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How Pharmaceutical Companies Destroyed Our Sleep
Yoho Preamble
A friend whom I will call Sally has destroyed her ability to get restful sleep. She takes five separate sleep prescriptions and says she has not slept well in several years. The medications multiplied over time—one drug failed, then another was added, then another. Now she is trapped in a pharmacological nightmare from which there seems no escape.
A “physician” convinced Sally that bioidentical progesterone causes breast cancer, which is the reverse of the truth, for progesterone suppresses it. Taking a micronized, bioidentical formulation from a compounding pharmacy in high enough doses at bedtime would likely solve her sleep problems in just a few days. (This is not healthy for men, however, and some women require 800 mg.) Instead, she takes five dangerous drugs that leave her exhausted and desperate.
Xyrem (sodium oxybate) is the one medication that delivers quality sleep, but obtaining it has become nearly impossible. The drug exists under a restrictive distribution system that makes access difficult, and the price—often exceeding $15,000 per month without insurance—puts it beyond reach for most patients. It was somehow branded a “date rape” drug.
I have skin in this game. Parkinson’s disease causes neurological sleep interruption, and I wake up four or five times each night. My inquiries among young friends involved in the rave scene turned up no Xyrem, which is for the best because the penalties for possessing it are severe.
I spent a decade on clonazepam (Klonopin) before I realized that the drug had become the problem. Withdrawing from it took months, and I had extreme rebound anxiety during that time. I suspect that my decade of use permanently damaged my ability to sleep. See HERE for that story.
My current best, albeit imperfect, sleep results occur when I avoid pharmaceutical drugs and use natural approaches. I occasionally—rarely—resort to 1/6th of an indica marijuana gummy. This works better than the sativa type, which can be agitating and contains more THC and less CBD. This is an imperfect solution that has the same side effects of confusion, progressive tolerance, and escalating doses, just like the damn benzos.
The Foundation: Natural Sleep Solutions
Gentle remedies exist: magnesium supplementation, proper sleep hygiene, stress management, and most important of all, hormone replacement.
A detailed discussion of these approaches appears in the Apocalypse Almanac chapter on good sleep HERE. It emphasizes a crucial point: hormone replacement should always be evaluated first when sleep problems are present.
For women with inadequate progesterone—a common problem even among 40-year-olds—replacing this hormone with micronized, compounded bioidentical progesterone offers an effective, natural solution. The treatment is so safe that it should be available over the counter. The key is to take it at bedtime and increase the dose until sleep improves. Some women require 1,000 mg. And both testosterone and progesterone protect against breast cancer, contrary to what some physicians tell patients.
With that foundation established, here is the disaster that pharmaceutical companies have created.
Ambien
Ambien (zolpidem), approved by the FDA in 1992, exemplifies the pattern that dominates the sleep drug market: short-term apparent effectiveness followed by long-term disruption of sleep architecture.
Ambien works by binding to GABA receptors in the brain, producing sedation. For a few weeks, it appears to help. Patients fall asleep faster and report subjectively better sleep. But studies reveal that the quality of that sleep is damaged from the beginning.
Research shows that the drug suppresses REM sleep—the stage of sleep critical for memory consolidation, emotional processing, and psychological health. One study found that a hypothesized mechanism for zolpidem-induced sleepwalking was REM sleep suppression and increased slow-wave sleep duration. Another study in pediatric burn patients found that slow-wave and REM sleep were dramatically reduced to just 18-37% of normal levels, even though stage 2 sleep was restored to 99% of normal.
High-dose use reveals even more damage. A case study of a patient taking 200-300 mg daily (20-30 times the usual dose) showed that the drug caused elongation of REM latency, poor slow-wave sleep, and frequent nocturnal arousals. The patient spent excessive time in stage N1 sleep and had a REM sleep latency of 180 minutes. The study noted that prolonged exposure to zolpidem may cause damage to GABA interneurons and cholinergic neurons.
