Study Finds Covid Boosters Cause “Net Harm” In Young Adults

Authors:  QUOTH THE RAVEN QTR Finance September 16, 2022

It was just a couple of days ago that I wrote about the explosive chronology of events laid out by Rutgers professor and Harvard PhD Dr. Richard Ebright that made it clear to me that the Covid “lab leak” origin was the most reasonable explanation for the pandemic.

And now, before we’ve even had a chance to digest that information, it looks as though we are getting another desperately needed Covid reality check: a new study conducted by scientists from University of Washington, Harvard and Johns Hopkins, emerged just hours ago and makes arguments against vaccine booster mandates for young adults. The findings of the study were stunning.

The study, which is still in pre-print and has not yet been peer reviewed, is called “COVID-19 Vaccine Boosters for Young Adults: A Risk-Benefit Assessment and Five Ethical Arguments against Mandates at Universities”.

The study looks at how, as of May 2022, at least 1,000 colleges and universities have required vaccination, with over 300 of them requiring boosters. Despite “more than fifty petitions” in writing against these mandates, “young people, parents and faculty have been ignored by administrators and mandate proponents”, the study says.

Led by researchers from the University of Washington, University of Oxford, Harvard and Johns Hopkins University, it set out to look at the problems of students facing disenrollment at North American universities due to third dose COVID-19 vaccine mandates.

The says that “two main factors” are driving scientific controversy over boosters: “a lack of evidence that booster doses provide meaningful reduction in hospitalisation risk among young people and mounting evidence that (widespread) prior infection confers significant protection against hospitalisation 50 due to (re-)infection.”

Remember earlier this year when the idea of “natural immunity” all of a sudden went from conspiracy theory topic to widely accepted by Dr. Fauci?

The paper seeks to provide the first “risk benefit assessment of SARS-CoV-2 boosters for young previously uninfected adults under 40 years old”.

The study found that requiring third boosters may provide “net expected harm”, as the study estimated that “22,000 – 30,000 previously uninfected adults aged 18-29 must be boosted with an mRNA vaccine to prevent one COVID-19 hospitalisation.”

COVID-19 vaccine may not stop long term effects on older adults

Authors: Associated Press

New U.S. research on long COVID-19 provides fresh evidence that it can happen even after breakthrough infections in vaccinated people, and that older adults face higher risks for the long-term effects.

In a study of veterans published Wednesday, about one-third who had breakthrough infections showed signs of long COVID.

A separate report from the Centers for Disease Control and Prevention found that up to a year after an initial coronavirus infection, 1 in 4 adults aged 65 and older had at least one potential long COVID health problem, compared with 1 in 5 younger adults.

Long COVID refers to any of more than two dozens symptoms that linger, recur or first appear at least one month after a coronavirus infection. These can affect all parts of the body and may include fatigue, shortness of breath, brain fog and blood clots.

Coronavirus vaccines that help prevent initial infections and serious illnesses provide some protection against long COVID but mounting research shows not as much as scientists had first hoped.

The veterans study published in Nature Medicine reviewed medical records of mostly white male veterans, aged 60, on average. Of the 13 million veterans, almost 3 million had been vaccinated last year, through October.

About 1%, or nearly 34,000, developed breakthrough infections. Lead author Dr. Ziyad Al-Aly noted that the study was done before the highly contagious omicron variant appeared at the end of the year and said the rate of breakthrough infections has likely increased.

Breakthrough infections and long COVID symptoms were more common among those who had received Johnson & Johnson’s single-dose shot compared with two doses of either Moderna or Pfizer vaccines. Whether any had received booster shots is not known; the first booster wasn’t OK’d in the U.S. until late September.

Overall, 32% had long COVID symptoms up to six months after breakthrough infections. That’s compared with 36% of unvaccinated veterans who had been infected and developed long COVID.

Vaccination reduced the chances for any long COVID symptoms by a “modest” 15%,” although it cut the risk in half for lingering respiratory or clotting problems, said Al-Aly, a researcher with Washington University and the Veterans Affairs health system in St. Louis. These symptoms included persistent shortness of breath or cough and blood clots in lungs or veins in the legs.

Patients who have taken Johnson & Johnson’s COVID-19 vaccine have tested positive for virus more often than their Moderna and Pfizer counterparts.FREDERIC J. BROWN/AFP via Getty Images

Infectious disease expert Dr. Kristin Englund, who runs a center for long COVID patients at the Cleveland Clinic, said the Nature Medicine study mirrors what she sees at her clinic. Long COVID patients there include people who were vaccinated and received boosters.

“As we have no clear treatments for long COVID, it is important for everyone to get vaccinated and use other proven methods of prevention such as masking and social distancing in order to prevent infections with COVID and thus long COVID,” Englund said.

The CDC report, released Tuesday, used medical records for almost 2 million U.S. adults from the start of the pandemic in March 2020 to last November. They included 353,000 who had COVID-19. Patients were tracked for up to a year to determine if they developed any of 26 health conditions that have been attributed to long COVID.

Those who had COVID were much more likely than other adults without COVID to develop at least one of these conditions, and risks were greatest for those aged 65 and older. Information on vaccination, sex and race was not included.

Breathing problems and muscle aches were among the most common conditions.

Older adults’ risks were higher for certain conditions, including strokes, brain fog, kidney failure and mental health problems. The findings are worrisome because those conditions can hasten older adults’ needs for long-term care, the report authors said.

They stressed that routine assessment of all COVID patients “is critical to reduce the incidence” of long COVID.

Long COVID after breakthrough SARS-CoV-2 infection

Authors: Ziyad Al-AlyBenjamin Bowe & Yan Xie 

Nature Medicine volume 28, pages1461–1467 (2022)

Abstract

The post-acute sequelae of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection—also referred to as Long COVID—have been described, but whether breakthrough SARS-CoV-2 infection (BTI) in vaccinated people results in post-acute sequelae is not clear. In this study, we used the US Department of Veterans Affairs national healthcare databases to build a cohort of 33,940 individuals with BTI and several controls of people without evidence of SARS-CoV-2 infection, including contemporary (n = 4,983,491), historical (n = 5,785,273) and vaccinated (n = 2,566,369) controls. At 6 months after infection, we show that, beyond the first 30 days of illness, compared to contemporary controls, people with BTI exhibited a higher risk of death (hazard ratio (HR) = 1.75, 95% confidence interval (CI): 1.59, 1.93) and incident post-acute sequelae (HR = 1.50, 95% CI: 1.46, 1.54), including cardiovascular, coagulation and hematologic, gastrointestinal, kidney, mental health, metabolic, musculoskeletal and neurologic disorders. The results were consistent in comparisons versus the historical and vaccinated controls. Compared to people with SARS-CoV-2 infection who were not previously vaccinated (n = 113,474), people with BTI exhibited lower risks of death (HR = 0.66, 95% CI: 0.58, 0.74) and incident post-acute sequelae (HR = 0.85, 95% CI: 0.82, 0.89). Altogether, the findings suggest that vaccination before infection confers only partial protection in the post-acute phase of the disease; hence, reliance on it as a sole mitigation strategy may not optimally reduce long-term health consequences of SARS-CoV-2 infection. The findings emphasize the need for continued optimization of strategies for primary prevention of BTI and will guide development of post-acute care pathways for people with BTI.

Main

The post-acute sequelae of SARS-CoV-2 infection—also referred to as Long COVID—have been characterized1. Increasingly, vaccinated individuals are being diagnosed with COVID-19 as a result of breakthrough SARS-CoV-2 infection (BTI)2,3. Whether people with BTI experience post-acute sequelae is not clear. Addressing this knowledge gap is important to guide public health policy and post-acute COVID-19 care strategies.

Here we leverage the breadth and depth of the electronic healthcare databases of the US Department of Veterans Affairs to address the question of whether people with BTI develop post-acute sequelae. We characterize the risks and 6-month burdens of a panel of prespecified outcomes in a cohort of people who experienced BTI after completion of vaccination in the overall cohort and by care setting of the acute phase of the disease (that is, whether people were not hospitalized, hospitalized or admitted to an intensive care unit (ICU) during the first 30 days after a positive test). We then undertake a comparative evaluation of the magnitude of risk in people with BTI versus those with SARS-CoV-2 infection and no prior vaccination and, separately, hospitalized people with BTI versus those hospitalized with seasonal influenza.

Results

Post-acute sequelae in BTI versus controls without SARS-CoV-2 infection

There were 33,940 and 4,983,491 participants in the BTI group and a contemporary control group of users of the Veterans Health Administration from 1 January 2021 to 31 October 2021 with no record of a positive SARS-CoV-2 test, respectively. BTI participants had a positive SARS-CoV-2 test with prior record of a complete vaccination defined following Centers for Disease Control and Prevention (CDC) guidelines at 14 days after first Janssen (Johnson & Johnson)(Ad26.COV2.S) vaccination and 14 days after second Pfizer-BioNTech (BNT162b2) or Moderna (mRNA-1273) vaccination. The demographic and health characteristics of the BTI and the control groups before and after weighting are presented in Supplementary Tables 14. During the enrollment period, the overall rate of BTI within those fully vaccinated was 10.60 (95% CI: 10.52, 10.70) per 1,000 persons at 6 months; rates of breakthrough by vaccine type are presented in Supplementary Data Table 1.

For all analyses, we provide two measures of risk: (1) we estimated the adjusted HRs of a set of incident prespecified outcomes in people with BTI versus the control group; and (2) we estimated the adjusted excess burden of each outcome due to BTI per 1,000 persons 6 months after a positive SARS-CoV-2 test on the basis of the difference between the estimated incidence rate in individuals with BTI and the control group. Assessment of standardized mean differences of participant characteristics (from data domains including diagnoses, medications and laboratory test results) after application of weighting showed that they are well-balanced in each analysis of incident outcomes (Supplementary Fig. 1).

Compared to the contemporary control group, people who survived the first 30 days of BTI exhibited an increased risk of death (HR = 1.75, 95% CI: 1.59, 1.93) and excess burden of death estimated at 13.36 (95% CI: 11.36, 15.55) per 1,000 persons with BTI at 6 months; all burden estimates represent excess burden and are given per 1,000 persons with BTI at 6 months (Fig. 1). People with BTI also had an increased risk of having at least one post-acute sequela of SARS-CoV-2 (PASC) (HR = 1.50, 95% CI: 1.46, 1.54; burden of 122.22, 95% CI: 115.31, 129.24) (Supplementary Table 5).

figure 1
Fig. 1: Risk and 6-month excess burden of post-acute sequelae in people with BTI compared to the contemporary control group.

Compared to the control group, 30-day survivors of BTI exhibited increased risk of post-acute sequelae in the pulmonary (HR = 2.48 (2.33, 2.64); burden of 39.82 (36.83, 42.99)) and several extrapulmonary organ systems, including cardiovascular disorders (HR = 1.74 (1.66, 1.83); burden of 43.94 (39.72, 48.35)), coagulation and hematologic disorders (HR = 2.43 (2.18, 2.71); burden of 13.66 (11.95, 15.56)), fatigue (HR = 2.00 (1.82, 2.21); burden of 15.47 (13.21, 17.96)), gastrointestinal disorders (HR = 1.63 (1.54, 1.72); burden of 37.68 (33.76, 41.80)), kidney disorders (HR = 1.62 (1.47, 1.77); burden of 16.12 (13.72, 18.74)), mental health disorders (HR = 1.46 (1.39, 1.53); burden of 45.85 (40.97, 50.92)), metabolic disorders (HR = 1.46 (1.37, 1.56); burden of 30.70 (26.65, 35.00)), musculoskeletal disorders (HR = 1.53 (1.42, 1.64); burden of 19.81 (16.56, 23.31)) and neurologic disorders (HR = 1.69 (1.52, 1.88); burden of 11.60 (9.43, 14.01)). Risk and excess burden of each individual sequela and by organ system are provided in Extended Data Fig. 1 (Supplementary Table 6) and Fig. 1 (Supplementary Table 5), respectively.

The results were consistent in analyses considering a historical control group (n = 5,785,273) as the referent category (Extended Data Fig. 2 and Supplementary Table 7) and, separately, people who were vaccinated for SARS-CoV-2 and did not experience a BTI (n = 2,566,369) as another alternative control group (Extended Data Fig. 3 and Supplementary Table 8).

