SSRI Drugs May Cause Serious Lung Disease And Fibrosis

haidut

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The study tries to downplay the risk by claiming that it is only relevant to "old, frail people". However, the specific lung issue linked to SSRI - bronchiectasis - is almost never found as an independent disease but rather almost always as a symptoms of cystic fibrosis. Given serotonin's primary role in development and progression of fibrosis I think the risks of SSRI drugs for ANY age group should immediately become apparent. As it is the case with so many other chronic and debilitating/lethal conditions lately, the rates of cystic fibrosis have been steadily increasing over the last 3 decades, which coincides almost perfectly with the prescription rate increase of SSRI drugs. Of course, instead of acknowledging the public health fiasco of the SSRI drugs, FDA and companies like Pfizer silently push anti-serotonin (5-HT2B) drugs like terguride through the system for quick approval as treatment for these serotonin-driven conditions. The system sells you both the poison and the remedy, and the pubic is oblivious.

[Full text] The relationship of SSRI and SNRI usage with interstitial lung disease | CIA
Bronchiectasis Study Links Antidepressants to the Disease in the Elderly
"...Research has shown a jump in antidepressant use in the past several decades. Their use increased by 400 percent in the United States between the late 1990s and 2008, for example. The most commonly prescribed antidepressants are selective serotonin reuptake inhibitors, or SSRIs, and serotonin norepinephrine reuptake inhibitors, SNRIs. Both classes of drugs are associated with the development of interstitial lung diseases such as bronchiectasis. Researchers hypothesised that the link between antidepressants and the development of bronchiectasis and other lung diseases is more prevalent than previous studies have reported. Their study, published in the journal Clinical Interventions in Aging, is titled “The relationship of SSRI and SNRI usage with interstitial lung disease and bronchiectasis in an elderly population: a case–control study.

"...The association between older people’s use of antidepressants and their developing a lung disease may be underreported, the researchers said. They think many doctors may be unaware of a lung disease because it has symptoms such as shortness of breath and fatigue that are common to this age group. The results suggest that doctors should prescribe antidepressants with care, minimizing the dose and period of treatment and considering alternative treatments where appropriate. Antidepressants “were significantly associated with the risk of ILD/B [bronchiectasis or another lung disease] in this elderly population,” the team wrote. “Because of their widespread usage, further studies should be done to validate these findings. Prescribers should cautiously monitor patients for development of insidious pulmonary [lung] symptoms when these drugs are used.”
 

Soren

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Continually amazed by the depth of the corruption and the depth of the ignorance. It's as if they want to keep you sick unto death.

Bizarrely I am still optimistic that truth will out and we will get a revolution in medicine. Technology is such a great equaliser that it is always getting more difficult for these monopolies to keep the truth hidden and to stop progress. Status quo's don't change, until they do.
 
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haidut

haidut

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Continually amazed by the depth of the corruption and the depth of the ignorance. It's as if they want to keep you sick unto death.

Bizarrely I am still optimistic that truth will out and we will get a revolution in medicine. Technology is such a great equaliser that it is always getting more difficult for these monopolies to keep the truth hidden and to stop progress. Status quo's don't change, until they do.

And the strange thing is that most studies I have seen on SSRI explicitly say that doctors should minimize treatment period with SSRI to the minimum needed to achieve remission. Yet every doctor I have ever talked to says antidepressants have to be taken for life.
 

Soren

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And the strange thing is that most studies I have seen on SSRI explicitly say that doctors should minimize treatment period with SSRI to the minimum needed to achieve remission. Yet every doctor I have ever talked to says antidepressants have to be taken for life.

The majority of doctors to me in many ways resemble an indoctrinated group of people blindly following the dogma that the church of the pharmaceutical industry and the FDA set from on high. Only a very small percentage seem to have the the gumption to look outside the mainstream beliefs. Yet so much trust and faith is put in them. People have this conception in their mind that every doctor has been given some unique insight and knowledge into the human body that we "normal" people can't possibly understand so they blindly follow them and anyone who challenges the dogma is ridiculed and marginalised.

On a side note do you see any movement away from SSRI drugs for the treatment of depression? Obviously terguride is a good sign that they are finally stumbling along the right path but that is not being marketed as a treatment for depression more the diseases that are caused by SSRIs and fibrosis. Perhaps the new drugs that are being researched for degenerative brain diseases (the ones similar to Allopregnanolone etc) will one day be marked as anti-depressants.
 
