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One of The Most Widely Used Antidepressants Has Just Been Implicated in Breeding Antibiotic Resistan

Discussion in 'Other Health News and Research' started by Jackb23, Sep 12, 2018.

  1. Jackb23

    Jackb23

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  2. RobR

    RobR

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    Oh Shi.......
     
    alkt likes this.
  3. Moof

    Moof Senior Member

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    Blimey O'Reilly!

    I took the dratted things for five months to prove to my doctor that I was willing to work with him to find solutions, even if some of his suggestions were frankly idiotic – it's bloody evil stuff if you don't suffer from depression. It made me feel as if I had some kind of depersonalisation disorder, and people kept asking me if I was all right mentally (I was fine until I started on it). Thankfully, a new GP started at the practice who actually knew that ME isn't caused by depression, and I was able to confess that I'd been shredding the prescriptions for over a year... :rofl:
     
  4. Mary

    Mary Moderator

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    A doctor prescribed this for me several years ago because I had unexplained (to him) fatigue - when in doubt, give a prescription AD! I took it for 2 days, hated how it made me feel, and stopped it. I later found out, through my chiropractor who does muscle testing, that my adrenals had tanked badly. The chiro gave me an adrenal glandular and within days my energy started returning. The way medicine is practiced in general is very scary to me. I only go see my doctor as a very last resort, and even then will do my own research about whatever it is he or she recommends before trying it.
     
  5. Mary

    Mary Moderator

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    My niece was given Paxil for 4 years (!) She said it made her numb so she didn't feel bad, she just didn't feel much of anything. I hate hate hate these drugs and how doctors hand them out. They don't know anything about how the body works, how depression can be tied to low vitamin D, low omega 3's and other things, how to increase serotonin naturally, etc.
     
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  6. Moof

    Moof Senior Member

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    I've no problem with these drugs when they work for people – depression's an awful illness, and some sufferers do well on antidepressants. The trouble is they're handed out inappropriately to so many patients, seemingly when doctors can't be bothered investigating why the person is ill. Can you imagine if other meds were viewed like this? "Oh, I don't really know what's wrong with you, but I'll try you on a treatment for cystic fibrosis. And if that doesn't work, we'll give prostate cancer drugs a go. Yes, I know you don't possess a prostate gland, but I heard somebody somewhere with something similar felt a bit better on them." :bang-head:
     
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  7. Hip

    Hip Senior Member

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    The study in question is here, but I don't really understand their approach.

    There are thousands of pharmaceuticals in use, as well as numerous other man-made chemicals in the environment. But the authors only appear to have tested Prozac for its bacterial mutagenic effects (and in an earlier study they also determined that triclosan, a common ingredient in toothpaste, has the same mutagenic effects).

    But how do we know that there are not hundreds of other common drugs and chemicals which might have these mutagenic effects on bacteria? (Unless other studies have previously singled out Prozac as having high bacterial mutagenic effects).
     
    Last edited: Sep 14, 2018
  8. Jackb23

    Jackb23

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    Another interesting study- There have been all kinds of purported reasons for antipsychotic weight gain (5HT2C receptor antagonism, etc). It will be interesting to learn more about the gut-dopamine connection as 90% of serotonin is in the gut (a similar monoamine neurotransmitter) and some scientists believe Parkinson’s might even start in peoples guts.

    https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0115225

    The Antipsychotic Olanzapine Interacts with the Gut Microbiome to Cause Weight Gain in Mouse


    First, we used germ-free C57BL/6J mice to demonstrate that gut bacteria are necessary and sufficient for weight gain caused by oral delivery of olanzapine. Second, we surveyed fecal microbiota before, during, and after treatment and found that olanzapine potentiated a shift towards an “obesogenic” bacterial profile. Finally, we demonstrated that olanzapine has antimicrobial activity in vitro against resident enteric bacterial strains. These results collectively provide strong evidence for a mechanism underlying olanzapine-induced weight gain in mouse and a hypothesis for clinical translation in human patients.



     
  9. Wolfcub

    Wolfcub Senior Member

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    I am not surprised.
     
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  10. RWP (Rest without Peace)

    RWP (Rest without Peace) Senior Member

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    While there may be many types of drugs that affect the gut, there is a specific relationship to SSRI's and other similar drugs and the gut due to the key regulation of the neurology of the gut muscles via serotonin. @Judee posted this article on her thread concerning her difficulty while taking 5-HTP for sleep. https://forums.phoenixrising.me/index.php?threads/ibs-and-serotonin.60999/#post-992893

    Here's the link and a quick quote:
    https://www.badgut.org/information-centre/a-z-digestive-topics/ibs-and-serotonin/
    Serotonin, or 5HT, is an integral neurotransmitter in the enteric nervous system that profoundly impacts bowel function. Of particular interest are the serotonin receptors 5HT3 and 5HT4 – key mediators of motility, secretion, and even pain sensation. After serotonin is released from enterochromaffin cells located in the lining of the gut, it flows to and binds to the receptors on nerve endings in the intestinal wall. A key to normal bowel function is how long free serotonin remains in the gut wall once it’s released. Serotonin transporter or SERT is an extremely important transporter protein that is responsible for the re-uptake of serotonin from the synaptic space. If re-uptake is blocked, the cells can’t inactivate serotonin.

