolley’s theory is that serotonin is a big molecule. Too big of a molecule, in fact, to cross the blood-brain barrier. Any serotonin injections would not be taken up by the brain because it can’t pass the blood-brain barrier. And, because it is such a biologically active hormone, it would instead interfere with other biological functions, notably contractions of the intestines and increased blood pressure. However, that does not mean that serotonin is not essential for neurological activity.

After Woolley’s death in 1966, his colleague, David Shaw, picked up the doctor’s work, determined to prove his predecessor right. Shaw theorized that if Woolley was right, and serotonin was the culprit for mental illness, he should be able to prove that people who have less serotonin in their brains experience the worst effects of depression and anxiety. But how do you measure serotonin in the brain of a living and thriving human being?

Well, the answer was surprisingly simple. You don’t. Shaw and his team conducted a study on recent suicide victims quickly post-mortem, analyzing their brain tessure for levels of 5-Hydroxytryptamine (aka serotonin). In the groundbreaking work that was ultimately published in the British Journal of Psychiatry, Shaw found that, on average, people who were diagnosed as depressed and then subsequently took their own lives demonstrated lower levels of central nervous system serotonin levels than non-depressed people17.

American pharmacist and inventor Eli Lilly ran with this chemtrail almost immediately. How logical would it be then, he argued, to conclude that depression is not a spiritual or emotional phenomenon but a biochemical reaction, or lack thereof, leading to the untimely death of thousands?  Like a dog with a bone, Lilly obsessively, hungrily, set out to find a compound that could selectively target the brain’s serotonin communication system without interfering with other neurological or hormonal pathways. In 1974, Lilly scientists created fluoxetine, a compound that blocks the removal of serotonin — and only serotonin — from synapses, making fluoxetine the first class of antidepressants called serotonin reuptake inhibitors, also known today as SSRIs. After more than a decade of clinical trials, the FDA finally approved fluoxetine for the treatment of depression in 1987, and mass-marketing began in 1988 under the brand name Prozac8.

In short order, American scientists have distilled the human condition down to a few simple and straightforward chemical reactions. And based on these reactions, mankind could master their own destiny, their hopes, dreams, and fears with nothing but a pill. SSRIs were the philosopher’s stone of the mind, promising health and freedom from human suffering.

The question now is, did they make good on that promise?

The Philosopher’s Stone

Think of it like a telephone call. Each phone is the ending of a nerve cell. Between the two nerve cells are chemicals traveling back and forth between receptors on the nerve ending. Once the chemical is received by the nerve ending, the chemical information is translated into electrical information, which stimulates the desired outcome across the brain and central nervous system. But instead of just one telephone call, it’s billions and trillions of calls, all communicating in unified and perfect harmony to allow for the fine-tuned regulation and function of our bodies. This is the function of our beloved neurotransmitter, serotonin, as it scurries to trigger the electronic signals between nerve cells in the brain9. 

Just as phones do not magically assemble themselves into a working call, our brains require a guiding mechanism to facilitate communication between nerve cells. This crucial role is played by hSERT, the serotonin transporter6. Similar to a diligent janitor, hSERT’s primary function is to efficiently remove excess serotonin from the synaptic cleft, the tiny space between nerve cells, after it has relayed its message. However, in some individuals, hSERT may work overly zealously, clearing away not only unnecessary serotonin but also essential serotonin before neighboring nerve cells have a chance to receive the signal. This overzealous cleanup process results in a situation akin to nerve cells whispering when they should be shouting.  Such a scenario hinders effective communication in the body.

Our bodies, however, are amazingly efficient. To allow the nerve to recover and receive the next message, the reuptake process cleverly recycles the neurotransmitters from the receptors and takes them back into the originating nerve. The goal of SSRIs is to slow down the collection of serotonin by transporters like hSERT and the process of returning the serotonin to the end of the neuron it comes from. SSRIs inhibit the serotonin transporter at the presynaptic axon terminal, and through inhibiting hSERT, an increased amount of serotonin can remain in the synaptic cleft and properly stimulate postsynaptic receptors for a more extended period. In essence, serotonin stays in the space between the cells longer and increases the chances that the second cell will get the message.