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haidut

haidut

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The majority of doctors to me in many ways resemble an indoctrinated group of people blindly following the dogma that the church of the pharmaceutical industry and the FDA set from on high. Only a very small percentage seem to have the the gumption to look outside the mainstream beliefs. Yet so much trust and faith is put in them. People have this conception in their mind that every doctor has been given some unique insight and knowledge into the human body that we "normal" people can't possibly understand so they blindly follow them and anyone who challenges the dogma is ridiculed and marginalised.

On a side note do you see any movement away from SSRI drugs for the treatment of depression? Obviously terguride is a good sign that they are finally stumbling along the right path but that is not being marketed as a treatment for depression more the diseases that are caused by SSRIs and fibrosis. Perhaps the new drugs that are being researched for degenerative brain diseases (the ones similar to Allopregnanolone etc) will one day be marked as anti-depressants.

Here is something you might enjoy in regards to why people act that way with doctors:
Human Pregnancy Length Controlled By Metabolism Speed, Not Pelvic Shape

More recent antidepressants seem to focus more on epinephrine reuptake inhbition, which probably has an effect on dopamine as well. A few serotonin antagonists and dopamine agonists (pramipexole) are about to be approved for depression as well. I am very curious to see how the pharma will sell these new drugs while still keeping sales of the SSRI intact, or at least explain the inconsistencies.
 

Soren

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Just read the post you linked. Couldn't agree more. Especially with the "something must be done" mentality. You see that in all levels of life, something happens and if someone suggests an idea to rectify it even if it is horrible people go along with it because they feel it is better than nothing. The fact that something is being done gives them comfort, people prefer to have an "expert" tell them what to do rather than discover for themselves.
 

mujuro

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My grandfather, 83, just came down with pneumonia. Scans revealed scarring on the lungs. His best guess was exposure to hay particles in a silo. He has been on escitalopram for 2 years now after the death of my grandmother. The doctors have him on steroids and an array of drugs to combat the side effects of other drugs. For 80 years of his life he didn't take a single drug.
 

Eilis

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The study tries to downplay the risk by claiming that it is only relevant to "old, frail people". However, the specific lung issue linked to SSRI - bronchiectasis - is almost never found as an independent disease but rather almost always as a symptoms of cystic fibrosis. Given serotonin's primary role in development and progression of fibrosis I think the risks of SSRI drugs for ANY age group should immediately become apparent. As it is the case with so many other chronic and debilitating/lethal conditions lately, the rates of cystic fibrosis have been steadily increasing over the last 3 decades, which coincides almost perfectly with the prescription rate increase of SSRI drugs. Of course, instead of acknowledging the public health fiasco of the SSRI drugs, FDA and companies like Pfizer silently push anti-serotonin (5-HT2B) drugs like terguride through the system for quick approval as treatment for these serotonin-driven conditions. The system sells you both the poison and the remedy, and the pubic is oblivious.

[Full text] The relationship of SSRI and SNRI usage with interstitial lung disease | CIA
Bronchiectasis Study Links Antidepressants to the Disease in the Elderly
"...Research has shown a jump in antidepressant use in the past several decades. Their use increased by 400 percent in the United States between the late 1990s and 2008, for example. The most commonly prescribed antidepressants are selective serotonin reuptake inhibitors, or SSRIs, and serotonin norepinephrine reuptake inhibitors, SNRIs. Both classes of drugs are associated with the development of interstitial lung diseases such as bronchiectasis. Researchers hypothesised that the link between antidepressants and the development of bronchiectasis and other lung diseases is more prevalent than previous studies have reported. Their study, published in the journal Clinical Interventions in Aging, is titled “The relationship of SSRI and SNRI usage with interstitial lung disease and bronchiectasis in an elderly population: a case–control study.

"...The association between older people’s use of antidepressants and their developing a lung disease may be underreported, the researchers said. They think many doctors may be unaware of a lung disease because it has symptoms such as shortness of breath and fatigue that are common to this age group. The results suggest that doctors should prescribe antidepressants with care, minimizing the dose and period of treatment and considering alternative treatments where appropriate. Antidepressants “were significantly associated with the risk of ILD/B [bronchiectasis or another lung disease] in this elderly population,” the team wrote. “Because of their widespread usage, further studies should be done to validate these findings. Prescribers should cautiously monitor patients for development of insidious pulmonary [lung] symptoms when these drugs are used.”

