We released our video on the topic about 2 years ago, which dives deep into the story of serotonin.
The monoamine hypothesis of depression has and continues to guide the medical establishment and collective consciousness on depression.
This theory states that a depletion of monoamine neurotransmitters, dopamine, norepinephrine and serotonin, leads to “depression.”
Reserpine, a drug that had been used for centuries by Indians.
Even Ghandi used it.
Reserpine works by inhibiting the release of all monoamines.
Despite showing benefit in humans, the narrative became that it induced depression in animals due to its sedative properties.
This "theory" lead to the creation of various drugs that are still in wide use today.
Monoamine oxidase inhibitors prevent breakdown of these compounds, while tricyclics act as dopamine, serotonin and norepinephrine reuptake inhibitors, also increasing their amount.
However, since then the reserpine-induced depression model has been characterized as a myth by various researchers.
Recent reviews have stated that reserpine, at best does not consistently induce depression, and in many cases can treat it! ncbi.nlm.nih.gov/pmc/articles/P…
This should come as no surprise given that these 3 neurotransmitters all have remarkably different effects on mood and perspective.
Some small studies suggested a link between lower serotonin levels in certain brain regions post mortem, further driving the hypothesis.
The authors cautioned that these findings were preliminary and did not do much but allow them to test more hypotheses.
Pharma giant Lilly went to work quickly on developing drugs that selectively increased serotonin.
In their original manuscript, they claim that there is multiple lines of evidence suggesting serotonin is low in depression,
but their references don’t remotely support this.
In fact, it supported the exact opposite: administering serotonin precursors caused sedation, numbness, convulsions, tremors and agitation.
Dopamine precursors produced alertness with none of these “side effects.”
They also note that 5HIAA cerebrospinal fluid concentrations, which is the “deactivated” version of serotonin, were decreased in certain mental illness.
They went ahead and assumed that this was because they had less serotonin generally, not because they had less turnover!
So it becomes clear rather quickly that tTeuptake Inhibitors (SSRIs) were not only completely unfounded, but were likely intentional given what we’ve discussed previously: that serotonin makes people easy to manipulate:
Documentation from LIlly in 1984 showed that severe agitation leading to suicide occurred in over 1% of patients, a figure large enough that it was required to be disclosed to regulatory agencies.
Of course, Lilly excluded this when seeking approval.
Lilly first tried to get Prozac approved in Germany, with their drug regulatory agency saying in a fax back to Lilly that “we think this preparation totally unsuitable for the treatment of depression.”
This hilarious reaction was driven by the fact that after reviewing Prozac’s trial data, it was painfully obvious that many patients would take the drug and go on to commit suicide.
“it refused to approve the antidepressant based on Lilly's studies showing that previously nonsuicidal patients who took the drug had a 5 fold higher rate of suicides and suicide attempts than those on older antidepressants, and a 3 fold higher rate than those taking placebos.”
Despite this clear evidence that Prozac was outright dangerous and made people kill themselves, the FDA approved Prozac in 1987, and it quickly became one of the hottest drugs on the market.
In 1987, the first lawsuit involving Prozac and violent tendencies was initiated.
A man who was taking Prozac shot and killed eight people, injured twelve others and then committed suicide at his workplace.
The verdict was that it had nothing to do with Prozac.
In 1990, shortly after Prozac’s approval, Harvard psychiatrist Martin H. Teicher reported that SSRIs could cause suicidal or homicidal tendencies. He described cases in disturbing, gory detail.
It was clear that these individuals had their reality distorted.
Lilly scientists were pressured by executives to alter records on doctor experiences with Prozac: changing mentions of “suicide attempts” to "overdose" and suicidal thoughts to "depression."
Once again we have clear indication that they knew exactly what they were doing
One LIlly employee stated:
“I do not think I could explain to [anyone] why we would do this especially on the sensitive issue of suicide and suicide ideation. At least not with the explanations that have been given to our staff so far.”
Lilly also withheld data demonstrating that “Prozac may produce nervousness, anxiety, agitation, or insomnia in 19% of users and sedation in 13% of users”
The FDA became aware of this deliberate manipulation. The chief FDA epidemiologist stated:
“Because of apparent large-scale underreporting, the firm's analysis cannot be considered as proving that fluoxetine and violent behavior are unrelated."
Despite massive evidence to the contrary, in 1991 the FDA concluded that there was no evidence for a causal link between Prozac and violence. Shocking.
Lilly also had hired guns to dismiss these notions. Researchers they had on staff churned out questionable statistical analysis that “disproved” Teicher’s concerns, but Teicher pointed out the flaws in their work.
