covid brain fog means antidepressant side effects function insertion took place

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sushi_chef
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covid brain fog means antidepressant side effects function insertion took place

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thats guesstimation, and, covid vax must have that too ..

"Can COVID-19 alter your personality? Here's what brain research shows.
PUBLISHED DECEMBER 29, 2021

At the height of the COVID-19 tsunami that engulfed New York City in early 2020, a highly respected emergency room doctor, Lorna Breen, died by suicide. She had been serving as medical director at Manhattan’s NewYork Presbyterian Allen Hospital, and she was regarded as brilliant, energetic, and organized. She had no history of mental illness. But that changed after Breen contracted the virus.

The 49-year-old doctor first showed symptoms on March 18. After a 10-day illness, she returned to work. Her family was alarmed: She was confused, hesitant, nearly catatonic, exhausted. Something was wrong. They brought her home to Charlottesville, and Breen checked into a psychiatric ward at University of Virginia Medical Center. Soon after she was released on April 26, she took her own life.

“She had COVID, and I believe that it altered her brain,” her sister Jennifer Feist said on NBC’s Today show.
..
While little is known about the mechanisms behind many of these symptoms, researchers increasingly believe that inflammation may play a key role. With COVID-19, a storm of inflammatory cytokine proteins can trigger an out-of-control immune response that might permanently damage or destroy brain cells.

And with damage to the brain, Boldrini says, “we may not be the same person anymore.”
..
The COVID connection
One common theme among these conditions is a sustained inflammatory process. It’s been implicated in head injuries and in neurological diseases such as Alzheimer’s, where it causes additional loss of brain cells and exacerbates the formation of plaques.

When the immune system launches an attack against a virus or another invader, waves of inflammatory cells circulate through the bloodstream like foot soldiers. With COVID-19 and other conditions, those immune cells may permeate the normally protective blood-brain barrier. If inflammation gets out of hand, the process may kill neurons, Bronstein says.

Kriegstein notes that “most of the neurological manifestations of SARS-CoV-2 infection appear to be the result of indirect effects likely mediated through inflammation or immune responses.”

Inflammation also seems to interfere with brain metabolism. Researchers suspect that the process interrupts the flow of serotonin and prompts the body to instead produce a cascade of substances that are toxic to neurons.
..
"
https://www.nationalgeographic.com/scie ... arch-shows
brain fog covid 19
https://duckduckgo.com/?q=%22brain+fog% ... =h_&ia=web

"We noticed that SARS-CoV-2-infected patients showed increased carboxypeptidase A3 (CPA3) and decreased serotonin levels in their serum when compared with symptomatic SARS-CoV-2-negative patients. CPA3
"
https://pubmed.ncbi.nlm.nih.gov/34057753/

"Antidepressants Actually Reduce Serotonin Levels
By Rob Wipond -February 28, 20152
5057
Common scientific beliefs about serotonin levels in depression and how antidepressants act on the brain appear to be completely backwards, according to a paper from Canadian and American researchers in Neuroscience & Biobehavioral Reviews.

The authors noted that it is impossible to measure serotonin levels directly in a human brain, but the dominant theory for fifty years has been that depressed people have lower serotonin levels, while SSRI antidepressants keep serotonin levels high by blocking its re-absorption.

However, in their review of the scientific literature they could find no evidence to support this theory, while there was compelling evidence to support an opposing theory: that serotonin levels increase substantially during depressive episodes.

“The best available evidence appears to show that there is more serotonin being released and used during depressive episodes, not less,” stated a press release about the study. This apparently indicated a greater allocation of the neurotransmitter to conscious thought over other body functions.

When SSRIs are added and serotonin levels increase even more, it is actually the brain’s own compensatory response to reduce the escalating serotonin levels that improves symptoms in some people. And because the brain’s response takes time, that is the reason, they argued, that SSRIs are typically said to take several weeks before they have any positive impact.

Over the long term, though, the brain’s regulating systems are destabilized by the drugs. In the press release, the lead author stated, “It’s time we rethink what we are doing. We are taking people who are suffering from the most common forms of depression, and instead of helping them, it appears we are putting an obstacle in their path to recovery.”

Science behind commonly used anti-depressants appears to be backwards, researchers say (McMaster University press release on ScienceDaily, February 17, 2015)
"
https://www.madinamerica.com/2015/02/an ... in-levels/

"In addition, when serotonin is deficient, the effects of noradrenaline are intensified.
and can lead to a tendency to lose one's temper and become aggressive.
" deepl ++

"Major side effects of SSRIs include, but are not limited to serotonin syndrome, nausea, diarrhea, increased blood pressure, psychomotor agitation (English version), headache, anxiety, irritability, emotional instability, increased suicidal ideation, suicide attempts, insomnia, drug-drug interactions, neonatal drug reactions, anorexia (English version), dry mouth, sleepiness, tremor, sexual dysfunction, decreased libido, impotence, dyspepsia, dizziness, and sweating, personality disorders, nosebleeds, frequent urination, hypermenorrhea, mania/hypomania[38], chills, palpitations, taste perversion, dysuria[39], somnolence, gastrointestinal irregularities, muscle weakness, prolonged weight gain.
" deepl ++

antidepressant harming others
https://duckduckgo.com/?q=antidepressan ... =h_&ia=web

ssri / snri and harming others actions
https://www.mhlw.go.jp/www1/kinkyu/iyak ... /261-2.pdf

