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The Herpes Viruses Are Activates By Stress, And Can Cause Cancer

Discussion in 'Scientific Studies' started by haidut, Feb 28, 2016.

  1. haidut

    haidut Member

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    Over the last few months, I received at least 20 emails from people questioning Peat's statements that viruses are activated by physical or emotional stress, estrogen, NO, prolactin, etc. Keep in mind that estrogen, NO, and prolactin are all biomarkers of stress themselves. This study explains how the cell's response to stress actually causes the virus reactivation and spread to other cells. What is even more important, a study like this provides evidence for a direct causative link between stress and certain types of cancer like sarcomas and lymphomas. Now, imagine that every type of cancer can be caused by this mechanism...

    Oncogenic Herpesvirus Utilizes Stress-Induced Cell Cycle Checkpoints for Efficient Lytic Replication
    How stress wakes up latent herpesviruses

    "...Herpesviruses establish lifelong infections in humans, and are known to reactivate in response to different kinds of stress. Researchers have now found an important link between cellular stress responses, cell cycle regulation and virus reactivation."

    "...Hiding their DNA genome inside the nucleus of infected cells, herpesviruses establish lifelong infections in humans. Poorly defined stress conditions are known to wake up these parasites from their dormancy – the latent phase – and reactivate the production of new viral progeny, eventually causing cell death by lysis – the lytic phase. This process allows the virus to multiply and spread usually through lesions of the skin, as in the case of the well known Herpes Simplex virus. Unlike Herpes Simplex, however, some herpesviruses are oncogenic, meaning they can cause cancer."

    "...While looking for cellular factors involved in the reactivation of an oncogenic human herpesvirus, the Kaposi's sarcoma associated herpesvirus (KSHV), the research group of Päivi Ojala, University of Helsinki, Finland, and collaborators identified a mechanism by which stress conditions favor the lytic reactivation and ensure the efficient production of progeny viruses. KSHV is the etiological agent for Kaposi’s sarcoma and primary effusion lymphoma (PEL), an aggressive form of lymphoma with reported median survival time shorter than six months after diagnosis. The study, a combination of the most advanced microscopy technologies and genetic manipulation techniques, shows that a variety of chemical stresses all lead to the activation of a set of cellular "stress-sensor" proteins – like p53 and p21clip – which slow down cell proliferation in the attempt of rescuing the cell from exogenous stress. This process seems to create an environment that favors the production of viral lytic genes, which a few hours after reactivation lead to massive damage to the cellular DNA and arrest the cell division cycle in a stage known as the Gap-2 phase or G2. In this status, cells are kept alive by viral proteins and all cellular nutrients and resources are redirected to the assembly of thousands of new virions. P21clip has a critical role in maintaining cells in the G2-arrested state, the research shows, as removal of this protein by genetic manipulation restored cell division in cells undergoing lytic replication. Importantly, reactivation of cell cycle progression coincided with a reduction in the kinetics of viral lytic gene expression, thus demonstrating that the efficiency of KSHV lytic replication depends on the inhibition of cell division. This finding provides an important direct link between cellular stress responses, cell cycle regulation and virus reactivation. Mutations in TP53 gene are rarely found in KSHV-associated malignancies. Therefore, the work now provides a mechanistic explanation as to why the virus has evolved to retain active p53. The researchers believe understanding the molecular events that connect cellular stresses with herpesvirus reactivation will lead to the development of next-generation antiviral strategies that can be used to treat human cancers caused by oncogenic herpesviruses, such as primary effusion lymphoma, for which there is currently no cure.
     
  2. Daimyo

    Daimyo Member

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    That's just an anecdotal evidence, but I know that 3 days of not sleeping enough is strong enough stress for me that I get a cold sore. Always.
     
  3. OP
    haidut

    haidut Member

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    It's not anecdotal at all, it has been replicated in human studies. Sleep deprivation increase flu infections, which is another "viral" disease. It could be due to higher cortisol suppressing the immune system. Sleep deprivation is known to raise cortisol.
     
  4. thebigpeatowski

    thebigpeatowski Member

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    It's a well known fact that bacteria, viruses and yeast etc. communicate not only amongst themselves (quorum sensing), but they can also communicate with their host (us). They can sense a person's hormone status: cortisol levels, epinephrine levels and overall metabolic status. Microbes use this ancient molecule signaling system to their advantage just like any other organism would assess it's environment and adapt accordingly....it's a matter of survival. A run down immune system gives the herpes virus an opportunity via a cold sore to spread to new hosts, yay.
     