    RWP
     
    Last edited: Sep 13, 2018
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  11. Eastman

    Eastman Senior Member

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    Art Ayers wrote the following blog post a few years ago:

    Common Medicines Make Superbugs, Not Prescription Antibiotics

    Excerpt:
     
  12. jesse's mom

    jesse's mom Senior Member

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    agreed... oh, shi......
     
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  13. RWP (Rest without Peace)

    RWP (Rest without Peace) Senior Member

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    A Quick clarification:

    I realize that the study was conducted in vitro, not on patients. So I was theorizing why they even bothered to do so, and I wonder if they already have some good hunches how the in vivo study (with patients) will turn out. Also, since the article postulated that the excess 11% of the drug that was not absorbed in patients and was still in circulation could be part of the cause of the effect, this could have an in-contact effect on gut bacteria. But the added effect of "messing with" the delicate serotonin balance could be an additional factor, so that's why I mentioned it. If the drug merely affected the neurology of the colon, it would be less severe than the combination of the two.

    Also, I wanted to mention that the link I cited (https://www.badgut.org/information-centre/a-z-digestive-topics/ibs-and-serotonin/ ) had the most advanced explanation of the gut as "the second brain," detailing the intricate neurology that mimics and closely interfaces with your "upper brain" more than I ever have heard explained. It's worth a read for anyone with ME because of the current research going on:


    "The altered bowel function, abdominal pain, and sensitivity symptoms indicative of IBS result from what appears to be a disturbance in the interaction among the gut, the brain, and the Autonomic Nervous System – which includes the Parasympathetic, Sympathetic, and the Enteric Nervous System – or ENS – now recognized as the “brain below.”

    “The status of our knowledge of the enteric nervous system has been, until recently, positively medieval,” said Dr. Michael Gershon, Professor and Chairman, Department of Anatomy and Cell biology at Columbia University, “but in recent times, significant advances in the understanding of this brain in the gut have resulted in a greater appreciation of its importance in clinical medicine, and no more so than in IBS.”

    The ENS consists of an extensive network of neurons supported by glia. Enteric glia are analogous to the astrocytes of the CNS. Enteric glial processes encircle large bundles of enteric axons. The small intestine contains about 100 million nerve cells, roughly equal to the number found in the spinal cord.

    Two neural plexuses comprise the ENS: a larger, myenteric plexus, positioned between the muscle layers of the muscularis externa, which is home to the neurons responsible for motility. A smaller, submucosal plexus houses sensory cells that talk to the neurons of the myenteric plexus and contain motor nerves cells, which stimulate luminal secretion.

    Signals from the brain to the gut play a critical role in maintaining optimal digestive function, reflex regulation of the GI tract, and modulation of mood states.

    The ENS can regulate peristalsis and secretion – independently of the central nervous system.

    If you cut the central nervous system connection to the gut, the bowel function persists. The ENS relies on a number of neuropeptides and small molecules to regulate both intestinal motility and secretion. Scientific evidence strongly suggests that serotonin – or 5HT – is one of the most important signalling molecules involved in the peristaltic reflex – and that alterations in serotonin signalling may be responsible for IBS symptoms. Ninety-five percent of the serotonin found in the body resides in the gut.

    “I first proposed that serotonin was an enteric neurotransmitter in the 1960s,” explained Dr. Gershon, “and by the early 1980s, my suggestion had been confirmed, and teams of scientists determined that serotonin was not only a neurotransmitter but also a signalling molecule that ultimately triggers peristaltic and secretory reflexes. Today, the gut is known to have at least seven different serotonin receptors.”

    In order for the gut to govern its own behaviour and trigger any reflexes, it has to sense what is going on in the lumen of the bowel. It does so using two detectors: the intrinsic primary afferent neurons of the intestine (IPANS) and enterochromaffin (EC) cells.

    “IPANs are activated by luminal content, such as pressure, nutrients, or acidity and they are the detectors that mobilize the neurons that control mixing and propulsion in the small intestine,” said Dr. Gershon. The large concentration of serotonin in EC cells is located in the basal granules of these cells because the serotonin is secreted into the wall of the gut, not the lumen.

    The ECs release serotonin into the underlying connective tissue space, which contains the nerve fibres that express serotonin receptors and thus respond to serotonin.

    These receptors include the 5-HT3 receptors known to send signals encoding pain, nausea and other noxious sensations to the CNS. This serotonin release occurs as the result of mucosal stimulation.

    The release of serotonin and activation of interneurons within the ENS triggers a cascade of other neurotransmitters, such as acetylcholine and Substance P, which excites peristaltic and secretary reflexes.

    “We now have extensive data confirming that serotonin stimulates the peristaltic reflex when it is applied to the mucosal surface and that serotonin is released when peristalsis is initiated. We also know that this reflex disappears when the mucosal actions of serotonin are blocked,” said Dr. Gershon.

    The more we know about serotonin’s role in the enteric nervous system, the closer we come toward creating effective therapeutic agents that can manipulate serotonin action and provide symptom relief.

    “As the true abundance of neurotransmitters, such as serotonin, in the gut finally become apparent, it has become possible to use the actions of these substances to unlock the secrets of the second brain and to use the data to bring solace to a troubled gut,” explained Dr. Gershon.
     
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