Recent research suggests that zolpidem may interfere with the brain’s waste-removal system. A 2025 study found that the drug suppresses the synchronized oscillations of norepinephrine, cerebral blood flow, and cerebrospinal fluid that drive the brain’s glymphatic system during non-REM sleep. This system clears metabolic waste linked to neurodegenerative diseases.
Beyond sleep architecture destruction, zolpidem produces dangerous behaviors. The FDA logged 66 incidents of semi-conscious behavior after taking Z-drugs that resulted in serious injury or death. A systematic review found that 88% of cases involving complex sleep behaviors, such as sleepwalking, sleep driving, and sleep eating, had a probable association with zolpidem.
The drug is also highly addictive. A 2012 meta-analysis found that Z-drugs work barely better than a placebo. When patients try to stop, they experience rebound insomnia, making the problem worse than before they started treatment.
Benzodiazepines are one of the most brazen frauds in pharmaceutical history.
These drugs, including Xanax (alprazolam), Klonopin (clonazepam), Valium (diazepam), and Ativan (lorazepam), were approved based on approximately two weeks of efficacy data. Everything that happened after those two weeks was ignored.
The UK’s National Institute for Health and Clinical Excellence reviewed the evidence and found that tolerance and physical dependence develop rapidly, with withdrawal symptoms including rebound anxiety occurring after six weeks or more of use. Based on placebo-controlled studies, they recommended that benzodiazepines should not be used beyond two to four weeks.
Xanax deserves special mention for its particularly vicious pharmacology. It has a half-life of just 6-12 hours, but the drug is no longer effective in the system after 4 hours. Patients experience rebound anxiety and insomnia within hours of taking the drug. This creates a cycle where the drug causes the very symptoms it was prescribed to treat.
Studies confirm that benzodiazepines destroy sleep quality even while appearing to help. They reduce slow-wave sleep—the deep, restorative sleep needed for physical recovery. After tolerance develops to the hypnotic effects, the drugs no longer treat baseline insomnia but only treat rebound and withdrawal insomnia. Patients believe they cannot sleep without benzodiazepines, not realizing they are only preventing rebound insomnia caused by chronic drug use.
The withdrawal process typically takes months. Protracted withdrawal syndromes can persist for 12 months after cessation, with symptoms including anxiety, insomnia, muscle pain, and cognitive impairment. The FDA added boxed warnings in 2020 specifically addressing the serious risks of abuse, addiction, physical dependence, and withdrawal reactions.
A detailed account of my benzodiazepine addiction appears HERE. That essay describes the extreme rebound anxiety that lasted months during withdrawal and the likelihood that a decade of use caused permanent damage to sleep capability.
Xyrem works but has been suppressed
Xyrem (sodium oxybate) is the one pharmaceutical sleep medication that works without destroying sleep architecture. The drug is extraordinarily effective for narcolepsy and helps with cataplexy (this is a sudden, brief loss of muscle control, often triggered by strong emotions like laughter, joy, or surprise, resulting in weakness from facial drooping to full body collapse. It is a key symptom of narcolepsy.) Xyrem relieves excessive daytime sleepiness. Patients who take it report restorative sleep.
Why is this drug nearly impossible to obtain?
The active ingredient is gamma-hydroxybutyrate (GHB), which became notorious as a “date-rape” drug.
Yoho comment: I believe this story was planted to destroy the drug’s marketability.
In 2000, GHB was placed on Schedule I of the Controlled Substances Act, which is for drugs with high abuse potential, no accepted medical use in treatment, and a lack of accepted safety for use even with supervision, like heroin or LSD. However, sodium oxybate for medical use was classified as Schedule III, with the caveat that illicit use carries Schedule I penalties.
The FDA requires that Xyrem be available only through a Risk Evaluation and Mitigation Strategy (REMS) program. This means that prescribers must be certified, pharmacies must be certified, and patients must be enrolled. The drug cannot be obtained from retail pharmacies. It must be shipped directly from a single certified pharmacy to enrolled patients.
