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.
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The use of mastic dates back to ancient time. Herodotus, a historian from the 5th century BC, mentioned chewing the resinous fluid secreted by the bark of the mastic tree.
Dioscorides, a prominent medical author from the 1st century AD, praised mastic for its therapeutic properties. He believed it was beneficial for blood coagulation, chronic cough, teeth cleaning, freshening breath, improving complexion and for stomach and intestinal disorders
We released our video on the topic about 2 years ago, which dives deep into the story of serotonin.
In the 1950s, serotonin was advertised as a "normal thinking" hormone. LSD, famous for inducing hallucinations, had been recognized to antagonize the effects of serotonin. The conclusion was simple: LSD made people crazy, so serotonin makes people sane.
Biological energy is really electron flow, like a wire or bolt of lightning. These electrons can get backed up for a number of reasons, which halts energy production, promotes oxidative stress, and other disease and aging related processes.
One of the ways is due to excess nitric oxide. NO binds and inhibits a crucial enzyme in the electron flow process, making its inappropriate elevation undesirable. We can see this when people are fed NO precursors, their metabolic rate drops substantially.
PREGNENOLONE: The closest you’ll get to the fountain of youth.
This protective hormone’s anti-aging properties, and how it bulletproofs your mitochondria and energy.
We just dropped a video detailing these effects of pregnenolone, so be sure to check that out if you want some more in depth analysis
“Anti-aging” as a phrase honestly really annoys me, so sorry I threw it in there to get your attention. I don’t like it as it seems like those using it most don’t have a functional idea of what constitutes aging in real life.
Adding this to my arsenal has been a complete game changer.
Harnessing the metabolic prowess of Methylene Blue to your advantage: a guide to its use, my experience, dosing, and what to expect. https://t.co/hdS9tAJjuntwitter.com/i/web/status/1…
We cover this in our video on Methylene Blue, so be sure to check that out:
My first time trying methylene blue was literally because I thought the name sounded cool. That should tell you the complexity of thought I had at this point in my life. I wasn’t an idiot, but certainly was looking for a tangible way to improve my energy and cognition.