I had been looking for your view on cystic fibrosis as this is a condition that has been widespread in my family. Ray mentioned in a conversation I think on Kmud that serotonin was linked with CF and when I had a look at pre-genetic Studies (obviously genetics have now clouded all relevant older research like thyroid and CF), there was one study that looked at serotonin as a marker for CF. I’m sure Ray had said serotonin while produced in the gut is broken down in the lungs...is this correct as I had trouble finding research on this. If so the correlation to bronchiectasis could be strong depending how effective this process is. CF also has a gut related issue for some patients depending on genetics....although not totally sure of this. Serotonin could be related to fast bowel transit when in excess, as is the case with many CF although blockage is another complication. I know in my individual case there has been no use of SSRis but the females have a line of inflammatory bowels and bowel cancer which may be linked with excess serotonin production. So if endogenous production of serotonin is high in gut how can this be prevented or what other mechanisms do I look at both for myself and family members with CF? Also how can you measure serotonin in lungs and is this directly altering CO2 levels. A widely accepted treatment now for the chronic CF lung is NO and there is a strong belief by patients that this holds merit and this is worrying. One family member with CF now uses a lot more caffeine as his metabolism has improved and some peating ideas. It’s helping for sure. But I remember you had said in an interview that NO was released from cells through magnesium. Just mentioned this as the use of magnesium has been hugely beneficial and this may in part be due to low thyroid, depletion of mag by CF medications etc...and releasing NO. Sorry about long post. I’ve been meaning to get on here and have some discussion about CF for ages. Thanks .
 
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haidut

haidut

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I had been looking for your view on cystic fibrosis as this is a condition that has been widespread in my family. Ray mentioned in a conversation I think on Kmud that serotonin was linked with CF and when I had a look at pre-genetic Studies (obviously genetics have now clouded all relevant older research like thyroid and CF), there was one study that looked at serotonin as a marker for CF. I’m sure Ray had said serotonin while produced in the gut is broken down in the lungs...is this correct as I had trouble finding research on this. If so the correlation to bronchiectasis could be strong depending how effective this process is. CF also has a gut related issue for some patients depending on genetics....although not totally sure of this. Serotonin could be related to fast bowel transit when in excess, as is the case with many CF although blockage is another complication. I know in my individual case there has been no use of SSRis but the females have a line of inflammatory bowels and bowel cancer which may be linked with excess serotonin production. So if endogenous production of serotonin is high in gut how can this be prevented or what other mechanisms do I look at both for myself and family members with CF? Also how can you measure serotonin in lungs and is this directly altering CO2 levels. A widely accepted treatment now for the chronic CF lung is NO and there is a strong belief by patients that this holds merit and this is worrying. One family member with CF now uses a lot more caffeine as his metabolism has improved and some peating ideas. It’s helping for sure. But I remember you had said in an interview that NO was released from cells through magnesium. Just mentioned this as the use of magnesium has been hugely beneficial and this may in part be due to low thyroid, depletion of mag by CF medications etc...and releasing NO. Sorry about long post. I’ve been meaning to get on here and have some discussion about CF for ages. Thanks .

People with CF often have pancreatic involvement and thus trouble digestive properly. The role of serotonin in chronic pancreatitis and the so-called exocrine pancreatic insufficiency (EPI) is known but not widely publicized and I posted a few studies showing anti-serotonin drugs can treat chronic pancreatitis, while taurine greatly improves fat absorption and protein utilization in those patients. I think NO is very dangerous for any patient and I am aware of its (criminally negligent) use in lung patients, especially newborn babies.
I don't think lungs break down serotonin buy they do store it, which explains why elevated blood serotonin levels affect lungs the most.
Lung serotonin metabolism. - PubMed - NCBI
https://www.openanesthesia.org/aba_lung_function_-_metabolic/
I think blood serotonin is a good proxy for lung serotonin load. Keeping the gut clean with antibiotics, fiber and charcoal would be what I would try as first line therapy and a doctor can prescribe TPH inhibitors off-label of serotonin levels are above 200. Serotonin antagonists like cyproheptadine can also help a lot but they do not resolve the underlying reason for increased serotonin - i.e. bacterial endotoxin overproduction.
Serotonin Production (gut) Depends On Bacteria
 

Kray

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Continually amazed by the depth of the corruption and the depth of the ignorance. It's as if they want to keep you sick unto death.

