Covid-19 News

    Not eating oily fish regularly can shorten life expectancy more than smoking, study reveals


    Study says not eating oily fish regularly can shorten life expectancy
    Scientists found that smoking knocked four years off life expectancy whereas low levels of the fatty acid - found in oily fish such as salmon and mackerel -…
    www.dailymail.co.uk


    Lack of omega-3 in the diet can short life even more than smoking, research says

    Scientists found low levels of the fatty acid could reduce expectancy by 5 years

    The oil found in oily fish is known to be good for heart and reduces blood clots

    A good level is 8% or higher, while intermediate is between 4% and 8%

    A lack of omega-3 oil in the diet can shorten life even more than smoking, new research warns.


    Scientists found that smoking knocked four years off life expectancy whereas low levels of the fatty acid — found in oily fish such as salmon and mackerel — could reduce it by five years.

    A good level is eight per cent or higher, intermediate is between four and eight per cent and low is four per cent and below.


    Study lead researcher Dr Michael McBurney, of the University of Guelph in Canada, said: 'It is interesting to note that in Japan, where the mean Omega-3 Index is greater than eight per cent, the expected life span is around five years longer than it is in the United States, where the mean Omega-3 Index is about five per cent.


    'Hence, in practice, dietary choices that change the Omega-3 Index may prolong life.

    'In the final combined model, smoking and the Omega-3 Index seem to be the most easily modified risk factors.


    'Being a current smoker, at age 65, is predicted to subtract more than four years of life, compared with not smoking, a life shortening equivalent to having a low vs. a high Omega-3 Index.'


    The study, published in the American Journal of Clinical Nutrition, used statistics from the Framingham Heart Study (FHS), one of the longest running studies in the world.


    Note: A boatload of vitamin D, pun intended

    Quote from THHuxleynew

    We do not yet have links, or a clear explanation of how you calculated the 15/1,000,000 figure.

    For this we have the official death statistic , That obviously show fewer deaths. But things are complex if you go into detail and look at subsets with different comorbities then for this we have no tables...

    But once more: Just compare with flu and we here end the discussion as you are only interested in finding excuses.

    Free masons are cricket brains so stay with them and believe what they think they could make the people believe...

    People with brains just laugh at you.

    Quote from THHuxleynew

    The Swiss seem to have been very unlucky? Unbelievably so.

    No we use the same open reporting system as the EU/USA. The official state sites are of now use as they only accept 100% certified death reasons and doctors have orders not to report any death as vaccine death...

    So please look up data in the UK adverse drug reaction database!

    Quote from stefan

    No, the data is all there.

    Same problem as with THH official link that is of almost no use. The question is who is allowed to enter data. You should go to the EU vigilence database and look up Sweden. If deaths there are 0 too then you know for sure that there is an order. USA so far has about 20'000 deaths in VAERS where about 1/3 was fully documented and and for 100% was vaccine related due to immediate onset of symptoms.

    So "0" deaths is a fairy tale. Or as I say magic mushrooms protect your country .... One more word :: Sweden in politics is not a left middle country is just the fake face for the elections. Socialists are members of Free masons since the fifties so its more close to right fascists in the inner circle thinking.

    Quote from Fm1

    Only 9.8% of these breakthrough infection cases required hospitalization, and deaths were associated with only 0.4% of the reported incidences.

    This is a huge number as normally fewer that 9.8% of the COV-19 infected people go to hospital. The typical figure is 2%! So if this is true vaccines make things worse e.g. among which people is the question.


    Switzerland cases raised now to 4x within 3 weeks but hospitals drain out. Delta must be very dangerous for hospitals...It's the no income virus..

    We have a database for reported medical possible side effects. Database for drug usage, database for the deaths, visits in hospital and then what not. To peek in the databases you need to go through a ethical board to do research. But the information is there. I think that the reported side effects is what's reported to EU. It's difficult to get hold of data one would like to have through internet though to really get good statistics but it's there ,complete and of good quality. I believe that especially the death statistics here are really good compared to other countries and if Swedish researchers do not factor in deaths in their study, they will many times in the peer review be requested to publish the number of deaths and the influence on the statistical analysis as the international reviewers is well aware that that information is available here.


    Now some information of deaths has been reported in the news by investigators that have gotten hold of the data. The deaths I found is a 2 or so possible blod cloath deaths (after that event, we got more careful regarding this risk) also there is a couple of hundreds of deaths from covid, at a specific time that also had gotten a vaccine shot that was reported in a news article. All other reports state that the data has been compared to natural frequencies of deaths and nothing remarkable has been seen apart from the blod cloths it seams. As I said if there was 10 cases with no co-morbidites of 35 year olds or such that within days dies by for example a heart attack, or blod cloth, this would be heavily investigated and reported. We probably do not have much data for really young people yet here like 18 years or such.


    If you have an idea of novel way to analyze the deaths from covid I highly recommend to team up with swedish researchers. Because our data are complete and rich, and the reporting is automatized, by professionals, and mandatory by law, you can get very good proofs of a deadly signal that does not have the issues of e.g. selection biases you get from more sloppy reporting and lack of complete death statistics. Also the death database means that one have a very good grip of the normal frequencies of deaths for quite detailed subgroups.


    my best link for a reference is to use google translate on


    Statistik om läkemedel
    www.socialstyrelsen.se



    there you can find a link to internet databases, but I did not find them good enough to do anything serious.

