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Cortisol And Serotonin Are Causative Agents In (male) Liver Cancer

Discussion in 'Scientific Studies' started by haidut, Aug 23, 2017.

  1. haidut

    haidut Member

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    The role of serotonin in all cancers of the billiary and GI tracts was well-known in the first half of the 20th century. The term carcinoid syndrome was used to describe the spectrum of such cancers and it was widely acknowledged that most of the patients died as a result of the fibrosis that serotonin caused, and not as a result of the primary cancer.
    It was not until the introduction of the poisonous SSRI class of drugs that this role started to get pushed into the background through skewed or directly fraudulent studies whose goal was to promote the use of the SSRI drugs. To add insult to injury, companies like Pfizer sell and openly market as beneficial the SSRI drugs while at the same time quietly running clinical trials with serotonin antagonists like terguride to reverse the fibrosis of various organs that serotonin is known to directly cause.
    This new study shows that serotonin and cortisol are directly causative for liver cancer development. The role of serotonin should not be surprising to anybody given the information above, and the fact that fibrosis is an immediate precursor to cancer (as Peat wrote). The more "surprising" finding is that cortisol is also a causative agent for liver cancer. This is arguably a more impactful findings given that glucocorticoids are the most widely prescribed anti-inflammatory agents today, and surpass even the SSRI drugs in terms of widespread use. Virtually all patients enduring a hospital stay or even childbirth (especially through C-section) are prescribed a glucocorticoid to control inflammation. As it often turns out these days, the very drugs prescribed to control an inflammatory condition end up exacerbating it and even turning it deadly.
    Finally, I am not convinced that cortisol and serotonin are only causative in males. The same mechanism is at play in both female and male liver cancer development and in fact serotonin levels are (on average) higher in females and non-cancer liver disease is also higher in females (as Peat wrote as well). So, unless I see a study vindicating these two hormones in females I am going to assume their role is equally detrimental for both sexes.
    Incidentally, cyproheptadine has recently been found to retard the growth of liver cancer. Given the ability of cyproheptadine to block both serotonin and cortisol I doubt this finding is a coincidence.

    Tumor-Associated Neutrophils and Macrophages Promote Gender Disparity in Hepatocellular Carcinoma in Zebrafish | Cancer Research
    http://www.cmghjournal.org/article/S2352-345X(17)30004-8/fulltext
    https://medicalxpress.com/news/2017-08-non-sex-hormones-sexing-liver-cancers.html

    "...However, clinical trials targeting sex hormones did not produce sufficiently convincing results, suggesting that other factors might also be involved. Liver cancer models based on zebrafish also show sex disparity. In particular, two non-sex hormone factors, cortisol and serotonin, appear to play critical roles in the sex disparity of liver cancers."

    "...Using a liver tumour model in krasv12 transgenic zebrafish, a research group led by Prof GONG Zhiyuan, including Ph.D. students YAN Chuan and YANG Qiqi from the Department of Biological Sciences, NUS found that some other factors which are not sex hormones play critical roles in the sex disparity of liver cancers. In one study, they found that a glucocorticoid hormone, cortisol, is produced more than usual in male zebrafish with liver cancers. This hormone could trigger two different types of white blood cells, neutrophils and macrophages, which in turn enhance the development of liver cancer. In another study, they found that serotonin, a neurotransmitter, is also produced more than usual in male oncogenic livers. This again can cause the growth of liver cancer through the activation of a major cell type involved in liver diseases (hepatic stellate cells)."
     
  2. Amazoniac

    Amazoniac Member

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    Stimulating healthy tissue regeneration by targeting the 5-HT2B receptor in chronic liver disease

    "Uninjured 5-HT2B knockout mice show no structural or biochemical evidence of liver defects"

    "Our understanding of the molecular regulation of liver regeneration is mainly derived from studies in "healthy" liver following hepatectomy. Here, we have addressed the additional regulatory complexity that is a feature of regeneration in the context of the diseased liver, and specifically a signalling network established by 5-HT2B-expressing activated HSC which are rare in healthy liver but abundant in diseased liver. It was originally reported that in the healthy liver, platelet-derived serotonin promoted the regenerative response to partial hepatectomy, with this function requiring the activities of the 5-HT2 subclass of receptors and in particular 5-HT2A which is expressed on hepatocytes[15]. However, expression of 5-HT2B is relatively low in healthy compared to diseased liver, where in the latter it is expressed on activated HSC in association with fibrotic tissue[17]. By focusing on models of progressive liver disease we have discovered that HSC are important suppressors of hepatocyte proliferation and that this function is provided by serotonin-induced expression of TGFβ1 via the 5-HT2B receptor (supplemental fig 13). Moreover, we suggest that this paracrine signalling pathway can feedback onto the HSC to further provoke their fibrogenic activities. 5-HT2B is also selectively expressed by activated human HSC (supplemental fig 14) and the signalling pathway we have described is conserved in human HSC. Antagonists of 5-HT2B are available and safe for use in humans, this class of drug may have exciting therapeutic potential in liver disease, both as a stimulant of hepatocyte regeneration and as an anti-fibrotic."

    This is exactly what Ray talks about: protective measures start to become contributors to the problem if they remain active for too long.​
     
  3. OP
    haidut

    haidut Member

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    Wait until Pfizer gets terguride through clinical trials. Once it gets approved probably ALL serotoni antagonists will disappear from the market. It already started happening with cyproheptadine and lisuride. It is impossible to get cyproheptadine in the USA through a doctor even though it is still approved for use in this country. Most doctors would either balk at prescribing it, or if they do the pharmacy will try to "convince" you to switch to an "equivalent" (which is just cetirizine) and even if you managed to make it past these hurdles, the pharmacy will usually be out and will tall you it is 2-3 months wait time.
     
  4. Amazoniac

    Amazoniac Member

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    The Stress guru wrote that when there's a stressor, you either combat or find a way to live in harmony with it.

    It's the gbolduev situation: PEAT is a menace, and since he cannot annihilate his articles and influence, he chooses to ignore him by being simply NOT interested while proposing his own system)) It ain't kindergarden stuff, it's biochemistry one-zero-one.

    I suppose it's similar with these drugs. If the inflammatory agent cannot be eliminated, you have to desanit- desins- to make yourself less sensitive to it.

    You know the first time that you playfully threaten a dog? A he gives you the scarying alert. The more you do it, the more likely he is to precipitate his action by much less. Even if you change your tone to tickling, he tends to keep the defense program running for a while before turning it off. This must be the body when it's under constant insults, it senses that there a serious imminent threat and it must keep inflammation elevated for protection tending to act too soon or unnecessarily because maybe it's expecting something worse.
     
  5. lollipop

    lollipop Guest

    Wow. Nervous for future generations who will not have or spend the time for proper education/information. To unravel the trail of lies will be almost impossible.
     
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