The risk of death was increased in the 30–90 days and also increased, but to a lesser extent, in the 90–180 days after a positive SARS-CoV-2 test (Supplementary Table 9). The risk of incident sequelae was increased in the 30–90 days after a positive SARS-CoV-2 test. In the period between 90 days and 180 days after testing positive, there was increased risk of both incident sequalae—albeit in lesser magnitude than the risk in days 30–90—and increased risk of recurrent or persistent sequalae (Supplementary Table 9).

Compared to the contemporary control group, there was increased risk of death, at least one PASC and organ involvement in people who were not immunocompromised before BTI (Extended Data Fig. 4a and Supplementary Table 10); the risks were generally higher in those who were immunocompromised before BTI (Extended Data Fig. 4a and Supplementary Table 10). Analyses of people with BTI showed that the risks of death, at least one PASC and organ system involvement were consistently higher in people who were immunocompromised versus those who were not before BTI (Extended Data Fig. 4b and Supplementary Table 10).

Of people with BTI, analyses by vaccine type suggested that there is no statistically significant difference in risk of post-acute death among the three SARS-CoV-2 vaccines (Pfizer-BioNTech (BNT162b2), Moderna (mRNA-1273) and Janssen (Johnson & Johnson) (Ad26.COV2.S)). Both BNT162b2 and mRNA-1273 were associated with decreased risk of at least one PASC: pulmonary and extrapulmonary organ involvement. There was no statistically significant difference in risk of any of these outcomes between BNT162b2 and mRNA-1273 (Supplementary Table 11).

Post-acute sequelae in BTI by care setting of the acute phase of the disease

The demographic and health characteristics of people with BTI who were not hospitalized, who were hospitalized and who were admitted to ICU during the acute phase of the disease before and after weighting are provided in Supplementary Tables 12 and 13. Evaluation of standardized mean differences of baseline participant characteristics after the application of the weighting suggested good balance (Supplementary Fig. 2).

Compared to the control group of people without evidence of SARS-CoV-2 infection, people who were not hospitalized during the first 30 days of BTI exhibited an increased risk of death (HR = 1.29 (1.12, 1.49); burden of 7.77 (5.62, 10.24)); the risk was further increased in those who were hospitalized (HR = 2.69 (2.33, 3.12); burden of 24.79 (20.39, 29.86)) and was highest in those who were admitted to ICU (HR = 5.68 (4.55, 7.09); burden of 60.02 (46.85, 76.19)). The risk of having at least one post-acute sequela was evident in non-hospitalized people (HR = 1.25 (1.20, 1.30); burden of 77.60 (68.40, 87.04)), was further increased in those who were hospitalized (HR = 2.95 (2.80, 3.10); burden of 334.10 (315.90, 352.53)) and was highest in those admitted to ICU (HR = 3.75 (3.38, 4.16); burden of 421.39 (383.37, 459.56)) (Fig. 2 and Supplementary Table 14).

figure 2
Fig. 2: Risk and 6-month excess burden of post-acute sequelae in those with BTI by acute phase care setting.

People who were not hospitalized exhibited small but significant increased risk of post-acute sequelae, including cardiovascular, coagulation and hematologic, gastrointestinal, mental health, metabolic, musculoskeletal and pulmonary disoders, as well as increased risk of fatigue (Fig. 2 and Supplementary Table 14). The risks were further increased in people who were hospitalized (Fig. 2 and Supplementary Table 14) and highest in those admitted to the ICU (Fig. 2 and Supplementary Table 14). Analyses of individual sequela are presented in Extended Data Fig. 5 and Supplementary Table 15.

Post-acute sequelae in BTI versus SARS-CoV-2 infection without prior vaccination

To place the magnitude of risk of post-acute sequelae in people with BTI in broad context of post-acute COVID-19 manifestations, we developed a comparative approach to evaluate the risk of organ system involvement in people with BTI (n = 33,940) versus people with SARS-CoV-2 infection and no prior history of vaccination (n = 113,474) (Supplementary Tables 1 and 16). Assessment of standardized mean differences of baseline characteristics in the weighted cohorts suggested good balance (Supplementary Figs. 3 and 4 and Supplementary Tables 4 and 17).

People with BTI exhibited lower risk of death (HR = 0.66 (0.58, 0.74); burden of −10.99 (−13.45, −8.22); negative values denote reduced burden in BTI relative to SARS-CoV-2 infection) and lower risk of post-acute sequelae (HR = 0.85 (0.82, 0.89); burden of −43.38 (−53.22, −33.31)) compared to those with SARS-CoV-2 infection and no prior history of vaccination (Fig. 3 and Supplementary Table 18). Comparatively, the risk of post-acute sequelae in all the examined organ systems was lower in people with BTI versus those with SARS-CoV-2 infection without prior vaccination. BTI was associated with lower risk of 24 of the 47 sequelae examined compared to those with SARS-CoV-2 infection without prior vaccination (Extended Data Fig. 6 and Supplementary Table 19). The reduced risk was evident (albeit weak) in those who were immunocompromised and in those who were not immunocompromised (Supplementary Table 20).

figure 3
Fig. 3: Risk and 6-month excess burden of post-acute sequelae in people with BTI compared to those with SARS-CoV-2 infection without prior vaccination.

Analyses within each care setting suggested that the risk reduction in BTI versus SARS-CoV-2 infection on both the relative (HR) and absolute (burden) scale generally becomes increasingly more pronounced as the acuity of the care setting increased (from non-hospitalized to admitted to ICU) (Fig. 4 and Supplementary Table 21). BTI was associated with less risk of death and at least one PASC in all care settings. There was also a consistently reduced risk of hematologic and coagulation disorders and pulmonary disorders in BTI versus SARS-CoV-2 infection without prior vaccination across all care settings.

figure 4
Fig. 4: Risk and 6-month excess burden of post-acute sequelae in those with BTI compared to those with SARS-CoV-2 infection without prior vaccination by acute phase care setting.

Post-acute sequelae in people hospitalized with BTI versus seasonal influenza

We developed a comparative analysis to better understand how people hospitalized with BTI (n = 3,667) fare relative to those who are hospitalized with seasonal influenza (n = 14,337). Demographic and health characteristics before and after weighting are provided in Supplementary Tables 22 and 23. Examination of standardized mean differences of baseline characteristics after application of overlap weighting demonstrated good balance (Supplementary Fig. 5).

Compared to people who were hospitalized with seasonal influenza, people with BTI who were hospitalized during the acute phase of the disease and survived the first 30 days exhibited an increased risk of death (HR = 2.43 (2.02, 2.93); burden of 43.58 (31.21, 58.26)) and increased risk of having at least one post-acute sequela (HR = 1.27 (1.19, 1.36); burden of 87.59 (63.83, 111.40)) (Extended Data Fig. 7 and Supplementary Table 24). People with BTI exhibited increased risk of sequelae in all the examined organ systems compared to those with seasonal influenza. Results of individual sequalae are presented in Supplementary Fig. 6 and Supplementary Table 25.

Positive and negative outcome controls

To assess whether our approach reproduces established knowledge, we tested the association between SARS-CoV-2 infection without prior vaccination and the risk of fatigue (a cardinal post-acute sequela of COVID-19, where, based on prior evidence, we would expect a positive association). The results showed that, compared to the contemporary control group, people with SARS-CoV-2 infection and without prior vaccination exhibited increased risk of fatigue (HR = 2.79 (2.57, 303)) (Extended Data Table 1a).

To assess the putative presence of spurious associations, we tested the association between BTI and several negative outcome controls where there was no biologic plausibility or epidemiologic evidence that an association is expected. We used the same data sources, cohort building process, covariate selection approach (including predefined and algorithmically selected high-dimensional covariates), weighting method and interpretation of results. The results suggested no significant association between BTI and risk of any of the negative outcome controls (Extended Data Table 1a).

To further test the rigor of our approach, we tested as a pair of negative exposure controls receipt of influenza vaccination in odd-numbered (n = 605,453) versus even-numbered (n = 571,291) calendar days between 1 March 2020 and 15 January 2021. Examination of the associations of receipt of influenza vaccine on odd-numbered versus even-numbered calendar days and each outcome yielded non-significant results, consistent with our a priori expectations for a successful application of negative exposure controls (Extended Data Table 1b).

Discussion

In this study of 33,940 people with BTI, 4,983,491 in the contemporary control, 5,785,273 in the historical control, 2,566,369 in the vaccinated control, 113,474 in the SARS-CoV-2 infection without prior vaccination group and 14,337 in the seasonal influenza group, we show that, compared to non-infected controls, people who survive the first 30 days of BTI exhibited increased risk of death and post-acute sequelae in the pulmonary and several extrapulmonary organ systems. The risks of death and post-acute sequelae were evident among non-hospitalized people, further increased among hospitalized people and highest among people who were admitted to ICU during the acute phase of the disease. Our comparative approach shows that risks of death and post-acute sequelae were lower in people with BTI versus people with SARS-CoV-2 infection without prior vaccination. Analyses of BTI versus SARS-CoV-2 infection without prior vaccination within the same care setting showed that this risk reduction was progressively more evident as care acuity of the acute phase of the disease increased from non-hospitalized to hospitalized and admitted to ICU and was consistently most pronounced for coagulation and pulmonary disorders. In comparative analyses among people who were hospitalized during the acute phase of the disease, those with BTI exhibited higher risks of death and post-acute sequelae than those with seasonal influenza. The constellation of findings shows that the burden of death and disease experienced by people with BTI is not trivial. Our comparative analyses provide a framework to better evaluate and contextually understand risks of the post-viral condition in people with BTI versus non-infected controls, versus SARS-CoV-2 infection without prior vaccination and versus seasonal influenza. The findings show that vaccination only partially reduces the risk of death and post-acute sequelae, suggesting that reliance on it as a sole mitigation strategy may not most optimally reduce the risk of the long-term health consequences of SARS-CoV-2 infection. Our results emphasize the need for continued optimization of primary prevention strategies of BTIs and will inform post-acute care approaches for people with BTI.

We examined the risk of death and post-acute sequelae in those with BTI versus several controls of people without evidence of SARS-CoV-2 infection, including (1) a contemporary control of people exposed to the same broader forces of the pandemic (lockdowns and economic, social and environmental stressors); (2) a historical control from a pre-pandemic era that represents a baseline unaffected by the disruptions of the pandemic; and (3) a vaccinated control group. The results show two key findings: (1) Long COVID, including increased risks of death and myriad post-acute sequelae in the pulmonary and extrapulmonary organ systems, also manifests in vaccinated individuals who experience a BTI; and (2) the range of post-acute sequelae in various organ systems in BTI does not appear to be different than COVID-19 without prior vaccination1,4,5,6,7,8,9,10,11,12. Our analyses of BTI versus SARS-CoV-2 infection without prior vaccination show that, comparatively, the magnitude of the risks of death and post-acute sequelae was lower in people with BTI versus those with SARS-CoV-2 infection who had not been previously vaccinated for it. These results show that, although vaccination may partially reduce the risks of post-acute death and disease, to most optimally reduce this burden requires continued emphasis on primary prevention of breakthrough SARS-CoV-2 infection as a goal of public health policy.

Although the absolute rates are smaller than in those with SARS-CoV-2 infection without prior vaccination, given the scale of the pandemic and the potential for breakthrough cases to continue to accumulate, the overall burden of death and disease after BTI will likely be substantial, will further add to the toll of this pandemic and will represent an additional strain on already overwhelmed health systems. In planning and development of health resources, governments and health systems should take into account the care needs of people with post-acute sequelae after BTI13.

Our analyses suggest that this risk reduction (of post-acute sequelae) was most pronounced in recipients of BNT162b2 and mRNA-1273 vaccines (compared to Ad26.COV2.S). Although these results recapitulate evidence of vaccine effectiveness in the acute phase of COVID-19, the mechanism or mechanisms underlying this carry-through effect of risk reduction from the acute to the post-acute phase of the disease is not entirely clear. One putative interpretation of these results is that vaccine-induced reduction in severity of the acute infection may then translate into less long-term risk of post-acute health outcomes. In other analyses, we also show that the reduced risk of post-acute sequelae in people with BTIs was partially eroded in people with immunocompromised status, suggesting a putative immune-related mechanism in the expression of post-acute sequelae that may be influenced by vaccination.