    Looking at the paper - they are saying that FA metrics correlate strongly with life expectancy, adjusting for age and sex. I don't think it means a lot unless they also adjust for wealth/socioeconomic status since that has a very high - possibly causative - correlation with life expectancy.


    Thus it may be that eating oily fish correlates (enough) with higher income. That then bring in lots of other lifestyle factors that increase life expectancy.


    To get meaningful FA info from this data you need to check whether income etc confounds this result.


    THH

    NIHR Awards $9.3m to Consortium Led by UCLH & UCL to Conduct UK-Wide Long-COVID Research Program Called STIMULATE-ICP


    NIHR Awards $9.3m to Consortium Led by UCLH & UCL to Conduct UK-Wide Long-COVID Research Program Called STIMULATE-ICP
    Thanks to a £6.8m ($9.3m) award from the National Institute of Health Research (NIHR), University College London Hospitals NHS Foundation Trust (UCLH) and
    trialsitenews.com


    Thanks to a £6.8m ($9.3m) award from the National Institute of Health Research (NIHR), University College London Hospitals NHS Foundation Trust (UCLH) and University College London (UCL) now head a comprehensive consortium to conduct a substantial clinical trial targeting long COVID over the next two years. This research program involves over 30 investigators, health professionals, patients, and industry partners involving over 30 organizations collaborating under what is formally known as STIMULATE-ICP (Symptoms, Trajectory, Inequalities, and Management: Understanding Long-COVID to Address and Transform Existing Integrated Care Pathways). There are high hopes in the UK for this program—that sufficient amounts of real-world data at scale will progress knowledge and inform clinicians as well as scientists, provide evidence to health policymakers, while bringing improved care directly to long-COVID patients. An ambitious effort, to improve recovery, the team seeks to understand what long COVID is, how to diagnose it, and how to manage it. They will interview patients and health professionals and analyze data from NHS records, informing the UK and global understanding of patterns of long COVID and the outcomes of current clinical practice.


    Taking on Long-COVID

    Long-COVID continues to be a mounting problem around the world as nations and health authorities struggle to cope and recover from successive waves of the pandemic, thus the importance of this substantial endeavor with a goal of informing medium- and longer-term policy and health system responses. Health systems, hospitals, and clinics, as well as local doctors and healthcare professionals, feel the pressure of long-COVID. As the condition can stretch on, ever more people will deal with the persistent symptoms over a period of months associated with their initial SARS-CoV-2 infection.


    Co-principal investigator Professor Amitava Banerjee commented, “Two million people in the UK are estimated to have had persistent symptoms for more than 12 weeks following initial COVID infection, with far-reaching impact on patients, healthcare, and the economy.”


    “More than 80 long COVID clinics have been established around England but we need to better understand, diagnose and treat this new disease. Inequalities in access to and provision of long COVID care have already become apparent.”


    The investigator continued, “Long COVID is challenging the NHS and healthcare systems around the world, which have had to deal with the acute consequences of coronavirus over the last 18 months,” said Prof Banerjee, professor of clinical science at the UCL Institute of Health Informatics and consultant cardiologist at UCLH.


    The Research Team

    An impressive group has come together to address long-COVID led by co-principal investigator Professor Amitava Banerjee as well as Dr. Melissa Heightman, another co-principal investigator. They span a wide range of clinical and academic fields from primary care to epidemiology, behavioral and mental health, and even health economics, reports UCLH in its recent press release. Even four patient groups have been recruited and are now engaged to help develop the research proposals—eliciting that patient point of view is key.


    The Study

    Within the overall program of research, a trial coordinated by the University of Central Lancashire will recruit over 4,500 people with long-COVID, starting with six sites in Hull, Derby, Leicester, Liverpool, London (UCLH), and Exeter.


    Individuals will be randomly assigned to usual care or a new pathway, including community-based, comprehensive MRI scan (using imaging technology called CoverscanTM developed by Perspectum), which can map the effects of COVID-19 on several of the body’s key organs) and enhanced rehabilitation (using a digital health platform called Living with COVID RecoveryTM developed by Living With).


    Co-principal investigator Dr. Melissa Heightman, who runs the UCLH post-Covid follow-up service, said: “We established our post-COVID clinic in London in May 2020 during the peak of the first wave, ‘building the plane while we were flying it’ and based in the hospital through necessity.


    Dr. Heightman, a consultant in respiratory medicine, added: “Individuals with long COVID need integrated services, working across traditional healthcare boundaries to best meet their complex care and rehabilitation needs. The aim will be to deliver timely high-quality care close to peoples’ homes with community-based diagnostics but access to specialist input when needed.”


    Whole Person Care


    Within this research program, another trial will test different drugs, such as aspirin and colchicine, to measure the effects of three months of treatment on symptoms, mental health, return to work, and other important outcomes.


    And researchers will also work alongside patients to co-develop ways of improving access to care and support, to address care inequalities.


    Denise Forshaw, Deputy Director of Lancashire Clinical Trials Unit and Principal Clinical Trials Manager from the University of Central Lancashire (UCLan), said:


    “Over the past year, it’s become clear that Long Covid is a serious and widespread issue that is likely to last for years to come, affecting over a million people in the UK alone. While dedicated Long Covid clinics are now in place, there is still much that we have yet to understand about the long-term impact and effective treatment of this illness.