  5. Seeweed65

    Seeweed65 Member

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    Hi Haidut,

    Is there any truth in this statment I found on the Internet.

    • #4
      03-12-2008 11:05 PM by norm11
      Re: Oral Herpes HSV1 Questions..Please Answer!!
      Intense persuasion, over expression of PPAR will initiate the adaptive immune system. A chronic immune response maybe interpreted as weak metabolic signaling. The involved dendritic cells, T cells and macrophages have not been provoked beyond tolerance. Using nicotinic acid to over express PPAR will cause unfurling of complement genes. Complete genes expression will improve dendrite cells to form MHC, T cells to increase TNF and macrophage phagocytotis. Improved functions of PPAR will also facilitate the ubiquitin-proteasome system, and other pathways. The enhanced metabolic signals will provoke the adaptive immune system to differentiate lymphocytes to memory T cells and memory B cells. Any chronic infection that has establishes suboptimal activation of dendritic cells, memory B cells and of macrophages can be eradicated once metabolic signals are enhanced.



      Achieving full immunity will occur between six to nine months. The ability of pathogens to use camouflage, such as ceramide, will not shield it. The efficacy of nicotinic acid can be impaired by agents (including lysine) that suppress transcription activities. Viral infected subjects must be healthy to endure the six to nine months. Those subjects with genital herpes should expect an outbreak each 28-days cycle for six months. Aspirin may help to limit the pro-inflammatory response. Subjects with drug resistant bacterial infection will be able to continue antibiotic therapy. The timescale for adaptive immunity is typical of a vaccine regiment.



      Nicotinic acid (flush-free or slow release) dosage is 1500 to 2000mg, divided doses, per day for six months. The dose is lowered to 1000 to 1500mg, divided doses, per day for the next six to twelve months
    • #6
      03-13-2008 11:57 AM by norm11
      Re: Oral Herpes HSV1 Questions..Please Answer!!
      Yes, I will. Once someone is infected with a pathogen, in this case a herpes virus, the body will respond by activating the innate immune system. The involved cells are dentritic cell, T cells and macrophage cells. The pathogen, herpes virus or bacteria has evolved ways to hide from or suppress the innate response. The PPAR, peroxisome proliferator-activated receptor, is responsible for communicating with the adaptive immune response. It is possible to heighten the metabolic signals of the innate immune system by over expressing PPAR with nicotinic acid (niacin).

      The increase volume from the innate immune system will initiate the adaptive immune response. The adaptive immune system recognizes and eliminate foreign invasion. The transition to an activated adaptive immune response will take between 6 to 9 months.

      It is important to know, while taking niacin to over-express PPAR, not to take any drug or agents whose actions include suppression of transcription activities. PPAR complement genes are sensitive to suppression. Without the PPAR complement genes the adaptive immune system will not become activated. Suppression drugs are anti-viral agents, including lysine.

      Once the adaptive immune system achieves activation then there will not be a need to take antiviral drugs. It will eradicate any pathogen whether viral or bacterial infection.

      If you decide to follow the regiment then I ask of you after 9 months to share your experience. There will be an outbreak each 28-days cycle for 6 months afterward the adaptive immune will become involved and the infection will be eliminated. The process will take 6 months to increase the metabolic signal from the innate immune system then another 6 to 12 months for complete coverage from the adaptive immune system.

      Regards

      Stephen
     
  6. PakPik

    PakPik Member

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    Those are very interesting posts, thanks!
    I don't know much about niacin yet, but I do know about niacinamide, and have been using it in order to help modulate my immune system in order to beat some very old and out of control infections. Niacinamide plus dietary interventions and other supplements have been amazing. These are an example of how niacinamide may help beat hard infections:
    JCI - C/EBPε mediates nicotinamide-enhanced clearance of Staphylococcus aureus in mice
    Nicotinamide: An Oral Antimicrobial Agent with Activity against Both Mycobacterium tuberculosis and Human Immunodeficiency Virus

    So it wouldn't surprise me if there was some truth to those posts regarding niacin; it would be nice to have references on what that person is claiming since niacin and niacinamide do have some differences.
     
  7. David PS

    David PS Member

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    Like many other things in this forum, most of this is over my head. I take high doses of B3 (3 grams spread out through the day per Abram Hoffer). In addition, I carefully monitor what I eat so that I ingest more lysine than arginine. Furthermore, I take additional lysine at times when I feel an outbreak in the making. I watch my lysine/arginine intake in an attempt to keep herpes in check. Chronometer.com helps as well as food tables like the one at Herpes Nutritional Guide | What's the Lysine Arginine ratio in foods?