We also show that the risk of post-acute sequelae is higher in people with BTI than in people with seasonal influenza—a well-characterized respiratory viral illness. This extends previous evidence showing that the risk of post-acute sequelae in people with SARS-CoV-2 infection was higher than those with seasonal influenza and again emphasizes the importance of prevention of both SARS-CoV-2 infection and BTI1.

This study has several strengths. To our knowledge, it is the first large study to characterize the risks of post-acute sequelae of BTI at 6 months. We leveraged the vast national healthcare databases of the US Department of Veterans Affairs (the largest nationally integrated healthcare delivery system in the United States) to characterize the risk and 6-month burden of a comprehensive set of prespecified incident health outcomes in patients who survived the first 30 days of BTI versus several control groups (contemporary, historical and vaccinated controls). In addition to evaluating risk of BTI versus those with no evidence of SARS-CoV-2 infection in the overall cohort and by care setting of the acute phase of the disease (non-hospitalized, hospitalized and admitted to ICU), we also undertook a comparative evaluation of BTI versus SARS-CoV-2 infection in people who had not been previously vaccinated and, separately, BTI versus seasonal influenza. We used advanced statistical methodologies and adjusted through weighting for a battery of predefined covariates selected based on prior knowledge and algorithmically selected covariates from high-dimensional data domains, including diagnoses, prescription records and laboratory test results. We evaluated the rigor of our approach by testing positive and negative outcome controls to determine whether our approach would produce results consistent with pre-test expectations.

The study also has several limitations. The BTI and SARS-CoV-2 infection groups included only those who had a positive test for SARS-CoV-2 and did not include those who may have had an infection with SARS-CoV-2 but were not tested; however, if present, this will bias the estimates toward the null. Although the Veterans Affairs population is comprised of mostly men, it includes 8–10% women, which, across the groups in our study, included 1,300,744 female participants. Although we adjusted through the overlap weighting approach for a large battery of predefined and algorithmically selected covariates, and although our approach demonstrated good balance for more than 734 covariates (including all those that were available in the data but not included in the weighting process) from several data domains, including diagnoses, prescription medications and laboratory test results, and resulted in successful testing of positive outcome controls and negative outcome controls, we cannot completely rule out residual confounding. Our approach does not evaluate the severity of each outcome. Finally, the COVID-19 global pandemic is highly dynamic. As vaccine uptake continues to increase, as vaccine schedules continue to be optimized, as vaccine effectiveness wanes over time since vaccination, as booster vaccinations are deployed, as treatment strategies of the acute phase of COVID-19 continue to improve and as new variants of the virus emerge, it is likely that the epidemiology of BTI and its downstream sequelae may also change over time.

In sum, our findings provide evidence of increased risk of death and post-acute sequelae in people with BTI compared to controls with no evidence of SARS-CoV-2 infection; the risks were reduced in comparative analyses involving BTI versus SARS-CoV-2 infection without prior vaccination. Our results show that SARS-CoV-2 vaccination before infection only partially reduced the risk of death and post-acute sequelae. Measures for the prevention of breakthrough infections are needed to most optimally reduce the risk of the long-term health consequences of SARS-CoV-2 infection.

Methods

All participants who were eligible for this study were enrolled; no a priori sample size analyses were conducted to guide enrollment. All analyses were observational, and investigators were aware of participant exposure and outcome status. A summary of the major design elements is presented in Supplementary Table 26, and an analytic flowchart is provided in Supplementary Fig. 7.

Setting

Cohort participants were identified from the US Veterans Health Administration (VHA) electronic health databases. The VHA provides healthcare to discharged veterans of the US armed forces in a nationally integrated network of healthcare systems that includes more than 1,415 healthcare facilities. Veterans enrolled in the VHA have access to a comprehensive medical benefits package that includes outpatient services; preventive, primary and specialty care; mental health care; geriatric care; inpatient hospital care; extended long-term care; prescriptions; home healthcare; medical equipment; and prosthetics. The VHA healthcare databases are updated daily.

Cohorts

We first identified users of the VHA who were alive on 1 January 2021 (n = 5,430,912). Use of the VHA was defined as having record of use of outpatient or inpatient service, receipt of medication or use of laboratory service with the VHA healthcare system in the 2 years prior (Supplementary Fig. 8). Among these, 163,024 participants had a record of a first positive SARS-CoV-2 test from 1 January 2021 to 31 October 2021, and 5,140,387 had no record of any positive SARS-CoV-2 test between 1 January 2020 and 1 December 2021. Participants were followed until 1 December 2021.

To construct a group of people with BTI, we selected, from those with a positive SARS-CoV-2 test (n = 163,024), those with a record of completion of an Ad26.COV2.S, mRNA-1273 or BNT162b2 vaccination before the date of their first positive SARS-CoV-2 test (n = 34,863). Completion of vaccination was defined following CDC guidelines at the 14th day after the second shot of the mRNA-1273 or BNT162b2 vaccination series or the 14th day after the first shot of the Ad26.COV2.S vaccination. Setting the date of first positive SARS-CoV-2 test as time zero (T0), we then selected those alive 30 days after T0, resulting in a cohort of 33,940 participants in the BTI group.

We then constructed several control groups; the rationale for each of these control groups is provided in Supplementary Fig. 9. To build a contemporary control group of people with no evidence of SARS-CoV-2 infection, we then used the 5,140,387 users of the VHA who had no record of a SARS-CoV-2-positive test. Among these participants, we randomly assigned a T0 to each participant in the group on the basis of the distribution of the T0 dates in those with BTI. We finally selected those who were alive 30 days after their T0 (n = 4,983,491). The contemporary control group represents contemporaneous users of the VHA who were subject to the broader forces of the pandemic but did not contract SARS-CoV-2 infection. Of these, the 2,566,369 who had record of a SARS-CoV-2 vaccination before their T0 served as a vaccinated control group. The vaccinated control group represents contemporaneous users of the VHA who share the characteristic of being vaccinated with the breakthrough group and have a major distinction in that they did not contract SARS-CoV-2 infection subsequent to their vaccination.

To build an alternate control group during a period of time where participants were not subject to the influence of the pandemic, we identified users of the VHA who were alive on 1 January 2018 (n = 6,084,973) and who had no history of a positive SARS-CoV-2 test (n = 5,938,519). After randomly assigning a T0 in 2018 on the basis of the distribution of the calendar dates of T0 in those with BTI, 5,785,273 were alive 30 days after T0. Participants were followed until 1 December 2018. This group served as the historical control group.

To build the group of people with SARS-CoV-2 infection and without prior vaccination as a means of investigating the effect of prior vaccination on the risk of post-acute sequalae, we identified, from the 163,024 people with a first positive SARS-CoV-2 test from 1 January 2021 to 31 October 2021, 118,185 who had no record of any SARS-CoV-2 vaccination up through 30 days after first positive SARS-CoV-2 test (T0). We then selected the 113,474 who were alive 30 days after T0 to comprise the group of people with SARS-CoV-2 infection and no prior vaccination.

Finally, to compare post-acute sequelae of those hospitalized with BTI during the acute phase of the illness to those hospitalized with seasonal influenza, we separately identified 15,160 VHA users hospitalized with positive seasonal influenza test 5 days before or 30 days after the test between 1 October 2016 and 29 February 2020. We set the date of the positive seasonal influenza test as T0. To ensure no overlap with the BTI group, participants who had no record of a positive SARS-CoV-2 test were then selected (n = 14,431). From these, we selected 14,337 who were alive 30 days after their T0 to constitute the seasonal influenza group. Duration of follow-up was randomly assigned on the basis of follow-up in the BTI group.

Data sources

Data used in this study were obtained from the VHA Corporate Data Warehouse (CDW). Within CDW, the patient data domain provided information on demographic characteristics; the outpatient encounters domain and inpatient encounters domain provided information on health characteristics, including data on timing and location of interactions with the healthcare system, diagnoses and procedures; the pharmacy and barcode medication administration domains provided medication records; and the laboratory results domain provided laboratory test information in both outpatient and inpatient settings5,6. The COVID-19 Shared Data Resource provided information on SARS-CoV-2 test results and SARS-CoV-2 vaccination status. The 2019 Area Deprivation Index (ADI) at each cohort participant residential address was used as a contextual measure of socioeconomic disadvantage14.

Post-acute sequelae

We prespecified a set of outcomes based on prior evidence on the post-acute sequelae of SARS-CoV-2 infection—also referred to as Long COVID4,5,6,7,8,9,10,11,12. Outcomes were defined using validated definitions leveraging information from several data domains, including diagnoses, prescription medications and laboratory test results, at the time of first record of occurrence in the data5,6,15,16,17,18,19,20,21. Incident post-acute sequelae were examined in a cohort with no record of the health condition in the 2 years before T0. We additionally examined outcomes of death and having at least one of post-acute sequelae that was defined at the time of the first incident prespecified post-acute sequelae in each participant.

Additionally, we defined a set of outcomes where we aggregated the prespecified post-acute sequelae, where applicable, by organ system. These included cardiovascular disorders, coagulation and hematologic disorders, fatigue, gastrointestinal disorders, kidney disorders, mental health disorders, metabolic disorders, musculoskeletal disorders, neurologic disorders and pulmonary disorders. All outcomes were assessed starting from 30 days after T0.

Covariates

We included a set of predefined covariates based on prior knowledge4,5,6,7,8,9,10,11,12,19,22,23,24,25,26 and algorithmically selected covariates. Predefined covariates included demographic information (age, race and sex); contextual information (ADI); measures of the intensity of healthcare interaction in the 2 years before T0, including the number of outpatient visits, the number of inpatient visits, the number of unique medications the participant received a prescription for and the number of routine blood panels that were performed; and prior history of receiving an influenza vaccination. We also included smoking status as a covariate. Health characteristics included prior history of anxiety, cancer, cardiovascular disease, cerebrovascular disease, chronic kidney disease, peripheral artery disease, dementia, depression, type 2 diabetes mellitus and chronic obstructive pulmonary disease, and measures of estimated glomerular filtration rate, systolic and diastolic blood pressure, and body mass index (BMI). We also included, as measures of spatiotemporal differences, the calendar week of enrollment and geographic region of receipt of care defined by Veterans Integrated Services Networks (VISN).

In consideration of the dynamicity of the pandemic, for analyses that compared BTI, SARS-CoV-2 infection without prior vaccination and the contemporary control, additional covariates included SARS-CoV-2 testing capacity, SARS-CoV-2 positivity rates, hospital system capacity (the total number of inpatient hospital beds) and inpatient bed occupancy rates (the percentage of hospital beds that were occupied) as well as a measure of the proportions of SARS-CoV-2 variants by Health and Human Services region26. These measures were ascertained for each participant in the week before cohort enrollment at the location of the healthcare system at which they received care. In analyses of the vaccinated control, we additionally included calendar week of first vaccination shot. All continuous covariates were treated as natural cubic splines unless heavily skewed toward zero.

In addition to the predefined covariates, we leveraged the high dimensionality of VA data where we developed and deployed a high-dimensional variable selection algorithm to identify covariates that may potentially confound the examined associations27. Using classifications from the Clinical Classifications Software Refined version 2021.1, available from the Healthcare Cost and Utilization Project sponsored by the Agency for Healthcare Research and Quality, more than 70,000 ICD-10 diagnoses codes in the year before T0 for each participant were classified into 540 diagnostic categories28,29,30. Using the VA drug classification system, 3,425 different medications were classified into 543 medication classes31,32. Finally, laboratory results from 38 different laboratory measurements were classified into 62 laboratory test abnormalities, defined by being above or below the corresponding reference ranges, on the basis of the recorded Logical Observation Identifiers Names and Codes. Of the high-dimensional variables that occurred at least 100 times in participants in each group (up to 821), we selected the top 100 variables with the highest relative risk for differences in group membership for inclusion in models.