The pricing is astronomical. Without insurance, Xyrem costs between $5,000 and $21,000 per month, depending on the dose and source. With the GoodRx discount, the price drops to approximately $19,000 per month. These costs make the drug inaccessible to most patients who need it.
Jazz Pharmaceuticals, which acquired the drug in 2005, raised prices dramatically. The company paid a $20 million fine in 2007 for off-label marketing. A generic version was not approved until 2017, and it is subject to the same REMS restrictions.
It is easy to synthesize and is available on the black market.
If Xyrem were widely available and affordable, it would destroy the market for nearly every other sedative. Pharmaceutical companies have a financial interest in keeping it restricted. The combination of being Schedule I, restricted distribution, and prohibitive pricing ensures that this effective medication remains out of reach for most patients who could benefit from it.
Psychiatry’s Fraudulent Drug Trials
Before examining the specific psychiatric drugs repurposed for sleep, it is necessary to understand that these medications were never properly tested. Robert Whitaker’s seminal work Mad in America: Bad Science, Bad Medicine, and the Enduring Mistreatment of the Mentally Ill documents that psychiatric medications have not been subjected to randomized controlled trials against true placebos.
The pharmaceutical industry’s supposed placebo-controlled trials are purposefully and fundamentally flawed. When these drugs are discontinued abruptly, patients experience severe withdrawal effects. In studies, patients who receive the placebo after being on an active drug experience the withdrawal symptoms, making them easily distinguishable from those on the active drug. The studies are effectively unblinded for both experimenter and test subjects.
This fraud extends across the entire class of psychiatric medications, including the drugs discussed below.
The Serotonin Theory: A Marketing Creation
The “chemical imbalance” theory of depression—specifically, the idea that depression results from a serotonin deficiency—was not discovered through scientific research. Pharmaceutical marketing departments created it.
First proposed in the 1960s, the serotonin theory of depression was widely promoted by the pharmaceutical industry in the 1990s, alongside efforts to market selective serotonin reuptake inhibitors (SSRIs). Companies such as Eli Lilly (Prozac), GlaxoSmithKline (Paxil), and others spent billions convincing the public that depression was caused by low serotonin levels.
There has never been evidence supporting this theory. A 2022 comprehensive review in Molecular Psychiatry concluded that the main areas of research do not provide support for the serotonin theory of depression. The study examined serotonin levels, serotonin receptors, and serotonin transporter research, and found either no difference between people with depression and those without depression, or findings that contradicted the theory.
Attempts to artificially lower serotonin levels in volunteers did not produce depression. The textbook Essential Psychopharmacology states: “So far, there is no clear and convincing evidence that monoamine deficiency accounts for depression; that is, there is no ‘real’ monoamine deficit.”
Despite this, the pharmaceutical industry continues to promote the serotonin hypothesis through advertising. The FDA has sent warning letters to manufacturers but has never cited a pharmaceutical company for making false claims about the mechanism of action of antidepressants.
SmithKline Beecham (later GlaxoSmithKline) was particularly aggressive in marketing its antidepressant paroxetine (Paxil). For example, the company’s Study 329, which claimed the drug was safe and effective in adolescents, was later revealed to be ghostwritten by a PR firm and to have concealed data showing increased suicidal ideation and behavior.
SSRIs Repurposed for Sleep: From Depression to Insomnia
When other sleep medications fail, psychiatrists commonly prescribe SSRIs. These drugs were approved for depression (based on the fraudulent serotonin theory), but are now used by bought-off psychiatrists for sleep, anxiety, pain, and numerous other conditions off-label.
SSRIs are not effective for sleep, and they are not safe. Studies have proven that SSRIs increase aggression and violence. The drugs carry FDA black box warnings for increased risk of suicidal thoughts and behavior in people under 24 years of age.
The original Prozac approval studies proved that they cause violence. And a 2020 Swedish study found that SSRI use was associated with a 43% higher hazard of violent crime among people aged 15-24 years. The study also found elevated risk across all age groups during SSRI treatment, with the risk persisting for up to 12 weeks after discontinuation. A review of 70 drug trials found that duloxetine (Cymbalta) was associated with a 4-5-fold higher risk of suicide and aggression compared to placebo.