    My greater fear with regard to herpes is not cancer but Alzheimer's disease. There seems to be some sort of correlation between the two.
    herpes alzheimer's - PubMed - NCBI

    I was working under the assumption that lots extra lysine was a good thing to keep the virus as fully suppressed as possible. Any thoughts about keeping my lysine/arginine just barely above 1.0? And/or upping my daily dose of B3 so that over expressing PPAR will win out?
     
  8. Tenacity

    Tenacity Member

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    I had a wart on my right index finger since I was at least 12 years old, and at 20 years of age I noticed recently that it had entirely disappeared. My understanding is that warts are caused by HPV. I fully believe that it's due to my practicing of a Peat inspired diet. It might be due to reduced cortisol or it might be because of my consumption of liver, but either way I'll take it as a sign that my body is moving in the right direction.
     
  9. Giraffe

    Giraffe Member

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    How much niacinamide did you use? What were the other supplements?
     
  10. PakPik

    PakPik Member

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    Basically my main supplements have been:
    Niacinamide: anything from 500 mg to 5000 mg
    Aspirin (as sodium acetylsalicylate): anything from 650 mg to 4 grams (plus vit K2, of course)
    Cyproheptadine: anything from 1 mg to 8 mg
    Rarely applied methylene blue drops on the skin covering or close to infected areas.

    I should mention that Iron depletion (through aspirin and low iron diet), which has been proposed as a therapy for the treatment of chronic infections, and a very low PUFA, well designed diet have been just as important.
    I constantly adjust dosages; every week I would take a different combination according to my needs.
     
  11. Giraffe

    Giraffe Member

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  12. Seeweed65

    Seeweed65 Member

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    I'm not sure if over expressing PPAR is a good thing or not and from the infomation on this forum the use of niacin (nicotinic acid) is not recommended. There maybe a safer way to do it which is why I ask Haidut if there was some truth in the statement above.

    I was looking more along the lines of Caffenine and aspirin.


    Coffee Lowers Brain Tumor Risk

    Aspirin

    Aspirin inhibits MMP-2 and MMP-9 expressions and activities through upregulation of PPARalpha/gamma and TIMP gene expressions in ox-LDL-stimulated ma... - PubMed - NCBI

    Efficacy of peroxisome proliferator activated receptor agonist in the treatment of virus-associated haemophagocytic syndrome in a rabbit model. - PubMed - NCBI


    Regards
     
  13. lollipop

    lollipop Guest

    I once researched this subject for several clients that had herpes. They tried both the zinc and iodine with great results.

    http://george-eby-research.com/html/herpes.html?redirect=false

    Recently one woman called me and was horribly suffering. I gave her the above link and also suggested from reading on Ray Peat's website and this forum that high serotonin and high estrogen might be at play. As a way to help her pain, I suggested putting Progest-e on the outbreak. She called me and told me it was a bit miraculous and healed the outbreak almost overnight.

    Side note disclaimer: I am NOT a medical professional and do not fully understand the science. I am a compassionate friend that likes to see people free themselves from suffering. Take everything as a potential and do your own research...
     
  14. mujuro

    mujuro Member

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    My cousin came over last week with the worst cold sores she's had in recent memory. She had 5 lesions on her lips that erupted overnight. I gave her some colloidal silver to apply topically (20ppm) on the lesions and in 3 hours her lips were completely normal.
     
  15. OP
    haidut

    haidut Member

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    I just wanted to draw attention to the connection between this post and another recent thread I made recently.
    Self-reported Health Much Better Predictor Than "objective" Tests

    As you can see, it confirmed in humans that stress causes reactivation of herpes viruses and is one of the reasons people may feel shitty even if biomarkers do not show anything being amiss.
     
  16. lollipop

    lollipop Guest

    Nice @haidut - that was an interesting thread.
     
  17. LeVere

    LeVere Member

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    I think we can say that viruses don't exist at this point. All of these signatures that are being observed are really unspecific markers of stress and toxicity.
     
  18. michael94

    michael94 Member

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  19. michael94

    michael94 Member

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    Agreed. HIV/Aids patients probably die from the medicines they're given.
     
  20. LeVere

    LeVere Member

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    That maybe part of it. I don't think a Gallo positive test is meaningless though. I think it's factor of oxidative stress as well as bioenergetic morphostatic breakdown overall. A fusion of Ray Peat and The Perth Group's analysis. I'm not entirely against some of the ARVs for an intermediate period, but it should be part of an overall functionalist approach that includes The Perth Group protocol of anti-oxidants as well as dealing bioenergetic morphostatic issues.
     
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