Statistical analysis

Mean (standard deviation) and frequency (percentage) of select characteristics are reported in the BTI group, SARS-CoV-2-infected group without prior vaccination, the contemporary control group, the historical control group, the vaccinated control group and the seasonal influenza group, where appropriate. Characteristics of those with BTI by hospitalization status are additionally presented. Vaccination characteristics for those with BTI are reported as well as BTI rates per 1,000 persons at 6 months for those vaccinated from 1 January to 31 October 2021.

To balance baseline characteristics, including predefined and high-dimensional variables across comparison groups, we applied an overlap weighting approach in our analyses. In brief, logistic regressions were constructed for probability of group membership of the groups being compared, using the predefined and high-dimensional covariates as independent variables, in separate subcohorts with no prior history of the outcome being examined, estimating propensity scores of the probability of group assignment33,34. In consideration of variability in duration of potential follow-up, calendar week of enrollment was included to balance length of follow-up between cohorts (uncensored duration of follow-up was included for comparison versus seasonal influenza). Propensity scores were then used in construction of the overlap weights whose application achieved similar baseline characteristic distributions across groups while providing higher weights to those with baseline characteristics more similar to those in other groups. Weights were then applied to Cox survival models to estimate HRs, where follow-up started 30 days after the date of testing positive. Standard errors were estimated by applying the robust sandwich variance estimator method. Covariate balance among all predefined and high-dimensional variables were assessed for each model through the standardized mean difference, where a difference <0.1 was taken as evidence of balance. We estimated the incidence rate difference (referred to as excess burden) between groups per 1,000 participants at 6 months after the start of follow-up based on the difference in survival probability in the relevant groups.

We first examined the risk and excess burden of individual post-acute sequelae, post-acute sequelae by organ system, at least one post-acute sequela and death between the BTI group, those with SARS-CoV-2 infection without prior vaccination and the contemporary control. We then compared risks of the BTI group with the historical control and, separately, with the vaccinated control.

Further analyses were conducted to better understand the risk in BTI versus the contemporary control. To investigate risk of post-acute sequalae before and after 90 days of follow-up, we conducted analyses that examined risk during the first 30–90 days, and during the 90–180 days, after T0. Examination of the risk from the 90–180 days was done overall, for incident outcomes during this period (where there was no record of the outcome during the 30–90-day period) and for recurrent or persistent outcomes during this period (where there was a prior record of the outcome during the 30–90-day period). We then comparatively evaluated the risks between the BTI and contemporary control based on their immunocompromised status, where immunocompromised status was defined (according to the CDC definition) by a history of organ transplantation, advanced kidney disease (an estimated glomerular filtration rate of less than 15 ml/min/1.73 m2 or end-stage renal disease), cancer, HIV or conditions with prescriptions of more than 30-day use of corticosteroids or immunosuppressants, including systemic lupus erythematosus and rheumatoid arthritis. We lastly compared the risks and burden of death, at least one PASC, pulmonary disorders and extrapulmonary disorders within those with BTI by type of vaccination received.

We then examined the risk and excess burden associated with BTI by care setting of the acute phase of the disease. Risks were estimated for individual sequelae and risks and excess burden of organ system involvement, at least one post-acute sequela and death in those with a BTI who were not hospitalized, who were hospitalized and who were admitted to ICU during the 5 days before and 30 days after their positive SARS-CoV-2 test compared to the contemporary control group.

We additionally examined differences in risk and burden between BTI and SARS-CoV-2 infection without prior vaccination by severity of the acute phase of the disease (non-hospitalized, hospitalized and admitted to ICU).

Finally, we compared the risks and excess burden of individual post-acute sequelae, post-acute sequelae by organ system, at least one post-acute sequela and death between those hospitalized with BTI and those hospitalized with seasonal influenza.

Positive and negative controls

We examined, as positive outcome controls, the risks of fatigue in those with SARS-CoV-2 infection without prior vaccination compared to the contemporary and historical control groups as a means of testing whether our approach would reproduce established knowledge8,9,10,11,12.

The application of negative outcome control may help detect both suspected and unsuspected sources of spurious biases. We, therefore, tested comparing BTI to the contemporary and historical controls, the risk of atopic dermatitis, accidental poisoning, accidental injury, fitting of a hearing aid or contact lenses, ingrown toenail and scarring as negative outcome controls—where no prior knowledge suggests that an association is expected. Additionally, we tested a pair of negative-exposure controls; we expected that receipt of the influenza vaccine on odd-numbered (n = 605,453) versus even-numbered (n = 571,291) calendar days between 1 March 2020 and 15 January 2021 would be associated with similar risks of the outcomes examined in our analyses. The successful testing of positive outcome controls, negative outcome controls and negative exposure controls may lessen concerns about biases related to study design, covariate selection, analytic approach, outcome ascertainment, unmeasured confounding and other potential sources of latent biases35,36.

All analyses were two-sided. In all analyses, a 95% CI that excluded unity was considered evidence of statistical significance. All analyses were conducted in SAS Enterprise Guide 8.2, and all figures were generated in R version 4.0.4. This study was approved by the VA St. Louis Health Care System Institutional Review Board (protocol no. 1606333).

Reporting summary

Further information on research design is available in the Nature Research Reporting Summary linked to this article.

Data availability

The data that support the findings of this study are available from the US Department of Veterans Affairs. VA data are made freely available to researchers behind the VA firewall with an approved VA study protocol. For more information, visit https://www.virec.research.va.gov or contact the VA Information Resource Center at VIReC@va.gov.

Code availability

The analytic code is available at https://github.com/BcBowe3/Breakthrough.

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COVID-19 Vaccine Boosters for Young Adults: A Risk-Benefit Assessment and Five Ethical Arguments against Mandates at Universities

Authors: Kevin Bardosh University of Washington; University of Edinburgh – Edinburgh Medical School Allison Krug Artemis Biomedical Communications LLC Euzebiusz Jamrozik University of Oxford Trudo Lemmens University of Toronto – Faculty of Law Salmaan KeshavjeeHarvard University – Harvard Medical School Vinay Prasad University of California, San Francisco (UCSF) Martin A. Makary Johns Hopkins University – Department of Surgery Stefan Baral John Hopkins University Tracy Beth Høeg Florida Department of Health; Sierra Nevada Memorial HospitalDate Written: August 31, 2022

Abstract

Students at North American universities risk disenrollment due to third dose COVID-19 vaccine mandates. We present a risk-benefit assessment of boosters in this age group and provide five ethical arguments against mandates. We estimate that 22,000 – 30,000 previously uninfected adults aged 18-29 must be boosted with an mRNA vaccine to prevent one COVID-19 hospitalisation. Using CDC and sponsor-reported adverse event data, we find that booster mandates may cause a net expected harm: per COVID-19 hospitalisation prevented in previously uninfected young adults, we anticipate 18 to 98 serious adverse events, including 1.7 to 3.0 booster-associated myocarditis cases in males, and 1,373 to 3,234 cases of grade ≥3 reactogenicity which interferes with daily activities. Given the high prevalence of post-infection immunity, this risk-benefit profile is even less favourable. University booster mandates are unethical because: 1) no formal risk-benefit assessment exists for this age group; 2) vaccine mandates may result in a net expected harm to individual young people; 3) mandates are not proportionate: expected harms are not outweighed by public health benefits given the modest and transient effectiveness of vaccines against transmission; 4) US mandates violate the reciprocity principle because rare serious vaccine-related harms will not be reliably compensated due to gaps in current vaccine injury schemes; and 5) mandates create wider social harms. We consider counter-arguments such as a desire for socialisation and safety and show that such arguments lack scientific and/or ethical support. Finally, we discuss the relevance of our analysis for current 2-dose CCOVIDovid-19 vaccine mandates in North America.

Download Complete Study Publication

https://papers.ssrn.com/sol3/Delivery.cfm/SSRN_ID4206070_code5055014.pdf?abstractid=4206070&mirid=1

COVID VAX REGRET: Horrific injuries, lack of support, and inexcusable “black hole” for injury claims against pharma and US government

Authors: S.D. Wells 09/06/2022 / Pandemic News

Impaired immunity is about the worst “side effect” from COVID vaccines that the majority of Americans would want to avoid, not run towards, seeing as how so many people are already suffering from obesity, cancer, heart disease, diabetes and dementia. Fear of COVID outweighed the fear of this because people have been brainwashed by their televisions, their newspapers and those pharma-shilling websites, so they run out and get jabbed up with Fauci Flu shots to try to save themselves from sure destruction, when that ironically is what they are injected with.

The already-immune-compromised “sheeple” are getting “shot” up with millions of toxic prions (that keep multiplying as mRNA) that drive chronic inflammation, while devastating the immune system, which in turn exacerbates their current health “conditions,” (preventable diseases and disorders), and sometimes to the point of “unexplainable” sudden death.

Is it too late for the injected sheeple? Can they sue? Will the next “flu” kill them all off, or will it be unexplainable, sudden-inflicted myocarditis? Are all the microscopic blood clots the REASON for the heart irregularities, cancer reemergence and spontaneous abortions? This deserves careful consideration. Time to take an inside look.

While fighting cancer with chemicals that spread cancer, Dan Bongino went and did the unthinkable – he got “vaccinated” with millions of prions that cause all of the body system issues that literally fuel cancer development, including inflammation, immune system dysfunction, pollution of the cleansing organs and massive stress. That’s why health advocates avoid the Fauci Flu shots like the plague, and that’s why they’re nicknamed “clot shots” and “death stabs.”

Dan Bongino, a former Secret Service agent, just blew the whistle on the establishment, the vaccine industrial complex, and he says he fell for the ploy because he was “scared.” Well, fear is big business in America, and Pharma is running the whole gamut, play by play.

As Tucker Carlson revealed on Fox News (he’s the only real truth seeker left at the network), the COVID vaccine’s suppression of the immune system has a “wide range of consequences, not the least of which include the reactivation of latent viral infections and the reduced ability to effectively combat future infections.”

Let that sink in for a minute … “the reduced ability to effectively combat future infections.” Isn’t that cancer? That’s the last thing any person fighting cancer should ever do to their body, but it’s the first thing everyone jumped to do that lost the virus mania “fear” battle with their (fake news) television and the highly corrupt CDC – Centers for Disease Continuance.

There’s a huge black hole for the COVID-vaccine-injured sheeple who hope to win lawsuits trying to sue anyone who pushed the vaccines on them

Law firms are litigating more vaccine-related injury claims than ever before in the history of vaccines, but that doesn’t mean they’re winning the cases or even gaining settlements for their clients. Big Pharma and crooked Congress have created a massive wall, a legal barrier, to protect their own interests and agenda in depopulation and population control. How? They can’t be sued for injury, wrong-doing, conspiring to kill – anything. The entire industry (the vaccine industrial complex) is immune from the Constitution.

Law firms are covered up trying to handle all the vaccine-related injury cases that involve people suddenly suffering from blood clots and cardiac inflammation. In fact, these lawyers are so covered up with filings, while gaining little traction as far as winning cases or money, that they’re starting to turn people away, saying “you have the right to file” but that you also “have the right to lose.”

Bookmark Vaccines.news to your favorite independent websites for updates on experimental “vaccines” that cause blood clots, myocarditis, chronic inflammation and post-vaccine-regret.

FDA restricts J&J’s COVID-19 vaccine due to blood clot risk

Authrsors: Associated Press

WASHINGTON (AP) — U.S. regulators on Thursday strictly limited who can receive Johnson & Johnson’s COVID-19 vaccine due to the ongoing risk of rare but serious blood clots.

The Food and Drug Administration said the shot should only be given to adults who cannot receive a different vaccine or specifically request J&J’s vaccine. U.S. authorities for months have recommended that Americans starting their COVID-19 vaccinations use the Pfizer or Moderna shots instead.

FDA officials said in a statement that they decided to restrict J&J’s vaccine after taking another look at data on the risk of life-threatening blood clots within two weeks of vaccination.

J&J’s vaccine was initially considered an important tool in fighting the pandemic because it required only one shot. But the single-dose option proved less effective than two doses of the Pfizer and Moderna vaccines.

Under the new FDA instructions, J&J’s vaccine could still be given to people who had a severe allergic reaction to one of the other vaccines and can’t receive an additional dose. J&J’s shot could also be an option for people who refuse to receive the mRNA vaccines from Pfizer and Moderna, and therefore would otherwise remain unvaccinated, the agency said.