    Through this research, we hope to establish effective investigation, treatment, and rehabilitation pathways that can mitigate the physical and mental health impacts of Long Covid, and create a more certain future for those affected regardless of their socio-economic background.”


    The Patient POV

    Lyth Hishmeh, who has suffered with long COVID since the first wave of the pandemic, sees the benefit of research that considers all aspects of the patient pathway: “Patients and health professionals faced and continue to face difficulties in knowing what to do for long COVID. A comprehensive study like STIMULATE-ICP is needed to look at the big picture and improve patient access to the right care at the right time in the right place.”


    Lead Research/Investigator

    Dr. Amitava Banerjee


    Dr. Melissa Heightman


    Call to Action: TrialSite will monitor this important study. Ensure you sign up for the daily newsletter for updates. Also, download the app—available for IOS or Android.

    I would agree if you were looking at the United States but western Pacific and Scandinavian countries would skew those results as their main diet is oily fish.

    Quote from Fm1

    I would agree if you were looking at the United States but western Pacific and Scandinavian countries would skew those results as their main diet is oily fish.

    Swedens dark secret of longlivety must be surströmming. We have big parties (surströmmings skivor) in the autum where we eat this. Right now we are experiencing a national trauma as big EU fishing boats have vacuumed the whole eastern sea from herring and local fishers can't find any herring for surströmming. So we might have to try something else, perhaps we can do as the vikings and get high on fly agaric which is commonly found here in the autumn. So expect our life expectancy to tank in the years to come.


    All big feasts in Sweden have basically the same food, (Christmas, eastern and midsummer) pickled herring spiced in many ways is a popular dish at those events.

    Salmon is a popular dish all year around. My favorite salmon (lax) is "gravad lax" with "hovmästarsås" and boiled potatos. Basically you freeze a salmon side in the freezer and then let it unfreeze and salt it in a couple of days. Hovmästarsås is basically a dill vinaigrette salt white pepper and mustard combo where you drip in oil and wip it very much like making a spiced mayonnaise without egg.


    In Sweden It looks like the most popular dish is spaghetti and a tomato minced meat sauce followed by chicken and fish. As said salmon is very popular here and we salt it, smoke it and make different dishes in the oven with it.

    Quote from Fm1

    I would agree if you were looking at the United States but western Pacific and Scandinavian countries would skew those results as their main diet is oily fish.

    You ned to look at who funded that study. It is not that it is wrong, just a bit misleading. A lot of the "this food is beneficial" studies are like that. There are definite advantages of omega-3.


    DEFINE_ME



    https://thefnc.com/research/dha-versus-epa-in-fish-oil/#:~:text=EPA%20has%20anti%2Dinflammatory%20effects,%2C%20black%20cod%2C%20and%20bluefish.


    EPA / DHA fish Omega 4


    ALA - Omega-3 from nuts etc - can be conveted to EPA / DHA but there are some questions about how well this happens


    EPA - good for heart and circulatory system - definite (from above paper - but see below)

    DHA - good for brain function - definite


    EDIT - I'm going to reduce (my) certainty on the above. These dietary things are very difficult to be sure about. What are the relative merits of EPA and DHA? It is not straightforward and I've not looked into it recently. Perhaps somone else has.

    You are going to hate this - I'd choose RCTs over received wisdom from US doctors...


    No Benefit from Fish Oil
    One day I was cooking pasta when the kitchen started to fill with the odor of fish. I happen to hate fish, so this was not a pleasant experience. It was also a…
    sciencebasedmedicine.org


    Having said that - anything to do with food and health is very complex, which is why mostly people just advise "have a healthy and varied diet".


    It seems pretty clear that the much higher than normal carbohydrate, salt intake in much processed food is bad. Anything to do with good or bad about fat intake gets very very complicated!


    Very low carbohydrate diets work for reducing weight - but it is a pretty weird thing to do.


    Lots of veg and nuts seems a good idea :)

    If anyone understands the whole omega-3 thing It would be great if they could explain it with references? Every time I look at it (I do every few years) I get confused and reckon it is unclear except it is probably a good idea to have omega-3 fats rather than omega-6 ones. Personally, since I love olive oil, I just eat and cook with lots of that. Who can tell if that is good or bad? (Frying with olive oil is not great - unless you do it very quickly).

    • Official Post
    Quote from THHuxleynew

    If anyone understands the whole omega-3 thing It would be great if they could explain it with references? Every time I look at it (I do every few years) I get confused and reckon it is unclear except it is probably a good idea to have omega-3 fats rather than omega-6 ones. Personally, since I love olive oil, I just eat and cook with lots of that. Who can tell if that is good or bad? (Frying with olive oil is not great - unless you do it very quickly).

    Good analogy with Ivermectin. The same mixed medical reviews, both are safe, might work/might not...so those that think it works will take, while those that think it is bupkis, will not. Only difference is the health care institutions try to block Iver use for COVID, while they take a laissez-faire approach to Omega's.

    NYU Scientists Study: Vaccines vs. Infection—Does Immunity Vary from Natural SARS-CoV-2 Infection to mRNA Vaccine?