But does it actually work?

The horrifying reality of the matter is that scientists, psychiatrists, and clinicians do not actually know. Even after 60 years of research, scientists still do not fully understand the role that serotonin plays in neurochemistry, much less all of biology. It is now evident that serotonin does not modulate single functions but rather a multiplicity of activities and behaviors present in both normal brain function and several pathological conditions in a less deterministic way than previously assumed. 

This was particularly evidenced by Simon Young from McGill University and his team, who conducted thorough depletion studies to see if they could artificially induce patients with depression through the lowering of serotonin levels25. The acute tryptophan depletion (ATD) technique employed by Young and his team, which involves manipulating dietary intake to lower neurological serotonin levels, has been widely employed by multitudes of researchers across the country to investigate the effects of low serotonin in the human brain. By altering participants’ diets, researchers can artificially induce depressive symptoms, providing valuable insights into the role of serotonin in mood regulation. Across eight studies, there was no observable trend or link between the lowering of serotonin and the onset of depressive symptoms. Joana Moncrieff, horrified by these findings, picked up the research and analyzed an enormous cross-section of studies to determine the efficacy of chemical imbalance theory as a whole. Across seventeen studies, Moncrieff concluded in 2022 that:

“The main areas of serotonin research provide no consistent evidence of there being an association between serotonin and depression, and no support for the hypothesis that depression is caused by lowered serotonin activity or concentrations11.” 

For nearly sixty years, the mental health industry has tethered itself to the foundation of chemical imbalance theory only to find that it was anchored to a bed of sand. As the tides of reality rolled in and washed away the sediment, many are now left adrift at sea, promises weathered, hopes dashed. 

The truth had been there all along. In reality, if anyone paused to think it through, it would seem obvious. If SSRIs are believed to stop hSERT, then that would lead to a rapid increase of serotonin in the brain. Depression and anxiety-ridden patients should have seen results instantly. And yet, doctors would prescribe these drugs for weeks, months, and years and remind their patients that these things take time. But why? If their theory was on solid ground, they should have seen results instantly. Some psychopharmacologists may clap back at this question with the argument that, while some SSRIs, like Lexapro, bind directly to the transporter, the direct binding is not the underlying mechanism of action14. Instead, antidepressants target our DNA, in particular the genes that code for the serotonin transporter20. They make these genes less active, so fewer serotonin transporter molecules are available in the brain. This, it is argued, explains the delayed action of antidepressants. They say this as if knowing that SSRIs target our genetic code rather than the neurotransmitters they were previously advertised to target would reassure us of their intentions and the soundness of the theorem. As if saying that SSRIs behave in one way while obscuring the dark reality does not shatter the trust between every depressed patient and the psychopharmacologist who tends to him.

Psychiatrists do not even know for certain that what they are treating is what they are treating. They do not collect blood or urine samples to test for low levels of serotonin. They do not do brain scans to determine if there is anything clinically wrong with a patient’s brain. They analyze a person’s emotions, insist on the reliability of the person’s self-reporting, and conclude that there is something broken, something wrong in the make of that person. Rather than searching deeper for the truth, many simply reach out for the quick fix, the band-aid solution to the gunshot wound problem. SSRIs were a false philosopher’s stone, one on which many scientists hinged their faith. But a faith built on a foundation of sand cannot withstand the storm.

This is not to mischaracterize good clinicians who strive to use cognitive behavior therapy (CBT) to search for the underlying problem. This criticism is directed at those who seek chemicals first, who are beholden to the pharmaceutical industry, and have built their practice on false promises. These clinicians are no better than the snake oil salesmen of old. But rather than selling very expensive placebos, these drugs have very serious long-term side effects that are only just now being realized.