A J&J spokesman said in an emailed statement: “Data continue to support a favorable benefit-risk profile for the Johnson & Johnson COVID-19 vaccine in adults, when compared with no vaccine.”

Despite the restriction, FDA’s vaccine chief Dr. Peter Marks said J&J’s vaccine “still has a role in the current pandemic response in the United States and across the global community.”

The FDA based its decision on “our safety surveillance systems and our commitment to ensuring that science and data guide our decisions

Nearly 15 million deaths associated with COVID-19, WHO says

The clotting problems first came up last spring, with the J&J shot in the U.S. and with a similar vaccine made by AstraZeneca that is used in other countries. At that time, U.S. regulators decided the benefits of J&J’s one-and-done vaccine outweighed what was considered a very rare risk — as long as recipients were warned.

COVID-19 causes deadly blood clots, too. But the vaccine-linked kind is different, believed to form because of a rogue immune reaction to the J&J and AstraZeneca vaccines because of how they’re made. It forms in unusual places, such as veins that drain blood from the brain, and in patients who also develop abnormally low levels of the platelets that form clots. Symptoms of the unusual clots include severe headaches a week or two after the J&J vaccination — not right away — as well as abdominal pain and nausea.

The New Brunswick, New Jersey-based company announced last month that it didn’t expect a profit from the vaccine this year and was suspending sales projections.

The rollout of the company’s vaccine was hurt by a series of troubles, including manufacturing problems at a Baltimore factory that forced J&J to import millions of doses from overseas.

Additionally, regulators added warnings about the blood clots and a rare neurological reaction called Guillain-Barré syndrome.

Pfizer and Moderna have provided the vast majority of COVID-19 vaccines in the U.S. More than 200 million Americans have been fully vaccinated with the companies’ two-dose shots while less than 17 million Americans got the J&J shot.

UK Bans COVID Vax for Kids – Investigation Finds Vaccine Affects Sexual Development in Little Boys

Authors:  Jim Hoft September 7, 2022 Gateway Pundit

The UK Health Security Agency banned the COVID vaccine from childrenwho had not turned five by the end of last month. The UK will no longer offer the vaccine to children aged 5 to 11.

Wolf also discussed a recent investigation that revealed the devastating affects of the vaccine on little boys. According to Dr. Naomi Wolf, the vaccine is hindering the development of the testes of pre-adolescent boys. This is a catastrophe.

The vaccines hurt the testes and hurt the parts of the testes that develop the masculinity and secondary sex characteristics of little boys, and baby boys, and teenage boys. So they literally harm the chances of your little boy child to grow up normally as a male human adult.

Risk of Myocarditis After Sequential Doses of COVID-19 Vaccine and SARS-CoV-2 Infection by Age and Sex

Authors: Martina Patone, PhD; Xue W. Mei, PhD; Lahiru Handunnetthi, PhD; Sharon Dixon, MD; Francesco Zaccardi, PhD; Manu Shankar-Hari, PhD; Peter Watkinson, MD; Kamlesh Khunti, PhD; Anthony Harnden, PhD; Carol A.C. Coupland, PhD; Keith M. Channon, MD; Nicholas L. Mills, PhD; Aziz Sheikh, MD; Julia Hippisley-Cox, MD August 28, 2022 ORIGINAL RESEARCHARTICLECirculation. 2022;146:00–00. DOI: 10.1161/CIRCULATIONAHA.122.059970 xxx xxx, 20223Patone et al

BACKGROUND: Myocarditis is more common after severe acute respiratory syndrome coronavirus 2 infection than after COVID-19 vaccination, but the risks in younger people and after sequential vaccine doses are less certain.

METHODS:

A self-controlled case series study of people ages 13 years or older vaccinated for COVID-19 in England between December 1, 2020, and December 15, 2021, evaluated the association between vaccination and myocarditis, stratified by age and sex. The incidence rate ratio and excess number of hospital admissions or deaths from myocarditis per million people were estimated for the 1 to 28 days after sequential doses of adenovirus (ChAdOx1) or mRNA-based (BNT162b2, mRNA-1273) vaccines, or after a positive SARS-CoV-2 test.RESULTS: In 42842345 people receiving at least 1 dose of vaccine, 21242629 received 3 doses, and 5934153 had SARS-CoV-2 infection before or after vaccination. Myocarditis occurred in 2861 (0.007%) people, with 617 events 1 to 28 days after vaccination. Risk of myocarditis was increased in the 1 to 28 days after a first dose of ChAdOx1 (incidence rate ratio, 1.33 [95% CI, 1.09–1.62]) and a first, second, and booster dose of BNT162b2 (1.52 [95% CI, 1.24–1.85]; 1.57 [95% CI, 1.28–1.92], and 1.72 [95% CI, 1.33–2.22], respectively) but was lower than the risks after a positive SARS-CoV-2 test before or after vaccination (11.14 [95% CI, 8.64–14.36] and 5.97 [95% CI, 4.54–7.87], respectively). The risk of myocarditis was higher 1 to 28 days after a second dose of mRNA-1273 (11.76 [95% CI, 7.25–19.08]) and persisted after a booster dose (2.64 [95% CI, 1.25–5.58]). Associations were stronger in men younger than 40 years for all vaccines. In men younger than 40 years old, the number of excess myocarditis events per million people was higher after a second dose of mRNA-1273 than after a positive SARS-CoV-2 test (97 [95% CI, 91–99] versus 16 [95% CI, 12–18]). In women younger than 40 years, the number of excess events per million was similar after a second dose of mRNA-1273 and a positive test (7 [95% CI, 1–9] versus 8 [95% CI, 6–8]).CONCLUSIONS: Overall, the risk of myocarditis is greater after SARS-CoV-2 infection than after COVID-19 vaccination and remains modest after sequential doses including a booster dose of BNT162b2 mRNA vaccine. However, the risk of myocarditis after vaccination is higher in younger men, particularly after a second dose of the mRNA-1273 vaccine.

We recently reported an association between the first and second dose of COVID-19 vaccination and myocarditis, which generated considerable scientific, policy, and public interest.1 It added to evidence emerging from multiple countries that has linked exposure to BNT162b2 mRNA vaccine with acute myocarditis.2–8In the largest and most comprehensive analysis to date, we reported an increased risk of hospital admission or death from myocarditis after both adenoviral (ChAdOx1) vaccines and mRNA (BNT162b2 or mRNA-1273) vac-cines. It is important that we also demonstrated across the entire vaccinated population in England that the risk of myocarditis after vaccination was small compared with the risk after a positive SARS-CoV-2 test.1However, myocarditis is more common in younger people younger than the age of 40 years and in men in particular.9,10 Additional analyses stratified by age and sex are important because vaccine campaigns are rap-idly being extended to include children and young adults. Furthermore, given the consistent observation that the risk of myocarditis is higher after the second dose of vac-cine compared with the first dose,1,11 there is an urgent need to evaluate the risk associated with a booster dose because booster programs are accelerated internation-ally to combat the omicron variant.12Because new data were available, we have extended our analysis to include people ages 13 years or older and those receiving a booster dose to further evaluate the association between COVID-19 vaccination or infection and risk of myocarditis, stratified by age and sex.

METHODS

Transparency and Openness Promotion This analysis makes use of multiple routinely collected health care data sources that were linked, deidentified, and held in a trusted research environment that was accessible to approved individuals who had undertaken the necessary governance training. Because of the sensitive nature of the data collected for this study, requests to access the dataset from qualified researchers trained in human subject confidentiality proto-cols may be sent to National Health Service Digital and the United Kingdom Health Security Agency. Simulated data and the analysis code are available publicly at https://github.com/qresearchcode/COVID-19-vaccine-safety. National Health Service Research Ethics Committee approval was obtained from the East Midlands–Derby Research Ethics Committee (Reference 18/EM/0400]. Anonymized data are analyzed, so there is no requirement for written informed consent. Data Sources We used the National Immunisation Database of COVID-19 vaccination to identify vaccine exposure. This includes vaccine type, date, and doses for all people vaccinated in England. We linked National Immunisation Database vaccination data, at the individual level, to national data for mortality (Office for National Statistics), hospital admissions (Hospital Episode Statistics and Secondary User’s service data), and SARS-CoV-2 infection data (Second Generation Surveillance System).Study Design and Oversight We undertook a self-controlled case series design, originally developed to examine vaccine safety.12 The analyses are conditional on each case, so any fixed characteristics during the study period, such as sex, ethnicity, or chronic conditions, are inherently controlled for. Age was considered as a fixed variable because the study period was short. Any time-varying factors, such as seasonal variation, need to be adjusted for in the analy-ses. Hospital admissions were likely to be influenced by the pressure on the health systems because of COVID-19, which was not uniform during the pandemic study period. To allow for these underlying seasonal effects, we split the study observation period into weeks and adjusted for week as a factor vari-able in the statistical models.Study Period and Population We included all people ages 13 years or older who had received at least 1 dose of ChAdOx1 (AstraZeneca), BNT162b2 (Pfizer), and mRNA-1273 (Moderna) vaccine and were admit-ted to hospital or died from myocarditis between December 1, 2020, and December 15, 2021.OutcomeThe primary outcome of interest was the first hospital admis-sion caused by the myocarditis, or death recorded on the death Clinical PerspectiveWhat Is New?•We performed an evaluation of the risk of myocar-ditis after COVID-19 vaccine in >42 million vacci-nated people 13 years or older, including 21 million people receiving a booster dose, stratified by age and sex.•We extend our previous findings demonstrating that the risk of hospitalization or death from myo-carditis after SARS-CoV-2 infection is substantially higher than the risk associated with a first dose of ChAdOx1, and a first, second, or booster dose of BNT162b2 mRNA vaccine.

•Associations were stronger in younger men <40 years for all vaccines and after a second dose of mRNA-1273 vaccine, where the risk of myocarditis was higher after vaccination than SARS-CoV-2 infection. What Are the Clinical Implications?•Our findings will inform recommendations on the type of vaccine offered to younger people and will help to shape public health policy on booster pro-grams enabling an informed discussion of the risk of vaccine associated myocarditis when considering the net benefit of vaccination.

Myocarditis After COVID-19 Vaccine and Infection certificate with the International Classification of Diseases, Tenth Revision code (Table S1) related to myocarditis within the study period (December 1, 2020, to December 15, 2022). We used the earliest date of hospitalization or date of death as the event date.ExposuresThe exposure variables were a first, second, or booster dose of the ChAdOx1, BNT162b2, or mRNA-1273 vaccines, and SARS-CoV-2 infection, defined as the first SARS-CoV-2–positive test in the study period. All exposures were included in the same model. We defined the exposure risk intervals as the following prespecified time periods: 0, 1 to 7, 8 to 14, 15 to 21, and 22 to 28 days after each exposure date, under the assumption that the adverse events under consideration are unlikely to be related to exposure later than 28 days after expo-sure. A pre-risk interval of 1 to 28 days before each exposure date was included to account for potential bias that might arise if the occurrence of the outcome temporarily influenced the likelihood of exposure. The baseline period for the vaccination exposures was the remaining time from December 1, 2020, until 29 days before the first dose date and from 29 days after the first or second dose until 29 days before the second or booster dose (if applicable), and from 29 days after the booster dose until December 15, 2021, or the censored date if earlier. We assumed that the risks might be different after each vac-cine dose, and hence we allowed for a dose effect, by defining a separate risk interval after each dose: 0, 1 to 7, 8 to 14, 15 to 21, or 22 to 28 days after the first, second, or booster dose. To avoid overlapping risk periods, we assumed that later expo-sures take precedence over earlier ones, except for the 1- to 28-day pre-risk period for the second or booster dose. A posi-tive SARS-CoV-2 test was considered as a separate exposure in the models, which allowed overlapping risk windows with vaccination exposure.Statistical AnalysisWe described the characteristics of the whole study population by vaccine dose and type, and in those with myocarditis strati-fied by age and sex.In vaccinated people with myocarditis, the self-controlled case series models were fitted using a conditional Poisson regression model with an offset for the length of the expo-sure risk period. Incidence rate ratios (IRR), the relative rate of hospital admissions or deaths caused by myocarditis in expo-sure risk periods relative to baseline periods, and their 95% CIs were estimated by the self-controlled case series model adjusted for calendar time. We investigated if associations between vaccine exposure and the myocarditis outcome were sex- or age-dependent by performing subgroup analyses strati-fied by sex and age (men age <40 years, men age≥ 40 years, women age <40 years, and women age ≥40 years). We also conducted analyses stratified by vaccination history, restricted to those who had the same type of vaccine in the first and sec-ond dose and by lag in days between the first and second dose (≤65, 66 to 79, and ≥80 days).We conducted sensitivity analyses to assess the robustness of results to assumptions, such as that the occurrence of an outcome event did not influence the probability of subsequent exposures by (1) excluding those who died from the outcome and (2) restricting analysis to the period after the first dose and (3) after the second dose, without censoring at death; and to assess potential reporting delays in the data by (4) restricting the study to the period up to December 1, 2021.We also performed sensitivity analyses (5) removing patients who had outcomes in the 28 days after a first dose, but before a second dose, and (6) removing patients who had outcomes in the 28 days after a second dose, but before a booster dose, because they are less likely to have a second dose if they experienced an adverse event after the first. Last, we conducted a sensitivity analysis (7) restricted to those with-out a positive SARS-CoV-2 test during the observation period.We used Stata (version 17) for these analyses.