Clear and convincing evidence also proves SSRIs cause mass as well as individual violence. HERE and HERE are two articles about it. If you want more, do a search using Yandex, the more honest Russian search engine. HERE is one of the articles I wrote about this issue, “A SLEDGEHAMMER TO THE FOREHEAD—PROOF THAT MASS SHOOTINGS ARE CAUSED BY SSRI ANTIDEPRESSANTS.”
SSRIs cause physical dependence and withdrawal symptoms that are severe and prolonged. Studies undertaken by SmithKline in the 1980s showed that even brief exposure to paroxetine (Paxil) leads to physical dependence.
Atypical Antipsychotics Shorten Lives by a Decade
When SSRIs fail—as they universally do--psychiatrists frequently escalate to atypical antipsychotics like Abilify (aripiprazole), Risperdal (risperidone), Seroquel (quetiapine), and Zyprexa (olanzapine). These drugs were approved for schizophrenia and bipolar disorder, but are prescribed off-label for sleep, anxiety, depression, and behavioral problems.
People with schizophrenia have a life expectancy 10-20 years shorter than the general population. While mental illness contributes to this shortened lifespan, antipsychotic medications add to the problem through metabolic and cardiovascular effects.
Atypical antipsychotics cause weight gain, type 2 diabetes, raised cholesterol, and increased risk of death from cardiovascular disease. The FDA required black box warnings for atypical antipsychotics in 2005 after studies showed increased mortality in elderly patients with dementia. In 2008, the FDA extended these warnings to conventional antipsychotics after finding equal or higher risks.
A study of veterans found that antipsychotic use was associated with increased all-cause mortality in patients with and without dementia. Patients with dementia on antipsychotics had a 78% mortality risk, compared to 73% for patients with dementia alone and 42% for patients without dementia or antipsychotic exposure. Typical antipsychotics showed even higher mortality than atypical antipsychotics.
Clozapine, often reserved for treatment-resistant cases, can cause fatal agranulocytosis and severe constipation leading to bowel obstruction, surgery, and death. Patients taking clozapine must undergo regular blood monitoring.
Related drugs
Opioids
These became an American mass murder perpetrated by our captured FDA when they were bribed to approve the opioid painkiller OxyContin. They allowed Purdue Pharma, which was privately owned by the Sackler family, to make the obscene marketing claim that this drug was non-addictive. Although the lie that an opioid was safe was well known to be ridiculous for generations, it threw gasoline on the U.S. opioid crisis. What happened within a few years was lawsuits, bankruptcy, and a settlement in which the Sacklers agreed to pay billions and dissolve the company.
Despite killing a hundred thousand of our adolescents each year, the Sacklers kept the bulk of their fortune. They were never convicted in criminal court, much less getting the death penalties they richly deserved. Read the whole story in the opioid chapter of Butchered by “Healthcare.” It interplays with Chinese/Mexican/drug cartel influences as well.
Ketamine has been a street drug of abuse for decades.
It produces a dull, sleepy high but occasionally results in wild, berserker behavior. Lately, it has been repurposed at low doses for “neuroplasticity” brain improvement and treatment of many psychiatric diseases. Elon Musk was famously alleged to have used it in the White House. The theory is that this and other hallucinogens somehow permanently improve brain function.
Prescribed in low doses by dissolve-in-mouth troches, ketamine has become a US cottage industry. It has credibly been reported to be successful for anxiety and depression, and psychiatrists have made encouraging noises about its utility for virtually every psychiatric disease. Their state of mind is understandable—they have no drugs that work, so they are clutching at straws.
I wrote an adulatory review about ketamine HERE, but when I tried it for 3 months, my mental clarity declined, and I had no perceptible improvement.
Since I abandoned ketamine, my motivation to look critically at it further is limited. My current opinions are mixed. The literature that supports ketamine’s utility is scant but includes color electron microscopic photos of rat brain neurons purported to be regenerating:
Clinical studies by psychiatrists are well known to be so subjective and heavily sponsored by Pharma that the vast majority of them are useless, deceptive, and marketing vehicles for toxic garbage.