    NYU Scientists Study: Vaccines vs. Infection—Does Immunity Vary from Natural SARS-CoV-2 Infection to mRNA Vaccine?
    Recently published in SSRN, a large group of prominent New York City-based researchers recently completed a study thanks to the funding from NYU Grossman
    trialsitenews.com


    Recently published in SSRN, a large group of prominent New York City-based researchers recently completed a study thanks to the funding from NYU Grossman School of Medicine as well as grants, including multiple from the National Institutes of Health. Led by NYU’s Ellie Ivanova (Department of Pathology) and NYU Grossman School of Medicine’s Joseph Devlin (Institute of Systems Genetics), the team conducted a study called ‘Discrete Immune Response Signature to SARS-CoV-2 mRNA Vaccination Versus Infection,” investigating the impact of the Pfizer-BioNTech BNT162b2 mRNA vaccine as compared to natural immune response to the SARS-CoV-2 pathogen. While noting that both the mRNA vaccine and the virus itself triggers healthy and natural, not to mention adaptive, immune responses, the New York City-based scientists found “significant qualitative differences between the two types of immune challenges.” For example, the natural immune response, that is, an individual that fell ill from SARS-CoV-2 infection, recovering on their own could be “characterized by a highly augmented interferon response,” which for the most part didn’t materialize in vaccinated recipients. This and other deltas between the two responses lead to significant questions about the differences between vaccine-induced or natural immunity to SARS-Cov-2.


    This recent study was uploaded to Elsevier’s SSRN as a not yet peer-reviewed manuscript. TrialSite provides a brief breakdown for the audience. What are the implications for this study? Could immune response to natural SARS-CoV-2 exposure be superior in human response as compared to vaccine antigen exposure?


    Ethics Committee

    This and all studies at NYU must be authorized by the NYU Institutional Review Board. All volunteers gave written informed consent in accordance with the Declaration of Helsinki.


    The Basis for the Study

    As reported in the authors’ manuscript, the authors point out that beyond antibody production, the knowledge behind COVID-19 vaccine immune response “remains largely uncharacterized.” Thus the authors sought out to provide more clarity to this important topic.


    The Study

    As described in their abstract, the study team conducted a study in a lab based on “multimodal single-cell sequencing on peripheral blood of patients with acute COVID-19” as well as a cohort of healthy volunteers before and after they received the mRNA vaccine known as BNT162bs developed by Pfizer-BioNTech.


    Their mission: compare the immune response elicited by the natural pathogen and in parallel compare to the response triggered by the vaccine product in emergency use authorization (EUA). Then the investigational team employed phenotypic and transcriptional profiling of each of the patient samples’ immune cells along with “reconstruction of the B and T cell antigen receptor rearrangement of individual lymphocytes,” affording the team the opportunity to characterize and compare the host responses to both A) the virus and B) defined viral antigens.


    Findings Summary

    Both the natural infection and mRNA vaccination-induced robust innate and adaptive responses but the authors noticed material differences in the two cohorts. TrialSite provides a brief table:


    Observation Natural SARS-CoV-2 Infection mRNA Vaccination

    High augmented interferon response High Close to Absent

    Dramatic upregulation of cytotoxic genes located in peripheral T cells & innate-like lymphocytes High Absent

    Clonal B & T Cells Effector Cells Circulating Memory Cells

    Implications

    The authors concluded that “far-reaching implications for immunity to SARS-CoV-2″ are implicated from their research: that is, the gap in two immune responses, transcriptional variance in the key immune populations, and the delta in maturation of adaptive immune cells call for further investigation.


    Funding

    NYU Grossman School of Medicine

    National Institutes of Health (NIH) (multiple grants)

    Leo Foundation Grant

    NYU Cancer Center Pilot Grant

    Judith and Stewart Colton Center for Autoimmunity Pilot Grant

    Danish Cancer Society

    Disclosures

    Mark J. Mulligan, NYU Langone, works with Lilly and Pfizer (exclusive of the current work), as well as Sanofi for vaccines or mAb versus SARS-CoV-2. Fees from a firm called Meissa Vaccines Inc. and Pfizer for Scientific Advisory Board services.


    Lead Research/Investigators

    Ivanova, Ellie and Devlin, Joseph and Buus, Terkild and Koide, Akiko and Cornelius, Amber and Samanovic, Marie and Herrera, Alberto and Zhang, Chenzhen and Desvignes, Ludovic and Odum, Niels and Ulrich, Robert and Mulligan, Mark J. and Koide, Shohei and Ruggles, Kelly V. and Herati, Ramin and Koralov, Sergei B.

    Cellular Immune Responses are Preserved and May Contribute to Chadox1 ChAdOx1 nCoV-19 Vaccine Effectiveness Against Infection Due to SARS-CoV-2 B·1·617·2 Delta Variant Despite Reduced Virus Neutralisation


    Cellular Immune Responses are Preserved and May Contribute to Chadox1 ChAdOx1 nCoV-19 Vaccine Effectiveness Against Infection Due to SARS-CoV-2 B·1·617·2 Delta Variant Despite Reduced Virus Neutralisation by Ramachandran Thiruvengadam, Amit Awasthi,…


    Abstract

    Background: The emergence of SARS-CoV-2 variants of concern (VoC) has threatened the effectiveness of vaccination due to decreased neutralisation ability of the vaccine generated antibodies. Our objective was to assess ChAdOx1 nCoV-19 vaccine effectiveness during the massive surge from 1st April to 31stMay 2021 predominantly due to the more infectious B·1·617·2 (Delta) in India.