RESULTS

Between December 1, 2020, and December 15, 2021, there were 42 842 345 people vaccinated with at least 1 dose of ChAdOx1 (n=20 650 685), BNT162b2 (n=20 979 704), or mRNA-1273 (n=1 211 956) (Table 1). Of these, 39 118 282 received a sec-ond dose of ChAdOx1 (n=20 080 976), BNT162b2 (n=17 950 086), or mRNA-1273 (n=1 087 220), and 21 242 629 people received a third vaccine dose: ChAdOx1 (n=53 606), BNT162b2 (n=17 517 692), and mRNA-1273 (n=3 671 331).Among people receiving at least 1 vaccine dose, 5 934 153 (13.9%) tested positive for SARS-CoV-2, including 2 958 026 (49.8%) before their first vac-cination.Of the 42 842 345 people in the study population, 2861 (0.007%) were hospitalized or died from myocar-ditis during the study period; 345 (<0.001%) patients died within 28 days from a hospital admission with myo-carditis or with myocarditis as cause of death recorded in the death certificate. A total of 617 (0.001%) of these events occurred 1 to 28 days after any dose of vaccine (Table 2). Of the 524 patients admitted to the hospital with myocarditis in the 1 to 28 days after any first or sec-ond vaccine dose, 151 (28.8%) had received a booster dose: 34.4% (79/230) of those who had ChAdOx1 in the first or second dose and 29.7% (72/243) of those who had BNT162b2 in the first or second dose (Table 2). Of the 5 934 153 patients with a SARS-CoV-2 infection, 195 (0.003%) were hospitalized or died with myocarditis in the 1 to 28 days after the positive test; 114 (58.5%) of these events occurred before vaccination (Table S2).Vaccine-Associated MyocarditisIn the study period, we observed 140 and 90 patients who were admitted to the hospital or died of myocardi-tis after a first and second dose of ChAdOx1 vaccine, respectively. Of these, 40 (28.6%) and 11 (12.2%)‚ re-spectively, died with myocarditis or within 28 days from hospital admission. Similarly, there were 124, 119, and 85 patients who were admitted to the hospital or died

After COVID-19 Vaccine and Infection Table 1.Baseline Demographic Characteristics of People Receiving ChAdOx1, BNT162b2, or mRNA-1273 Vaccines or Testing Positive for SARS-CoV-2 Virus (in Those Vaccinated) in England Between December 1, 2020, and December 15, 2021 ChAdOx1BNT162b2mRNA-1273ChAdOx1BNT162b2mRNA-1273ChAdOx1BNT162b2mRNA-1273SARS- CoV-2 positive*One dose (n=42 842 345)Two doses (n=39 118 282)Booster doses (n=21 242 629)(n= 5 934 153)% (n)% (n) % (n)% (n)% (n)% (n)% (n)% (n)% (n)% (n)Total no. of people20 650 68520 979 7041 211 95620 080 97617 950 0861 087 22053 60617 517 6923 671 3315 934 153SexWomen49.5(10 215 079)49.1(10 295 561)38.7(469 114)49.5(9 945 533)50.1(9 000 748)39.5(429 705)61.2(32 792)54.2(9 489 364)48.4(1 778 317)52.3(3 103 168)Men43.3(8 933 572)40.4(8 476 032)42.0(508 416)43.3(8 697 560)39.8(7 148 539)42.1(457 629)34.8(18 674)41.4(7 244 858)44.2(1 623 230)40.5(2 405 336)Not recorded7. 3(1 502 034)10.5(2 208 110)19.3(234 426)7. 2(1 437 882)10.0(1 800 799)18.4(199 886)4.0(2140)4.5(783 471)7. 3(269 784)7. 2(425 649)Age, yMean age (SD)54.9 (14.8)43.0 (22.4)32.3 (9.7)55.0 (14.7)46.5 (21.7)32.7 (9.8)63.1 (17.0)61.8 (15.9)53.7 (12.4)41.4 (18.0)13–17 <0.1(10 214)10.6(2 219 006)0.1(838)<0.1(9105)2.6(468 569)0.1 (623)0.1 (31)0.1(23 826)0.1(2961)8.3(493 728)18–29 5.2(1 081 177)24.4(5 127 151)43.1(521 916)5.1(1 022 847)24.9(4 472 159)41.3(449 436)3.7(1964)3.6(624 465)4.0(146 688)21.6(1 279 933)30–39 7. 9(1 634 841)21.5(4 517 781)35.6(431 515)7. 8(1 556 785)23.1(4 146 117)36.1(392 581)5.8(3102)6.1(1 067 916)8.6(315 936)18.3(1 084 406)40–49 22.1(4 564 393)8.5(1 784 664)18.4(222 849)22.0(4 414 864)9.3(1 665 983)19.5(212 187)11.5 (6171)11.1(1 949 092)19.2(706 004)19.4(1 152 196)50–59 2 7. 5(5 673 878)8.0(1 684 013)1.8(22 320)2 7. 6(5 549 187)9.1(1 636 430)1.9(20 463)19.9(10 644)20.8(3 635 337)35.3(1 295 168)16.7(989 499)60–69 19.8(4 083 887)8.5(1 777 370)0.7(8330)20.0(4 013 588)9.8(1 753 552)0.7(8145)19.3(10 371)22.5(3 938 515)24.8(910 586)8.5(505 389)70–79 13.4(2 763 041)9.4(1 979 901)0.3(3241)13.5(2 717 638)10.9(1 959 318)0.3(2789)22.6(12 090)23.1(4 049 042)6.5(237 287)4.2(248 415)80–89 3.1(630 457)7. 7(1 621 129)0.1(842)3.0(604 788)8.9(1 591 216)0.1(837)12.5 (6710)10.8(1 888 973)1.3(47 228)2.2(132 459)90+ 1.0(208 753)1.3(268 563)<0.1(103)1.0(192 162)1.4(256 698)<0.1(158)4.7(2523)1.9(340 498)0.3(9473)0.8(48 117)Not recorded<0.1 (44)<0.1 (125)<0.1 (2)<0.1 (11)<0.1 (44)<0.0 (1)0<0.1 (29)0<0.1 (11)Women age groups, y <40 14.8(1 510 119)51.7(5 325 910)7 7. 9(365 443)14.4(1 437 517)45.9(4 131 123)76.4(328 311)9.2(3020)10.9(1 032 366)14.2(252 054)4 7. 6(1 477 776)≥40 85.2(8 704 960)48.3(4 969 651)22.1(103 671)85.5(8 508 009)54.1(4 869 604)23.6(101 394)90.8(29 772)89.1(8 456 981)85.8(1 526 263)52.4(1 625 385) Not recorded<0.1 (16)<0.1 (59)0<0.1 (7)<0.1 (21)0000<0.1 (7)Men age groups, y<40 11.2(998 025)56.2(4 762 038)78.2(397 521)10.9(949 865)49.4(3 533 806)76.7(35 074)8.8(1650)7. 5(541 432)10.5(171 132)46.2(1 110 723)≥40 88.8(7 935 546)43.8(3 712 994)21.8(110 895)89.1(7 747 692)50.8(3 614 721)23.3(106 834)91.2(17 024)92.5(6 703 416)89.5(1 452 098)53.8(1 294 609) Not recorded<0.1 (21)<0.1 (42)<0.1 (2)<0.1 (3)<0.1 (12)<0.1 (1)000<0.1 (4)EthnicityWhite6 7. 9(14 012 353)63.6(13 344 722)53.0(642 168)68.0(13 656 716)64.2(11 530 182)54.0(587 123)74.3(39 827)73.6(12 891 303)69.6(2 553 453)66.9(3 971 366)Indian2.0(406 066)2.2(469 302)1.1(13 385)2.0(395 171)2.2(394 274)1.1(11 902)2.1(1141)2.0(354 433)1.4(51 193)2.6(153 403)Pakistani1.2(253 523)1.6(335 100)1.0(12 213)1.2(239 511)1.4(249 446)0.9(9732)0.9(477)0.6(109 038)0.5(19 186)2.0(118 522)Bangladeshi0.5 (96 392)0.5 (111 314)0.5 (5966)0.5 (92 835)0.5 (83 524)0.5 (4902)0.4 (217)0.2 (43 360)0.3 (10 775)0.7 (40 093)Other Asian0.9 (177 629)1.1 (238 245)1.0 (11 859)0.9 (171 863)1.1 (191 996)1.0 (10 365)0.8 (436)0.7 (128 434)0.6 (23 284)1.1 (67 392)Caribbean0.6 (117 507)0.5 (96 994)0.4 (4265)0.6 (110 470)0.4 (80 146)0.3 (3296)1.3 (706)0.4 (77 095)0.3 (11 820)0.5 (28 327)(Continued)ORIGINAL RESEARCHARTICLECirculation. 2022;146:00–00. DOI: 10.1161/CIRCULATIONAHA.122.059970xxx xxx, 20225Patone et alMyocarditis After COVID-19 Vaccine and Infectionof myocarditis after a first, second, and third dose of BNT162b2 vaccine, respectively. Of these, 22 (17.7%), 14 (11.8%), and 13 (15.3%) patients died with myo-carditis or within 28 days from hospital admission. Last, there were 11, 40, and 8 patients who were admitted to the hospital for myocarditis after, respectively, a first, second, and third dose of mRNA-1273 vaccine. None of these patients died with myocarditis or within 28 days from hospital admission with myocarditis (Table2).In the overall population, we confirmed our previous findings that the risk of hospitalization or death from myocarditis was higher after SARS-CoV-2 infection than vaccination and was greater after the first 2 doses of mRNA vaccine than after adenovirus vaccine (Table3; Table S3; Figure). There was an increased risk of myo-carditis at 1 to 28 days after the first dose of ChAdOx1 (IRR, 1.33 [95% CI, 1.09–1.62]) and BNT162b2 (IRR, 1.52 [95% CI, 1.24–1.85]).There was an increased risk of myocarditis at 1 to 28 days after a second dose of BNT162b2 (IRR, 1.57 [95% CI, 1.28–1.92]) and mRNA-1273 (IRR, 11.76 [95% CI, 7.25–19.08]); and after a booster dose of BNT162b2 (IRR, 1.72 [95% CI, 1.33–2.22]) and mRNA-1273 (IRR, 2.64 [95% CI, 1.25–5.58]).Vaccine-Associated Myocarditis in MenOf the 17918020 men vaccinated in England in the study period, 6158584 (34.4%) were younger than 40 years, and 11759 436 (65.6%) were 40 years or older (Table1). Analysis restricted to younger men age younger than 40 years showed an increased risk of myocarditis Black African0.9 (185 852)1.0 (218 158)1.0 (12 121)0.9 (176 094)0.9 (164 260)0.9 (9258)1.1 (588)0.6 (98 216)0.5 (16 997)1.0 (57 157)Chinese0.3 (63 180)0.3 (70 206)0.4 (5176)0.3 (61 902)0.3 (58 438)0.5 (4902)0.3 (149)0.3 (47 390)0.3 (11 899)0.2 (11 732)Other1.8 (378 719)2.4 (502 815)2.6 (31 811)1.8 (363 257)2.2 (388 674)2.5 (27 107)1.7 (902)1.4 (245 301)1.4 (50 501)2.3 (138 024)Not recorded24.0(4 959 464)26.7(5 592 847)39.0(472 992)24.0(4 813 156)26.8(4 809 146)38.5(418 633)1 7. 1(9163)20.1(3 523 123)25.1(922 223)22.7(1 348 137)History of myocarditis Previous myo-carditis<0.1 (1837)<0.1 (1632)<0.1 (69)<0.1 (1778)<0.1 (1511)<0.1 (56)<0.1 (18)<0.1 (1885)<0.1 (272)<0.1 (687)COVID-19 status†No COVID-1986.3(17 815 732)86.0(18 052 842)85.8(1 039 833)86.3(17 334 448)8 7. 3(15 674 125)86.2(937 147)88.4(47 367)90.5(15 846 583)88.0(3 230 055)…COVID-19 previous vac-cination5.9(1 227 131)7. 8(1 629 334)8.4(101 484)5.9(1 183 882)6.5(1 170 434)7. 8(85 166)6.3(3398)4.7 (815 805)5.3(194 056)49.8(2 958 026)COVID-19 after first dose0.7(143 526)2.8(594 914)3.2(38 200)0.5(99 981)2.2(401 516)3.0(32 222)0.9(456)0.6 (108 097)0.4(15 316)13.1(776 725)COVID-19 after second dose6.7(1 383 490)3.0(638 578)2.7(32 215)6.9(1 381 868)3.6(639 976)3.0(32 452)1.8(969)3.5 (621 836)5.8(213 627)34.6(2 054 331)COVID-19 after booster dose0.4(80 807)0.3(64 035)<0.1(224)0.4(80 796)0.4(64 035)<0.1(233)2.6(1416)0.7(125 372)0.5(18 277)2.4(145 071)No. of dosesOne dose only2.3(467 328)14.8(3 114 034)11.9(144 026)………………12.8(761 515)Two doses only36.0(7 430 747)45.1(9 464 269)80.8(979 495)36.5(7 328 422)53.2(9 550 989)91.7(996 599)………51.5(3 054 000)Two doses + booster61.8(12 752 610)40.0(8 401 400)7. 3(88 435)63.5(12 752 553)46.8(8 399 097)8.3 (90 621)100.0(53 606)100.0(17 517 692)100.0(3 671 331)35.7(2 118 638)Type of vaccinesTwo doses of ChAdOx19 7. 0(20 040 458)……99.8(20 040 458)……83.0(44 472)55.8(9 780 549)79.1(2 903 545)46.2(2 741 419)Two doses of BNT162b2…84.9(17 815 058)……99.2(17 815 058)…5.1(2760)43.7(7 653 274)19.6(720 535)38.0(2 256 069)Two doses of mRNA-1273……8 7. 5(1 060 277)……9 7. 5(1 060 277)<0.1(8)0.3(45 269)1.2(42 783)2.5(146 385)*Among vaccinated individuals. †Determined by a SARS-CoV-2 test. Table 1.ContinuedChAdOx1BNT162b2mRNA-1273ChAdOx1BNT162b2mRNA-1273ChAdOx1BNT162b2mRNA-1273SARS- CoV-2 positive*One dose (n=42 842 345)Two doses (n=39 118 282)Booster doses (n=21 242 629)(n= 5 934 153)% (n)% (n) % (n)% (n)% (n)% (n)% (n)% (n)% (n)% (n)