Sinister Realities

The side effects of SSRIs are just now coming to light on the national stage as thousands of patients everywhere testify to how their doctors, clinicians, therapists, and psychologists failed them – gravely so. Some patients prescribed SSRIs experience insomnia, skin rashes, headaches, joint and muscle pain, stomach upset, nausea, or diarrhea. Thankfully, these issues are typically transient, mild, or both. A more serious potential concern is diminished blood clotting ability due to reduced serotonin levels in platelets. This raises the risk of internal bleeding, especially in patients concurrently taking aspirin or another NSAID, such as ibuprofen or naproxen. And perhaps the most hidden and horrifying side-effect is a tragic condition known as PSSD.

Post-SSRI sexual dysfunction, or PSSD, is a sexual disorder that may arise during the administration of SSRIs and persist long after their discontinuation4. These persistent side effects include decreased libido, genital anesthesia, erectile dysfunction, and anorgasmia. Researchers admitted that the prevalence of persistent sexual side effects after discontinuing SSRIs is not well known. Worse still, there is no definitive treatment for PSSD; however, there are some proposed management options. Lowering SSRI dosage could decrease the sexual side effects but weaken the drug’s initial treatment strategy. Strategies that had patients taking other medications alongside the SSRIs to reduce the possibilities of PSSD, drugs like Buspirone, trazodone, donepezil, ketamine, metformin, and mirtazapine have met with little to no success19. 

Across the nation, patients who are promised relief from their inner turmoil instead find their emotions blunted. They are walled off from feelings of sorrow, certainly, but find that joy cannot penetrate the neurological barrier that has been erected either. Feelings of love have been stunted, and even eliminated, in many. TikTok is brimming with testimonies of men and women who have lost the ability to enjoy their spouse or partner because they simply cannot feel anything. As human creatures driven by emotion, this psychological walling not only cuts us off from one another but cuts off the part of us that makes us human. 

And it gets worse. Not only do SSRIs cause people to find diminished joy in sexual activities, they also decrease their overall fertility15. A study published in 2022 by Frontiers in Pharmacology, which did an in-depth and detailed study on the effects of SSRIs on sperm, found that: 

“Our meta-analysis demonstrated that SSRIs have a statistically significant impairment on semen quality, such as sperm concentration, sperm morphology, sperm motility, and the DFI, but not on semen volume. Furthermore, the damage to sperm morphology and concentration were all observed in the 3-month period of SSRIs use but had no significant effect after 1 month of SSRIs use. Therefore, during the period of SSRIs treatment, patients of reproductive age may consider not conceiving or taking other drugs that have a lower potential for infertility22.”

In addition, the Journal of Epidemiology published an extensive study on the effect of SSRIs on pregnant women. The researchers conducted a prospective cohort study of 2,793 pregnant women oversampled for a recent episode of major depression or use of an SSRI.  The results showed that SSRI use was associated with preterm birth24.

The psychologists and pharmacologists promoting SSRIs are shooting arrows in the dark. Instead of protecting those they promised to defend from medical harm, they have struck their own patients with horrifying conditions that have left them feeling empty and less than human. Rather than encouraging people to seek out methods of recovery that do not utilize drugs, America has overmedicated its citizens into infertility, emotionlessness, and isolation. All in the name of science.

A Better Tomorrow In Overmedicated America

America’s mental health crisis is a tragic reality, one our nation’s scientists have ignored for far too long. They have hitched their faith to methodologists that have fallen short time and again. It is difficult to uproot such a pervasive weed in the scientific community. Yet, in the face of such overwhelming evidence, the path must be corrected. Research into PSSD must continue to undo the damage done by the pharmaceutical industry. Alternative methods of addressing mental illness should be better researched. Already, promising alternatives in cognitive behavioral therapy, community efforts, and spiritual practices have shown themselves to be viable alternatives to medication. Rather than seeking the pill first, going for the quick fix, and hinging our hopes on a false philosopher’s stone, psychologists should turn to more long-lasting and enduring strategies that do not compromise their patient’s biochemistry, fertility, and neurological function. Because we are more than just a series of biochemical reactions. We are mind, body, and spirit. We are soul. Created in the image of God. Some things simply cannot be medicated away. Rather than blunting the human experience with chemicals, let us find our better tomorrow in a foundation that will stand the test of time, a foundation built on rock rather than sand. Only then will we find hope in the darkness.

References

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