    Methods: We conducted a test-negative case-control study to assess the effectiveness of ChAdOx1 nCoV-19 vaccine. Cases were RT-PCR positive for SARS-CoV-2 infection. In addition, we tested live virus neutralisation and cellular immune responses against VoC among healthy recipients of ChAdOx1 nCoV-19 vaccine. The outcomes were effectiveness of ChAdOx1 nCoV-19 against infection and severe coronavirus disease-19, virus neutralisation effectivity and T-cell responses against the VoC among healthy vaccine recipients.


    Findings: Of the 2766 cases of confirmed SARS-CoV-2 infection, 3·1% were fully vaccinated compared with 7·1% of the 2377 controls giving an adjusted OR of 0·37 (95%CI 0·28, 0·48); this translated to 63·1% (95%CI 51·5, 72·1) vaccine effectiveness against SARS-CoV-2 B·1·617·2 variant, seen in 90% of the infected population as confirmed by whole-genome virus sequencing. Full vaccination prevented moderate-severe COVID-19 in 81·5% (95%CI: 9·9, 99·0). The effectiveness of single-dose vaccine was 46·2% (95%CI: 31·6, 57·7) against infection but 79·2% (95%CI: 46·1, 94·0) in preventing moderate-severe Covid-19. Among healthy vaccinated persons, plasma live virus neutralisation was 2·5-6·8 fold lower against B·1·1·7, B·1·351, B·1·617·1 and B·1·617·2 being lowest against B·1·617·2. However, T-cell responses were preserved against the recombinant mutant receptor binding domain antigens suggesting cell-mediated immune protection.


    Interpretation: Despite significantly reduced virus neutralisation, the effectiveness of ChAdOx1 nCoV-19 vaccine was 63% against B·1·617·2 infection and 81·5% in preventing severe disease. Spike specific T cells responses against virus variants were maintained and might contribute to immune protection following vaccination.


    Funding Information: Department of Biotechnology, Government of India; Council for Scientific and Industrial Research, India; Fondation Botnar.

    This is fascinating and important work, which raises more questions than it answers. It points towards COVID infection leaving long-lasting and dysfunctional marks on the immune system, as opposed to vaccination, which does not.


    In COVID-19 patients, transcriptional profiles of many immune populations were characterized by augmented interferon (IFN) signaling, upregulation of genes associated with cytotoxicity, and changes in metabolic pathways. Analysis of peripheral immune cells following vaccination with the SARS-CoV-2 BNT162b2 mRNA vaccine revealed alterations of transcriptional programs of several immune populations consistent with immune activation, but the highly augmented IFN signaling and cytotoxic signature observed in COVID-19 patients were largely absent.


    A number of studies have revealed a highly heterogenous picture of the anti-viral inflammatory responses in COVID-19 patients, likely due to variability of disease severity, stage of disease, and diversity of preexisting conditions2-7. However, our analysis revealed striking differences in the frequency of several key immune populations between COVID-19 patients and healthy volunteers prior to and following vaccination (Fig. 1). Our multimodal platform enabled us to resolve differences in major immune

    subsets (Supplemental Fig. 1B), and to resolve rare circulating populations as well (Supplemental Fig. 2). For example, we observed an expansion of circulating hematopoietic stem and progenitor cells (HSPCs) in COVID-19 patients that was absent from healthy volunteers and was not induced by immunization (Supplemental Fig. 1B). Increased frequency of circulating HSPCs is associated with emergency myelopoiesis elicited in response to acute viral infection33,34. Consistent with this, and despite the overall heterogeneity in myeloid responses to SARS-CoV-2 in COVID-19 patients, we also observed expansion of several key myeloid populations, including dendritic cell (DC) and monocyte populations (Fig. 1C, Supplemental Fig. 2A).


    For those like me annoyed at TSN never giving direct links to papers: https://doi.org/10.1101/2021.04.20.21255677


    It shows ways in which the COVID-19 interference with the immune system changes typical immune response - for example:

    • Replace memory cells by effector cells
    • Make augmented interferon response

    Overall does this reduce or increase the effectiveness of immune response relative to the COVID vaccine response, which do not suffer this COVID-specific interference? Who knows. But it is certainly dramatic. COVID not only mucks up with the immune system in a way which is harmful during infection - it leaves a strong signature of this in the immune response.


    I guess the big question here is could this altered immune response be responsible for aspects of long COVID? In which case it would make sense that vaccination could reset this.


    I have to say it is good that TSN publishes such a strongly pro-vaccine paper given its editorial slant - but maybe they did not understand the significance of this?


    Differences in SHM were suggestive of differences in germinal center (GC) biology between cohorts. Induction of effective high-affinity humoral immune responses and generation of memory B cells requires a specialized subset of CD4 Th cells known as T follicular helper (Tfh) cells. Tfh cells are essential for GC formation, affinity maturation, and the generation of most high-affinity antibody-producing and memory B cells59,60. A circulating population of Tfh cells, termed circulating Tfh (cTfh), are phenotypically and transcriptionally similar to lymphoid Tfh cells and their presence correlates with ongoing GC reaction and maturation of antibody response46,61,62. Indeed, we found significant expansion of the cTfh population in COVID-19 patients relative to healthy volunteers, with a minimal increase in the setting of vaccination (Fig. 1E). GSVA revealed that cells in this population are enriched for genes involved in type I and type II IFN responses, which were notably absent in cTfh cells found in healthy volunteers (Supplemental Fig. 5). In contrast, cTfh cells from vaccinated individuals were enriched for the transcriptional signature of TNF-NFκB pathway activation, which was associated with improved cTfh survival and more robust humoral immune responses63.