After COVID-19 Vaccine and Infectionafter a first dose of BNT162b2 (IRR, 1.85 [95% CI, 1.30–2.62]) and mRNA-1273 (IRR, 3.06 [95% CI, 1.33–7.03]); and a second dose of ChAdOx1 (IRR, 2.73 [95% CI, 1.62–4.60]), BNT162b2 (IRR, 3.08 [95% CI, 2.24–4.24]), and mRNA-1273 (IRR, 16.83 [95% CI, 9.11–31.11]). The risk of myocarditis for older men 40 years or more was associated with a booster dose of both mRNA vaccines, BNT162b2 (IRR, 2.15 [95% CI, 1.46–3.17]) and mRNA-1273 (IRR, 3.76 [95% CI, 1.41–10.02]) (Table 3).Vaccine-Associated Myocarditis in WomenOf the 20 979 754 women vaccinated in England in the study period, 7 201 472 (34.3%) were younger than 40 Table 2. Demographic and Clinical Characteristics of Patients Who Were Admitted to the Hospital for Myocarditis in the 1 to 28 Days After a COVID-19 Vaccine First Dose, Second Dose, and Booster Dose or SARS-CoV-2 Infection Among the Vaccinated Population in England from December 1, 2020, Until December 15, 2021VariableBaselineRisk set (1–28 days after exposure)ChAdOx1BNT162b2mRNA-1273 First dose Second dose Booster dose First dose Second dose Booster dose First dose Second dose Booster dose Total no. of people22441409001241198511408Sex Women40.4 (907)40.7 (57)26.7 (24)…41.1 (51)28.6 (34)45.9 (39)*** Men59.4 (1333)59.3 (83)73.3 (66)…58.1 (72)70.6 (84)54.1 (46)>5>5>5 Not recorded0.2 (4)00…0.8 (1)0.8 (1)0000Age Mean age (SD)53.8 (19.7)57.5 (17.5)54.2 (18.0)…48.7 (24.3)45.0 (24.8)67.2 (15.8)27.0 (9.5)24.9 (6.3)61.8 (14.8) <40 y26.3 (590)14.3 (20)25.6 (23)…46.8 (58)58.8 (70)7.1 (6)>5>5≥40 y73.7 (1654)85.7 (120)74.4 (67)…53.2 (66)41.2 (49)92.9 (79)>5Deaths with myocarditis or within 28 days of hospital admission with myocarditis No. of deaths10.9 (245)28.6 (40)12.2 (11)…17.7 (22)11.8 (14)15.3 (13)……… Mean age of death (SD), y68.7 (14.3)62.1 (17.4)65.2 (10.4)…67.8 (20.4)69.2 (21.6)78 (8.7)……… No. of deaths Women38.2 (92)35.0 (14)…57.1 (12)46.1 (6)……… Men61.8 (149)65.0 (26)>5…42.9 (9)53.9 (7)> 5……… Not recorded0.2 (4)000.8 (1)0.8 (1)0COVID-19 status (positive SARS-CoV-2 test) No COVID-19…72.9 (102)82.2 (74)…71.8 (89)88.2 (105)81.2 (69)54.5 (6)90.0 (36)100.0 (8) COVID-19 previous vac-cination…12.9 (18)11.1 (10)…10.5 (13)8.2 (7)… COVID-19 after first dose…11.4 (16)…15.3 (19)… COVID-19 after second dose…5.6 (5)…5.0 (6)… COVID-19 after booster dose…7.1 (6)…No. of doses One …45.7 (64)…53.2 (66)90.9 (10)* Two …23.6 (33)60.0 (54)…16.9 (21)70.6 (84)97.5 (39)* Two + booster…30.7 (43)40.0 (36)…29.8 (37)29.4 (35)100.0 (85)100.0 (8)Type of first 2 doses received ChAdOx1…50.7 (71)98.9 (89)………49.4 (42)……62.5 (5) BNT162b2…………43.5 (54)99.2 (118)50.6 (43)……* mRNA-1273………………100.0 (40)Lag between first and second doses (days)≤655.7 (8)16.7 (15)…8.1 (10)47.9 (57)24.7 (21)55.0 (22)* 6 6–7931.4 (44)55.6 (50)…25.8 (32)32.8 (39)54.1 (46)…22.5 (9)*≥8017.1 (24)27.8 (25)…12.9 (16)19.3 (23)21.2 (18)…22.5 (9)Cells with counts <5 are suppressed. ORIGINAL RESEARCH

After COVID-19 Vaccine and Infection Table 3. Incidence Rate Ratios (IRR [95% CI]) for Main Analysis and by Age Group (Age 40 Years or Older, Younger Than 40 Years) and Sex (Female and Male) for Myocarditis in Predefined Risk Periods Immediately Before and After Exposure to Vacci-nation and Before and After a Positive SARS-CoV-2 Test Result, Adjusted for Calendar Time From December 1, 2020, to December 15, 2021 (if 1 or no events, IRR has not been estimated and reported as n/a).Time periodChAdOx1 nCoV-19 vaccineBNT162b2 mRNA vaccinemRNA-1273 vaccine Positive SARS-CoV-2 test (before vaccine)Positive SARS-CoV-2 test (vaccinated) Events I RR (95% CI) Events I RR (95% CI)Events IRR (95% CI)Events IRR (95% CI)Events IRR (95% CI)Main analysis 1–28 days: first dose/positive test before any vaccination1401.33 (1.09–1.62)1241.52 (1.24–1.85)111.85 (0.93–3.66)11411.14 (8.64–14.36)815.97 (4.54–7.87) 1–28 days: second dose900.93 (0.74–1.17)1191.57 (1.28–1.92)4011.76 (7.25–19.08) 1–28 days: booster dose*n/a851.72 (1.33–2.22)82.64 (1.25–5.58)Women 1–28 days: first dose/positive test before any vaccination571.32 (0.97–1.81)511.59 (1.16–2.20)*1.07 (0.23–4.90)4714.23 (9.34–21.68)326.87 (4.38–10.78) 1–28 days: second dose240.54 (0.35–0.83)341.04 (0.72–1.50)*3.95 (1.20–13.04) 1–28 days: booster dose*n/a391.55 (1.06–2.27)*1.51 (0.35–6.47)Men 1–28 days: first dose/positive test before any vaccination831.33 (1.03–1.72)721.47 (1.14–1.90)92.35 (1.09–5.08)679.71 (7.03–13.40)495.55 (3.91–7.88) 1–28 days: second dose661.26 (0.96–1.65)841.93 (1.51–2.45)3614.98 (8.61–26.07) 1–28 days: booster dose*n/a461.89 (1.34–2.67)63.57 (1.48–8.64)Age <40 y 1–28 days: first dose/positive test before any vaccination201.31 (0.79–2.16)581.79 (1.33–2.41)102.76 (1.32–5.75)205.25 (3.11–8.86)81.18 (0.56–2.48) 1–28 days: second dose231.69 (1.06–2.71)702.59 (1.96–3.44)3913.97 (8.07–24.19) 1–28 days: booster dose*n/a61.53 (0.64–3.64)*n/aAge ≥40 y 1–28 days: first dose/positive test before any vaccination1201.21 (0.97–1.51)661.28 (0.97–1.71)*n/a9414.87 (10.98–20.14)7310.52 (7.61–14.54) 1–28 days: second dose670.72 (0.55–0.93)490.85 (0.62–1.16)*n/a 1–28 days: booster dose*n/a791.96 (1.48–2.59)72.97 (1.32–6.69)Women age <40 y 1–28 days: first dose/positive test before any vaccination71.20 (0.51–2.84)141.65 (0.91–2.97)*2.68 (0.54–13.25)79.80 (3.70–25.97)63.98 (1.52–10.42) 1–28 days: second dose/posi-tive test after any vaccination*0.32 (0.08–1.37)91.16 (0.57–2.34)*4.75 (1.11–20.40) 1–28 days: booster dose*n/a*0.83 (0.19–3.64)*n/aMen age <40 y 1–28 days: first dose/positive test before any vaccination131.34 (0.72–2.48)431.85 (1.30–2.62)83.06 (1.33–7.03)134.35 (2.31–8.21)*0.39 (0.09–1.60) 1–28 days: second dose212.73 (1.62–4.60)603.08 (2.24–4.24)3616.83 (9.11–31.11) 1–28 days: booster dose*n/a*2.28 (0.77–6.80)*n/a(Continued )ORIGINAL