Bizarrely I am still optimistic that truth will out and we will get a revolution in medicine. Technology is such a great equaliser that it is always getting more difficult for these monopolies to keep the truth hidden and to stop progress. Status quo's don't change, until they do.
 

Kray

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I had been looking for your view on cystic fibrosis as this is a condition that has been widespread in my family. Ray mentioned in a conversation I think on Kmud that serotonin was linked with CF and when I had a look at pre-genetic Studies (obviously genetics have now clouded all relevant older research like thyroid and CF), there was one study that looked at serotonin as a marker for CF. I’m sure Ray had said serotonin while produced in the gut is broken down in the lungs...is this correct as I had trouble finding research on this. If so the correlation to bronchiectasis could be strong depending how effective this process is. CF also has a gut related issue for some patients depending on genetics....although not totally sure of this. Serotonin could be related to fast bowel transit when in excess, as is the case with many CF although blockage is another complication. I know in my individual case there has been no use of SSRis but the females have a line of inflammatory bowels and bowel cancer which may be linked with excess serotonin production. So if endogenous production of serotonin is high in gut how can this be prevented or what other mechanisms do I look at both for myself and family members with CF? Also how can you measure serotonin in lungs and is this directly altering CO2 levels. A widely accepted treatment now for the chronic CF lung is NO and there is a strong belief by patients that this holds merit and this is worrying. One family member with CF now uses a lot more caffeine as his metabolism has improved and some peating ideas. It’s helping for sure. But I remember you had said in an interview that NO was released from cells through magnesium. Just mentioned this as the use of magnesium has been hugely beneficial and this may in part be due to low thyroid, depletion of mag by CF medications etc...and releasing NO. Sorry about long post. I’ve been meaning to get on here and have some discussion about CF for ages. Thanks .

Hi Eilis- Hope you're still checking in these days. I would really appreciate any update in your situation, and what you have found to be beneficial? I know someone who has CF and has really been having a hard time of late; she is a 20ish female. I want to reach out to her with anything that might show hope in helping her.

Thank you, and I pray you and your family are doing well with regard to your health challenges.
 

PaRa

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I have CF, I do use taurine a lot and caffeine too, they help with the mind, not always up, caffeine give a pleasant boost.
I can relate so to high serotonin type, low thyroid symptoms (TSH was 1.5 2 weeks ago tho), bad digestion, black ideas, no motivation, highly introverted, I clearly prefer dogs to people lol.

Salt, E, K, calcium and magnesium are heavily needed
Will give a try to NAC

I may try some antibiotics for cleaning the gut but don’t know what are the safest, cyproheptadin ? Erythromycin ?
 

Perry Staltic

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@haidut What does a 5HT2b agonist do? I can understand what an antagonist would do, but it's not clear to me what an 5HT receptor agonist does. Does it increase 5HT2b expression, ie, the number of receptors, or something else?

I'm reading this study that mentions agonist activity at 5HT2b causes fibrosis


And then this study says that all SSRIs are 5HT2b agonists, which implies to me that people who take SSRIs are susceptible to fibrosis. Thinking covid here because interstitial lung fibrosis is a key characteristic of severe covid, and that appears to be a pathology caused by 5HT2b agonism.

 

Perry Staltic

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Serotonin is a natural ligand of 5HT receptors. Do 5HT receptor agonists act as unnatural ligands mimicing serotonin? I'm confused about what 5HT receptor agonists exactly do.
 

Perry Staltic

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At this point I am convinced that 5HT receptor agonists act as functional analogs of 5HT, but are artificial, independent change-agents uncontrolled by natural biologic signaling.

5HT binds to 5HT2b receptors mediating fibrosis and tissue remodeling to promote healing. The body naturally keeps serum 5HT levels low via platelet storage and other mechanisms, but artificially introduced 5HT2b agonists are not subject to the same control mechanisms and continuously activate 5HT2b receptors independent of 5HT.

All SSRIs are 5HT2b agonists, so potentially, people who take SSRIs long term have an increased risk of fibrosis.
 

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