    • Official Post
    Quote from THHuxleynew

    I have to say it is good that TSN publishes such a strongly pro-vaccine paper given its editorial slant - but maybe they did not understand the significance of this?

    The study was not linked to, but from this quote in the TrialSiteNews (TSN) article about the study, it appears that Mother Nature won over the bodies vaccine response:


    "the New York City-based scientists found “significant qualitative differences between the two types of immune challenges.” For example, the natural immune response, that is, an individual that fell ill from SARS-CoV-2 infection, recovering on their own could be “characterized by a highly augmented interferon response,” which for the most part didn’t materialize in vaccinated recipients."


    What do you think? Overall, as you said it is interesting. There have been other studies indicating the vaccine triggers a more robust, protective response, and a few others that say the opposite. That seems to be the story of this pandemic: everything could be this or maybe it could be that, with studies backing each positiion; i.e. masks/no masks/only the right type of mask, lockdowns save lives/lockdowns kill more people, vaccine better/natural better, Ivermectin good/Iver bad, leaked from the lab/did not.


    No wonder this thing has become so political.

    Do Young Children Need to Participate in COVID-19 Vaccine Clinical Trials?


    Do Young Children Need to Participate in COVID-19 Vaccine Clinical Trials?
    That’s an important question. Given mounting concern about vaccine equity on the one hand, and the true risk factor(s) on the other hand for children
    trialsitenews.com


    That’s an important question. Given mounting concern about vaccine equity on the one hand, and the true risk factor(s) on the other hand for children under the age of 12, not to mention some fear (at least some segments within American society about safety concerns), a University of Pittsburgh professor of Pediatrics makes the case for continued vaccine research in pediatric populations. TrialSite appreciates Professor Judy Martin’s transparency and straight talk. A summary of her recent piece in The Conversation is followed by some considerations for a broader rational discussion across the nation. Some notions are challenged here, meant for meaningful debate, something that’s critically important in this age of COVID-19.


    First published in The Conversation, TrialSite breaks down the case made by Professor Judy Martin, a well-known principal investigator who receives funding from the National Institutes of Health to conduct SARS-CoV-2 vaccine research. Currently, both Pfizer and Moderna are sponsoring clinical trials with children participating in ages ranging from 11 years old down to six months old. This surprises many people that babies are included in these vaccine trials. With results not ready for translation into potential public policy modifications for several months, Professor Marin explains why this is occurring.


    The Credentials

    Prior to commencing a brief overview, we mention Martin’s credentials. She conducts her NIH-funded research out of the University of Pittsburgh’s Pittsburgh Vaccine Trials Unit, which is well-known in the world of vaccine research. In her Op-Ed, she shares that this unit conducts both adult and pediatric studies involving COVID-19 vaccines. The investigator shares that she’s been conducting pediatric vaccine research for over 20 years now.


    Ms. Martin emphasized that the Pittsburgh VTU participated in the heavily funded COVID-19 Prevention Network, which was the consolidation and rationalization, not to mention streamlining, of several NIH/NIAID trial site networks in a bid to take on the COVID-19 pandemic.


    Now Professor Martin shares with the world that the Pittsburgh-based VTU will conduct the mRNA vaccine investigating the safe dosage regimens for children 6 to 11 years old. This will require fully risk-informed and consented volunteers that have not been coerced or enticed (consented by parents or guardians, performed under ethical review board oversight). TrialSite supports this kind of transparency.


    The Clinical Trials

    Offering full transparency, Professor Martin shares with the world that their VCU has conducted three (3) adult clinical trials involving both Moderna and Johnson and Johnson vaccines. Moreover, they are a trial site for Moderna’s KidCove study, enrolling cohorts from 6 to 11 years of age down to 6 to 24 months of age in this Phase 2 trial investigating the safety and appropriate dosing regimen. Now the University of Pittsburgh trial site proposes to progress to a Phase 3 pediatric trial commencing in mid-August involving children aged 6 to 11 in both American and Canada.


    Information & Education

    This top Pittsburgh academic medical investigator shares with the reader how the COVID-19 vaccines were developed, noting that Operation Warp Speed pumped at least $18 billion into the vaccine development. She shares a summary of the vaccine development lifecycle, an overview of the rigorous process, and opines that these amazing products ultimately “work by tricking the body’s immune system into making proteins, called antibodies, that fight disease—but without giving a person the disease.” Further describing the phases of clinical trials and the regulatory process, the historical COVID-19 vaccine development effort in America has led to three authorized vaccines under EUA by the FDA for people 18 years and up while the BNT162b2 (Pfizer-BioNTech) is now available for young people 12-years of age and up. TrialSite suggests that her comments include a broad overstatement, in that the relative importance of antibodies versus T effector cells in providing protective immunity against death and disease is not well understood. Her comments also overlook and simplify the pattern of known and emerging adverse events associated with these vaccines, which presumably could be a key focus of the proposed Phase 3 trial, along with the expected effective rate. In risk assessment for clinical trials, one typically must assume that the experimental product confers no benefit, and therefore the risks must be completely disclosed and those risks must be proportional to the potential significance of the intervention for the intended population.