"When I remembered that the shooter in the 1999 Columbine High School shooting, in which 12 students were shot and killed, 24 were seriously injured, and two of the shooter's high school students committed suicide, I looked up the fact that the shooter was taking medication and learned that the shooter was taking SSRIs.
So I researched SSRIs and learned that SSRIs have a tremendous side effect called Activation Syndrome. It was described as "anxiety, agitation, hostility, impulsivity, panic attacks, and worse, suicidal behavior."
" deepl

thus should avoid all Antipsychotics drugs by all means too ..


history of antidepressant
"After the end of World War II, pharmaceutical companies obtained very cheap stocks of hydrazine, one of the fuels for the V2 rocket, and altered its structure to create new compounds [161]. Hoffman-La Roche discovered that the hydrazine compounds isoniazid and iproniazid had the properties of a drug that killed tuberculosis bacteria [161].

In 1952, treatment with this drug was known to have euphoric side effects, such as tuberculosis patients dancing joyfully, and in the process it was tested on psychiatric patients, and in 1956 iproniazid was found to be effective against depression [161]. Iproniazid is a monoamine oxidase inhibitor (MAOI) antidepressant (the Japanese product FP is not indicated for depression).

Around the same time, a type of antidepressant called tricyclic was also discovered: in 1856, the English chemist William Parkin discovered that a phenothiazine-like compound derived from coal tar could be used as a dye [162]. From this phenothiazine-like synthetic dye, iminobenzyl summer blue, the Swiss company Geigy synthesized imipramine [163]; in 1955, Roland Kuhn administered imipramine to a patient hospitalized for melancholy [163], and in 1957, at the International Psychiatric Conference reported that it reduced symptoms in depressed patients[164]. The following year, in 1958, imipramine was marketed under the trade name Tofranil [165].

Around the same time, another hypothesis to explain depression emerged: the neurotransmitter serotonin was reported to be present in the brain in 1954, and in 1960, George Ashcroft proposed the theory that serotonin levels may be low in depression [167]. In North America, noradrenaline is thought to be involved, and in 1965 Joseph Schildkraut of the U.S. National Institute of Mental Health (NIMH) proposed the catecholamine hypothesis of depression, which states that noradrenaline in the brain is reduced in depression and antidepressants increase it [ 168]. Schildkraut's theory is based on the fact that the hypertensive drug reserpine reduced serotonin, noradrenaline, and dopamine levels in rabbits [169], and an article published in the same issue of The Lancet just prior page that reserpine improved symptoms of depression and anxiety compared to a sham drug [ 170] that reserpine improved symptoms of depression and anxiety compared to sham medication [167]. However, an article in the same issue of The Lancet, on pages 116-117, found that reserpine users showed suicidal tendencies. The discovery of dopamine, for example, was later used to support the conclusion that serotonin was not decreased [167].

Arvid Carlson, a neuroscientist who later won the Nobel Prize for his discovery of dopamine, tried to create a drug that would only inhibit serotonin reuptake, and synthesized dimeridine (English version) at Astra in Sweden by modifying the chemical structure of the antihistamine chlorpheniramine, and in 1972, it was patented in several European countries. The patent was granted in several European countries in 1972, and the drug was approved in 1982 under the trade name Zelmid [172]. However, during approval by the U.S. Food and Drug Administration in the same year, a fatal side effect, Guillain-Barré syndrome, was reported, and it disappeared from the market [172]. This is believed to be the world's first selective serotonin reuptake inhibitor (SSRI). It was later discovered that chlorpheniramine itself had serotonin reuptake inhibitor-like effects, but it could not be patented, and without a patent, there was no prospect for profitable clinical trials, marketing, sales, and revenue [173].

Following Zermid, Juraal Le Fere of the French company Fournier developed Indulpin, a modified version of the antihistamine with a modified molecular structure, which was marketed under the trade name Upsten, but quickly disappeared from the market due to the side effect of leukopenia [174].

The first SSRI to survive on the market was fluvoxamine (Luvox), which was marketed in Switzerland in 1983 and approved in many countries, but was not approved in Germany due to suicides and suicide attempts during clinical trials [175].

Prozac (not approved in Japan) was approved in the U.S. and Canada in 1988 and in the U.K. in 1989, and by this time the topic of the dangers of benzodiazepines had become serious and was marketed on the basis that depression was behind anxiety disorders [176].

The word SSRI, a combination of acronyms, was coined by SmithKline Beecham (later GlaxoSmithKline) to market paroxetine, but became popularized to refer to a type of drug [177]. Paroxetine was marketed under the trade names Seroxat in the UK in 1991 and Paxil in the US in 1992.

Around 2000, the term "mental cold" was used in Japan for the marketing of Paxil, to refer to a mild case of depression as a disease [178].

In 2003-2004, David Healy claims that when the topic of a study that paroxetine induced suicides in children was covered up in Europe and the U.S., it turned into a marketing pitch for bipolar disorder [179]. Elsewhere, in 2003, the UK's Medicines and Healthcare Products Regulatory Agency (MHRA) told GlaxoSmithKline that suicides prior to the start of clinical trials should not be counted as part of the sham group, something that the FDA apparently did not notice, but the same was done with Prozac and Zoloft [180 ].
" deepl
:arrow:

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