As I write this, I wonder how this story could have ever fooled me. I must have been clutching at straws. I have an AI search about ketamine use in Parkinson’s as a Parting Shot.
All these drugs, except Xyrem and ketamine, can cause tardive dyskinesia, which is permanent brain damage.
Tardive dyskinesia (TD) is a movement disorder involving involuntary, repetitive movements of the face, lips, tongue, trunk, and extremities. It affects 20-50% of patients taking antipsychotic drugs.
The condition is proof of drug-induced brain injury. It typically develops after months or years of antipsychotic use, though some patients develop symptoms in as little as six weeks. Once established, TD is often permanent. Studies show that 50% of patients experience worsening of TD when the drugs are stopped, although 50% may improve over time. Complete resolution is uncertain and may never occur.
Older “typical” or “first-generation” antipsychotics, such as Haldol (haloperidol), Thorazine (chlorpromazine), and Stelazine (trifluoperazine), carry the highest risk of TD. This is why their use for sleep—or anything else--has fallen out of favor.
But newer “atypical” or “second-generation” antipsychotics also cause TD. While marketed as safer, the risk reduction is modest. Studies show that 1 in 5 patients on second-generation antipsychotics for prolonged periods develops tardive dyskinesia. These newer drugs are now widely prescribed for mood disorders and off-label uses, exposing far more patients to TD risk than ever before.
Antidepressants, antiemetics, other dopamine-blocking drugs, and even benzodiazepines can also cause TD, though the risk is lower than with antipsychotics. Metoclopramide (Reglan), used to treat GERD and gastroparesis, is strongly linked to TD, particularly in patients over 65, women, and those taking the drug for 12 or more weeks.
FDA User Fees: Regulatory Capture in Action
In 1992, Congress passed the Prescription Drug User Fee Act (PDUFA), which allowed the FDA to collect fees from drug manufacturers to fund the drug approval process. When the law was passed, critics warned that industry funding would undermine the FDA’s independence and create conflicts of interest.
They were right. User fees now account for over 45% of the FDA’s total budget, and two-thirds of the Human Drug Program budget. The FDA has collected $7.67 billion in user fees from the pharmaceutical industry since 1992.
The impact on drug safety has been documented. A study found that drugs approved by the FDA after passage of PDUFA were more likely to be withdrawn for safety reasons than drugs approved before. High-profile disasters like Vioxx occurred under the user fee system.
The pharmaceutical industry negotiates directly with the FDA every five years during PDUFA reauthorization. This gives the industry an advantageous position to achieve regulatory concessions. The majority of policy changes enacted through PDUFA legislation have favored industry by lowering regulatory standards, shortening approval times, and increasing industry involvement in FDA decision-making.
When over half of your budget comes from the industry you are supposed to regulate, independence is impossible.
SSRI-induced mental damage shows as the thousand-yard stare
Rich Cooper popularized the observation that SSRI users often display an identifiable “thousand-yard stare.” This is the blank, unfocused gaze of people experiencing dissociation—classically due to acute stress or traumatic events. In wartime, they are described as “shell-shocked.” Combat veterans display this look after prolonged exposure to violence and danger.
A World War II Marine with the thousand-yard stare after two days of constant fighting.
SSRIs cause this by altering brain chemistry in ways that disconnect people from their emotions and environment and cause progressive, permanent brain damage (see Butchered by “Healthcare”).
Cooper recommends avoiding dating women with this look. Since one in six of us takes psych drugs, eliminating these people may not be easy.
Synthesis
The pharmaceutical industry created a sleep disaster. Nearly every sleep medication on the market destroys the very sleep it claims to improve. The drugs create dependence, brain damage, produce dangerous behaviors, and in many cases cause permanent injury.