    The Rational for Children’s Trials

    Professor Martin argues that while about two-third of all adults in American have received at least one COVID-19 vaccine dose by mid-July, 2021 with a circulating Delta and people throughout the country engaging in seemingly normal, pre-pandemic behavior school’s just around the corner. All of those kids, under 12 who aren’t yet eligible for access to the emergency use authorized investigational products, this combination of A) uncertainty about what kinds of transmissibility will occur at school and B) delta variant transmissibility and potency lead to a growing risk for yet another surge. Unstated is that the total number of COVID-attributed deaths (in USA, per CDC) in this age cohort to date is less than 380. This means that out of approximately 610,000 deaths for an extremely low rate of .0063%. According to a recent entry in Nature deaths asociated with children and COVID-19 are extremely low. https://www.nature.com/articles/d41586-021-01897-w


    Importantly, she argues it’s the fact that “children have important differences in physiology and responses to vaccines from those of adults” and thus treating this cohort will be instrumental in finally ending the pandemic. That is, “children are not just little grownups; their bodies differ from adults in important ways.”


    While true in general, it does not logically follow that vaccination of children is necessary to “finally end.. the pandemic. “ This statement relies on the hypothesis that the current vaccines are highly effective in preventing infection, viral replication, and transmissibility. To date, this hypothesis is not supported by available data, and in fact, the converse appears to be true. It also relies on the hypothesis that childhood (versus adult) transmission plays an important role in viral transmissibility to high-risk individuals (including the aged, obese, and other high-risk populations). Again, there are no compelling data to support this. In general, the belief that these vaccines can prevent viral infection, replication, and transmission is not well supported, as evidenced by the epidemiology of delta variant infection, disease, and death in previously vaccinated individuals (as well as WHO’s advice regarding mask use to prevent infection and spread of delta in all cohorts).


    The University of Pittsburgh researcher goes on to emphasize some of the differences between adults and children, from the feature of a rapidly developing brain to the delta in immune systems, especially in babies and toddlers. Dr. Martin shares:


    “For the first few months of life, infants’ immune systems still possess the antibodies they received from their mothers across the placenta during late pregnancy. This changes how newborns respond to pathogens and makes them less able to mount an immune response to some vaccines. Young children’s bodies gradually ramp up their own immune systems as their protection from mom wears off.” While a general truism, in the specific case of the current US SARS-CoV-2 vaccines available under EUA, these maternal-fetal kinetics are not known. Characterization of this time would seem a useful precursor to initiating infant studies and should be performed prior to initiating such studies.


    Other factors include the change in dosage from a safe and effective adult vaccine to what’s tolerable safety in a child, as Martin emphasizes “there can be important differences in how their bodies respond to it.” TrialSite agrees, both in terms of immunogenicity and in terms of safety.


    The Key Drivers for Clinical Trials

    Martin declares for the key pivotal aforementioned reasons: “Vaccines often need to be tailored specifically for young children.” She offers up an example: made from polysaccharides—those sugar molecules that coat the outside of the pneumococcal bacteria—the Pneumococcal vaccine is designed to prevent pneumonia in adults yet this vaccine product doesn’t work in infants due to the fact that they’re not capable of eliciting an immune response to the molecules. Thus a modified vaccine for babies was designed and developed. And, of course, the dosage level in a safe and effective vaccine for adults may need to be modified considerably for children.


    Safety becomes of utmost importance, proclaims Martin, and clinical trials, with myriad safety layers and stage gates, can catch safety signals that weren’t produced in adult studies. Of course, much like most trials, the fully informed consent of volunteers is key, which necessitates awareness, trust, and engagement with volunteer communities. In the case of pediatric clinical trials, the “volunteer” is participating in the trial and incurring adverse event risks based on information provided to a parent or guardian. It will be crucial to demonstrate that the parent or guardian is free of external pressures and has not been coerced or enticed in any way to “volunteer” the participation of the child. TrialSite presumes that the relevant ethics review board will ensure that this is the case. Careful monitoring and validation of the absence of coercion will be crucial. Given the current public messaging concerning SARS-Cov-2/COVID-19 vaccines, it will be challenging to identify and verify parents or guardians that have not been pressured in any way to “volunteer” a child for such studies.


    TrialSite Commentary

    First, TrialSite again commends Dr. Martin for the transparency, candor, and outreach to a broader world. She makes the case why pediatric vaccine research is needed to progress vaccines against SARS-CoV-2. Some key factors she didn’t raise include what’s the actual risk of COVID-19 to children, and the practicalities of obtaining non-coerced informed consent. At what numbers are children infected during the first waves across America? What’s the rate of hospitalization and death? We know that, generally, about 90% of total COVID-19 cases end up as asymptomatic to mild-to-moderate in nature. Of the 10% or so that experience disease progression, the vast majority are adults. Despite fear-driven talk in the mainstream media, as noted above, the incidence of death and disease from COVID-19 is extremely low among children. TrialSite supports Dr. Martin, and also supports a more transparent analysis into the true risks associated with COVID-19, particularly when it comes to children, ensuring a more holistic and balanced discussion—and a less emotionally charged, fear-driven hyperbole. Then the proper risk-benefit analysis is possible. TrialSite suggests studies are different than mass vaccination programs, and detailed proper informed consent is necessary for parental or guardian authorization. Of course, the University of Pittsburgh’s VTU is one of the top in the country, if not the world, and understands these important principles.