Lilly later initiated a media smear campaign against another Harvard doctor published the book Prozac Backlash, detailing Lilly’s malpractice and tendency to hide or downplay harms of their drug. https://t.co/7h9PTqCGRItwitter.com/i/web/status/1…
Things came to a climax at the Tobin v. SmithKline trial, where an individual shot and killed his wife, daughter, granddaughter, and himself after just two doses of Praxil, another SSRI drug. Finally, Pharma was held (somewhat) accountable, as the jury found for the plaintiff.
Doctors testified, saying that there was already a extensive existing literature on how SSRIs could cause suicidal or homicidal tendencies. They presented substantial evidence that both Lilly and SmithKline were well aware of this. twitter.com/i/web/status/1…
Several other trials were held about similar issues: people starting to take SSRIs and then killing others and/or themselves.
By this point it didn’t matter. Prozac was a top 5 selling drug and was raking in billions. Paying off a few million to some families was well worth it.
In 2004, the FDA finally issued a blackbox warning on these medications of a “link” between taking them and violence and/or suicide and worsened depression. Zoloft, Lexapro, Prozac and Celexa continue to make billions, being handed out to tens of millions of Americans yearly.
Oh yeah, but you know, it was just an accident.
They didn’t know any better. More studies are needed.
Thanks for reading through this thread, we will have plenty of more content on this issue soon. Toss us a RT if you enjoyed, and be sure to check out all of our content, consultation options and supplements over at lnk.bio/analyze.and.op…
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High cortisol, anxiety, and can’t sleep? This is for you.
This is the ULTIMATE GUIDE to STRESS - the signs, the biological mechanisms and what to do about it:
There are TONS of symptoms that you might not have realized are from stress.
1. Can’t fall asleep 2. Waking up in the night to pee 3. Waking up in the night for no reason 4. Nightmares / sleep paralysis 5. Foamy urine 6. Hair loss 7. Hair graying 8. Gain weight easily 9. Gaining weight in the abdomen (visceral fat) 10. Low appetite 11. Cold extremities (fingertips, nose, toes, ears) 12. Menstrual cramps 13. Irregular menstruation or premenstrual syndrome 14. Irritability 15. Anger or aggression 16. Twitching 17. Headaches 18. Itchiness 19. Jitters 20. Anxiety / fear 21. Lack of confidence 22. Insatiable appetite or sweet cravings 23. Trouble catching your breath or breathing heavily 24. Pounding heart 25. Constipation 26. Nausea 27. Diarrhea 28. Gut pain 29. Acid reflux 30. Frequent urination
One of the simplest test for stress is the heartbeat / blood pressure.
Feel your pulse - if it feels like there’s pressure / pounding, good sign your body is under stress.
EVERYTHING originates in the brain - this is what allows us to perceive stress and mount a physiological response.
The amygdala in the brain is where a lot of this perception happens,
And the hypothalamus is the control center - coordinating the stress to other parts of the body.
The hypothalamus:
→ Stimulates the pituitary (with a hormone called CRH), which then sends another hormone (ACTH) to the adrenal cortex to produce CORTISOL (among other hormones). This is known as the hypothalamus-pituitary-adrenal (HPA) axis, the primary stress system in the body.
→ Transmits signals to the brain stem and then to the spinal cord - which sends nerve fibers throughout the body
→ Some of these fibers connect to the adrenal medulla, which secretes adrenaline and noradrenaline
There are tons of other stress hormones and signals, which we will get into, but ultimately they all work by or as a result of these core systems.
It is perfectly designed to respond to external threats, where you SHOULD be stressed,
But that’s not what we’re focused on. We are talking about excessive, chronic, inappropriate and/or overactive stress responses.
How can we live calmly while not becoming numb to things that necessitate stress?
Thiamine (vitamin B1) has powerful protective effects for the brain, reducing death from severe brain injury by >50% in multiple studies.
(🧵1/9)
This study came out in 2024 in Frontiers in Nutrition.
They examined people with traumatic brain injury who got thiamine treatment or those who didn't.
It wasn't an experiment - it was an associational study, but the design makes it pretty strong.
They did propensity score matching (PSM).
Essentially, this helps remove confounding variables by only including people who could be matched up with a similar "control" who did not receive the thiamine.
As you can see, about 1400 people were excluded from the non-thiamine group because they couldn't be matched up with someone similar who did get thiamine.
This ensured that the 402 people and their non-thiamine matches were similar in all measures so that any effect was attributable to thiamine.