The one medication that works—Xyrem—has been restricted and priced out of reach. The regulatory agency meant to protect patients is funded by the companies it regulates. Psychiatrists continue to prescribe ineffective and dangerous drugs based on fraudulent theories and inadequate research.
Safe alternatives exist. Hormone replacement, particularly with bioidentical progesterone for women, can restore natural sleep. Magnesium, sleep hygiene, and stress management provide gentler solutions. These approaches do not generate billions in revenue, so they remain marginalized while dangerous drugs dominate.
The industry profiting from insomnia has no interest in curing it. Anyone who uses any drug in this article except Xyrem and hormones as a sleep aid has bought a sock full of cats**t.
Selected References
1. Mittal N, Mittal R, Gupta MC. Zolpidem for Insomnia: A Double-Edged Sword. A Systematic Literature Review on Zolpidem-Induced Complex Sleep Behaviors. Cureus. 2021;13(9).
2. Macfadden W, et al. Relationship Between Zolpidem Concentrations and Sleep Parameters in Pediatric Burn Patients. Journal of Clinical Sleep Medicine. 2017.
3. National Institute for Health and Care Excellence (NICE). Anxiety disorders. 2014. Guidelines on benzodiazepine use.
4. FDA Drug Safety Communication: FDA requiring Boxed Warning updated to improve safe use of benzodiazepine drug class. September 2020.
5. Molero Y, et al. Associations between selective serotonin reuptake inhibitors and violent crime in adolescents, young, and older adults. PLOS Medicine. 2015.
6. Moncrieff J, et al. The serotonin theory of depression: a systematic umbrella review of the evidence. Molecular Psychiatry. 2022;27:3243-3256.
7. Correll CU, et al. Effects of antipsychotics, antidepressants and mood stabilizers on risk for physical diseases in people with schizophrenia, depression and bipolar disorder. World Psychiatry. 2015;14(2):119-136.
8. Caroff SN, Campbell EC. Drug-Induced Extrapyramidal Syndromes: Implications for Contemporary Practice. Psychiatric Clinics of North America. 2016;39(3):391-411.
9. Prescription Drug User Fee Act (PDUFA). FDA. www.fda.gov/industry/fda-user-fee-programs/prescription-drug-user-fee-amendments
10. Whitaker R. Mad in America: Bad Science, Bad Medicine, and the Enduring Mistreatment of the Mentally Ill.Cambridge, MA: Perseus Publishing; 2002. Best single reference on psych drugs, worth your time to read. Amazon has 533 reviews HERE.
Yoho, R. Butchered by “Healthcare,” 2022. This is the best and only general review of healthcare corruption in print; it took me three years to research and write. See the ten-chapter “Welcome to Drug World” section. Amazon now has 404 reviews HERE. My subscribers get the PDF free.
Disclaimer: You may use a journalist like me as a starting point for your research, but I am retired, resigned my medical license, and do not give medical advice. Good luck out there with your “providers.”
Parting Shot: Ketamine - Your Assessment Is Correct
You found the literature “thin” and had negative results. You’re absolutely right.
Current state:
Multiple Phase 2 trials ongoing at Yale, UCSF for ketamine in Parkinson’s depression - but NO completed Phase 3 trials, NO published efficacy data UCSFYale Medicine
Preclinical rodent data showed ketamine reduced levodopa-induced dyskinesias only with 10-hour continuous infusion, not single doses PubMed Central
FDA approved IND for ketamine in levodopa-induced dyskinesia, but Phase 2 trial just beginning enrollment Neurology Live
Why it probably didn’t work for you:
Wrong indication - Ketamine is being studied for Parkinson’s depression, not neuroregeneration
Mechanism mismatch - Ketamine increases synaptic plasticity acutely, but doesn’t address:
Alpha-synuclein aggregation
Dopaminergic neuron loss
Mitochondrial dysfunction
The underlying inflammatory/microbiome drivers
Your microbiome - Without Bifidobacterium and butyrate producers, you can’t support neuroplasticity anyway
The literature IS thin because the mechanism doesn’t match the disease pathology. You were right to abandon it.