    Lead Research/Investigator

    Professor Judy Martin, MD


    Call to Action: What are your thoughts?

    Quote from stefan

    All other reports state that the data has been compared to natural frequencies of deaths and nothing remarkable has been seen apart from the blod cloths it seams.

    I know this dissipative reports made by the pharma clerks. They do not use proper math. If cloths occur within 3-6 hours then you must take the survival rate for e.g. 1/8 of a day. Then you must take a mirror set of same age groups and look often such people did die after the flu shot within 3-6 hours. Crucial is the time point of onset of symptoms not the final death. You can always cheat this. A said in VAERS you can find a large set of cases with all details.


    To repeat in once more vaccine related deaths in all countries show the same bandwidth (20..40/mio) despite large under reporting.

    Quote from Shane D.

    Only difference is the health care institutions try to block Iver use for COVID,

    The difference here is:: "to be or not to be..." (Hamlet..)


    Quote from Fm1

    NYU Scientists Study: Vaccines vs. Infection—Does Immunity Vary from Natural SARS-CoV-2 Infection to mRNA Vaccine?

    The paperhttps://www.medrxiv.org/conten…04.20.21255677v1.full.pdf


    From multiple aspects it looks like RNA vaccine are of minor value compared to an infection. The only win (potential less cytokin storm risk) is also a risk as we in future will see much more vaccinated patients going to hospital (India! 9.8% instead of 2%). So first dark clouds on sky!


    Vaccine risks:


    However, we did not detect appreciable expansion of plasmablastsin circulation of individuals immunized with SARS-CoV-2 BNT162b2 mRNA vaccine,despite a robust antibody response.


    No nasal infection protection by vaccines:


    One recent study suggests that neutralizing antibodies are rarely detected in nasal swabs from subjects who received the BNT162b2 SARS-CoV-2 mRNA vaccine88, however,it remains to be determined whether the vaccine elicits protective mucosal immunity.


    Mixed value/risks::


    vaccines help from over regulating cytokines. But do block other critical paths (as we know from Pfizer induced immune suppression) interferon response to low.

    Critically, induction of IFNs by viral infection can radically reshape antigen presentation, cellular trafficking, and terminal differentiation of lymphocytes83,84. Infection with SARS-CoV-2 potently inducedIFNresponses, but we did not observe evidence of IFN induction by the BNT162b2 mRNA vaccine


    Some potential dangers from vaccines and CoV-19 that need more research


    Another consequence of high IFN activity could be aberrant humoral responses. Whereas SARS-CoV-2 vaccine development has mainly focused on antibody production,the role of antibodies in SARS-CoV-2 infection is less clear. Strong antibody responses often correlate with more severe All rights reserved. No reuse allowed without permission. (which was not certified by peer review) is the author/funder, who has granted medRxiv a license to display the preprint in perpetuity. The copyright holder for this preprintthis version posted April 21, 2021. ; https://doi.org/10.1101/2021.04.20.21255677doi: medRxiv preprint

    11illness and antibody-dependent enhancement of pathology has been described in COVID-19 patients17,92-96. In our study, antibody-producing cells were characterized by a type I IFNgene expression signature. A strongIFN signature has been associated with pathogenic autoantibodies in systemic lupus erythematosus(SLE)97,98. Previous studies have highlighted the shared IFN-induced gene signature in lymphocytes from patients with autoimmune disease and in subjects following viral infections98,99. Our observation that B lymphocyte transcriptional programs in COVID-19 patients are dominated by dramatic upregulation of IFN-response genes may be important for understanding the immunopathology of COVID-19, as there is growing evidence that autoantibodies could be driving severe disease and long-term sequelae in some COVID-19 patients92-94,96.Recent studies emphasize generation of antigen-specific T cells in protective immunity against SARS-CoV-2 infection and itisbecoming increasingly clear that successful vaccines need to engage the cellular adaptive immune response100-102. Indeed,humoral immune responses may be less effective against new SARS-CoV-2 variants88,103. Conversely, SARS-CoV-2-specific CD8 T cellresponses, which target a broad range of epitopes, remain largely intactagainst new variants presently in circulation104. Our analysis revealed that both SARS-CoV-2 infection and, to a lesser degree, vaccination elicit clonal CD8 effector T cell responses

    Happy "Freedom Day" for all the Brits out there! I hear most continue to wear their masks anyway. Still, "Freedom Day" sounds good doesn't it!


    Did you hear the one about the French cafe owners who were told that in a few days, if they don't check their customers for a Covid pass, they can get up to a year in jail and a 45K Euro fine? Spoiler : it's no joke.

Subscribe to our newsletter

It's sent once a month, you can unsubscribe at anytime!

View archive of previous newsletters

* indicates required

Your email address will be used to send you email newsletters only. See our Privacy Policy for more information.

Our Partners

Supporting researchers for over 20 years
Want to Advertise or Sponsor LENR Forum?
CLICK HERE to contact us.