After COVID-19 Vaccine and Infection years, and 13 778 282 (65.7%) were 40 years or older (Table 1). Analysis restricted to women younger than 40 years showed an increased risk of myocarditis after a second dose of mRNA-1273 (IRR, 4.75 [95% CI, 1.11–20.40]). For women 40 years or older, there was an in-creased risk of myocarditis associated with a first (IRR, 1.57 [95% CI, 1.05–2.33]) and third (IRR, 1.76 [95% CI, 1.17–2.65]) dose of BNT162b2 vaccine. It is important that for all subgroups, the higher risk of myocarditis was found in the 1 to 7 days or 8 to 14 days after vaccination (Table S4).Vaccine-Associated Myocarditis by Vaccination History Analyses restricted to people who had the same type of vaccine for the first and second doses (Table S5) showed that for patients having a first and second dose of ChAdOx1, there was an increased risk of myocarditis associated with a booster dose of BNT162b2 (IRR, 1.78 [95% CI, 1.22–2.60]) and mRNA-1273 (IRR, 2.97 [95% CI, 1.13–7.82]). For patients who had a first and second dose of BNT162b2 vaccine, there was an increased risk of myocarditis after the second dose of BNT162b2 (IRR, 1.53 [95% CI, 1.24–1.88]). Last, for patients who had a first and second dose of mRNA-1273 vaccine, there was an increased risk of myocarditis after a second dose of mRNA-1273 (IRR, 8.63 [95% CI, 3.98–18.75]).The risk after a second dose of BNT162b2 was higher for people who received the first 2 doses within 65 days of each other (IRR, 2.16 [95% CI, 1.60–2.91]) compared with people who received the first 2 doses with a longer lag: between 66 and 79 days (IRR, 1.01 [95% CI, 0.71–1.44]) and 80 days or more (IRR, 1.40 [95% CI, 0.88–2.21]). The risk after a second dose of mRNA-1273 was higher when the lag was of 80 or more days (IRR, 22.80 [95% CI, 7.48–69.48]) compared with when the lag was 65 days or less (IRR, 7.41 [95% CI, 3.98–13.77) (Table S6).SARS-CoV-2 Infection–Associated Myocarditis There was an increased risk of myocarditis in the 1 to 28 days after a SARS-CoV-2–positive test, which was higher if infection occurred before vaccination (IRR, 11.14 [95% CI, 8.64–14.36]) than in vaccinated individuals (IRR, 5.97 [95% CI, 4.54–7.87]). The risk of myocarditis associated with a SARS-CoV-2–positive test before vaccination was higher in people 40 years or older (IRR, 14.87 [95% CI, 10.98–20.14]) than in-dividuals younger than 40 years (IRR, 5.25 [95% CI, 3.11–8.86]), but no significant difference was observed between risks in women (IRR, 14.23 [95% CI, 9.34–21.68]) and men (IRR, 9.71 [95% CI, 7.03–13.40), al-though the point estimate for women was higher than the equivalent for men. A similar pattern of risk of myo-carditis was associated with a SARS-CoV-2–positive test occurring in vaccinated individuals; however, in this case, the increased risk was substantially lower and in particular was not observed for individuals younger than 40 years (IRR, 1.18 [95% CI, 0.56–2.48]) (Table 3).Absolute and Excess Risks After the first dose of the ChAdOx1 and BNT162b2 vaccines, an additional 2 (95% CI, 1–3) and 2 (95% CI, 1–3) myocarditis events per million people vaccinated would be anticipated, respectively. After the second dose of BNT162b2 and mRNA-1273, an additional 2 (95% CI, 2–3) and 34 (95% CI, 32–35) myocar-ditis events per million people would be anticipated, Women age ≥40 y 1–28 days: first dose/positive test before any vaccination501.30 (0.92–1.84)371.57 (1.05–2.33)*n/a4017.29 (10.70–27.96)268.65 (5.13–14.59) 1–28 days: second dose220.55 (0.35–0.86)250.98 (0.63–1.52)*n/a 1–28 days: booster dose*n/a371.76 (1.17–2.65)*2.00 (0.46–8.72)Men age ≥40 y 1–28 days: 1st dose/positive test before any vaccination701.16 (0.87–1.54)291.05 (0.69–1.59)*n/a5413.40 (9.04–19.88)4711.77 (7.77–17.85) 1–28 days: second dose450.85 (0.61–1.19)240.77 (0.49–1.18)*n/a 1–28 days: booster dose*n/a422.15 (1.46–3.17)53.76 (1.41–10.02)Day 0 of each exposure has been removed because of small numbers.*Cells with counts <5 are suppressed. Table 3. Continued Time periodChAdOx1 nCoV-19 vaccineBNT162b2 mRNA vaccinemRNA-1273 vaccine Positive SARS-CoV-2 test (before vaccine)Positive SARS-CoV-2 test (vaccinated) Events IRR (95% CI)Events IRR (95% CI)Events IRR (95% CI)Events IRR (95% CI) EventsIRR (95%

After COVID-19 Vaccine and Infectionres pectively. After a booster dose of BNT162b2 and mRNA-1273, an additional 2 (95% CI, 1–3) and 1 (95% CI, 0–2) myocarditis events per million people would be anticipated, respectively. These estimates compare with an additional 35 (95% CI, 34–36) and 23 (95% CI, 21–24) myocarditis events per million people in the 1 to 28 days after a SARS-CoV-2–posi-tive test before vaccination and in vaccinated individu-als, respectively (Table 4; Figure).In men younger than 40 years, we estimate an additional 4 (95% CI, 2–6) and 14 (95% CI, 5–17) myocarditis events per million in the 1 to 28 days after a first dose of BNT162b2 and mRNA-1273, respectively; and an additional 14 (95% CI, 8–17), 11 (95% CI, 9–13) and 97 (95% CI, 91–99) myocarditis events after a second dose of ChAdOx1, BNT162b2, and mRNA-1273, respectively. These estimates compare with an additional 16 (95% CI, 12–18) myocarditis events per million men younger than 40 years in the 1 to 28 days after a SARS-CoV-2–positive test before vaccination (Table 4; Figure).Robustness of the ResultsOverall, our main findings were not sensitive to censoring because of death (Table S7, sensitivity analyses 1 through 3), and IRRs for the second dose of vaccination agreed with main results when we removed those who had the outcome after the first dose of any vaccine, but before the second dose (Table S7, sensitivity analysis 5). Similarly, IRRs for the booster dose of vaccination agreed with main results when we removed those who had the outcome af-ter the second dose of any vaccine, but before the booster dose (Table S7, sensitivity analysis 6). There was no bias caused by possibly not complete data near the end of the study period (Table S7, sensitivity analysis 4). Estimates for vaccines exposures agreed with the main analysis when restricted to patients who never tested positive to SARS-CoV-2 (Table S8, sensitivity analysis 7).

DISCUSSIONIn

a population of >42 million vaccinated individuals, we re-port several new findings that could influence public health Figure. Risk of myocarditis in the 1 to 28 days after COVID-19 vaccines or SARS-CoV-2.(Left) Incidence rate ratios with 95% CIs and (right) number of excess myocarditis events for million people with 95% CIs in the 1 to 28 day risk periods after the first, second, and booster doses of ChAdOx1, BNT162b2,and mRNA-1273 vaccine or a positive SARS-CoV-2 test in (top) a population of 42 842 345 vaccinated individuals and (bottom) younger men (age <40 years), older men (age ≥40 years), younger women (age <40 years), and older women (aged ≥40 years).ORIGINAL

First, the risk of myocar-ditis is substantially higher after SARS-CoV-2 infection in unvaccinated individuals than the increase in risk observed after a first dose of ChAdOx1nCoV-19 vaccine, and a first, second, or booster dose of BNT162b2 vaccine. Second, although the risk of myocarditis with SARS-CoV-2 infec-tion remains after vaccination, it was substantially reduced, suggesting vaccination provides some protection from the cardiovascular consequences of SARS-CoV-2. Third, in contrast with other vaccines, the risk of myocarditis ob-served 1 to 28 days after a second dose of mRNA-1273 vaccine was higher and similar to the risk after infection. Last, vaccine-associated myocarditis was largely restrict-ed to men younger than 40 years with 1 exception; both younger men and women were at increased risk of myo-carditis after a second dose of mRNA-1273.Vaccination against COVID-19 has both major public health and economic benefits. Although the net benefit of vaccination for the individual or on a population level should not be framed exclusively around the risks of myocarditis, quantifying this risk is important, particularly in young people who are less likely to have a severe ill-ness with SARS-CoV-2 infection. Multiple studies have identified an increase in myocarditis after exposure to the BNT162b2 mRNA vaccine.1–8,13 Some of our find-ings are confirmatory, but we also demonstrate that the risk of myocarditis is not restricted to this vaccine but is observed after vaccination with adenovirus and other mRNA vaccines and after a booster dose.It is important to place our findings into context. One of the strengths of our analysis is that we quantify the risk of myocarditis associated with both vaccination and SARS-CoV-2 infection in the same population. Myocarditis is an uncommon condition. The risk of vaccine-associated myocarditis is small, with up to an additional 2 events per million people in the 28-day period after exposure to all vaccine doses other than mRNA-1273. This is substan-tially lower than the 35 additional myocarditis events observed with SARS-CoV-2 infection before vaccination. Furthermore, vaccination reduced the risk of infection associated myocarditis by approximately half, suggest-ing that the prevention of infection associated myocarditis may be an additional longer-term benefit of vaccination.The risk of vaccine-associated myocarditis is con-sistently higher in younger men, particularly after a second dose of mRNA-1273, where the number of additional events during 28 days was estimated to be 97 per million people exposed. An important consid-eration for this group is that the risk of myocarditis after a second dose of mRNA-1273 was higher than the risk after infection. Indeed, in younger women, although the relative risks of myocarditis were lower than in younger men, the number of additional events per million after a second dose of mRNA-1273 was similar to the number after infection. These findings may justify some reconsideration of the selection of vaccine type, the timing of vaccine doses, and the net benefit of booster doses in young people, particularly in young men. However, there are some important caveats that need to be considered. First, the num-ber of people vaccinated with mRNA-1273 was small compared with those receiving other types of vaccine, Table 4. Measures of the Effect of Vaccinations and SARS-CoV-2 Infections Presented as Excess Events Per 1 Million Exposed Excess myocarditis events per 1 000 000 exposed (95% CI)Main analysis Age <40 yAge ≥40 y Women Men Age <40 yAge ≥40 y Women Men Women Men ChAdOx1 First dose2 (1–3)………2 (0–4)………… Second dose…4 (0–6)…………14 (8–17)…… Booster dose………………………BNT162b2 First dose2 (1–3)2 (1–3)…2 (1–3)3 (1–4)…4 (2–6)3 (0–4)… Second dose2 (1–3)5 (4–5)……6 (4–7)…11 (9–13)…… Booster dose2 (1–3)…2 (2–3)1 (0–2)3 (2–4)……2 (1–3)3 (2–4)mRNA-1273 First dose…7 (3–9)……10 (1–14)…14 (5–17)…… Second dose34 (32–35)43 (41–44)…7 (2–9)73 (70–76)7 (1–9)97 (91–99)…… Booster dose1 (0–2)…1 (1–2)…3 (1–3)………3 (1–3)SARS-CoV-2 Positive test (before vaccine)35 (34–36)10 (9–11)63 (62–64)28 (27–29)50 (48–51)8 (6–8)16 (12–18)51 (49–52)85 (82–87) Positive test (vaccinated)23 (21–24)…39 (38–40)17 (16–19)34 (30–36)7 (3–8)…26 (24–27)61 (58–63)Only significant increased risks were reported during the 1 to 28 days after exposure. When incidence rate ratios were not significant during the 1 to 28 days after vaccine, absolute measures are not given.

Second, the average age of those receiving this vaccine was younger at 32 years compared with other vaccines where recipients were in their mid-40s and 50s. The observed excess risk related to mRNA-1273 may in part be a result of the higher probability of myocarditis in this younger age group. Our findings are consistent with 2 recent studies from the United States and Denmark in which the risks of myocarditis after mRNA-1273 and BNT162b2 were compared.7,14 In the Vaccine Adverse Event Reporting System, 1991 cases of myocarditis were reported to August 31, 2021, with a median age of 21 years and 82% male.14 Although our findings are not directly com-parable because the Vaccine Adverse Event Reporting System dataset relies on clinician reporting, the risks of myocarditis were higher after a second dose of both BNT162b2 and mRNA-1273 and were greater for mRNA-1273 in most younger age groups. In Denmark, a population-based study that applied both case-control and self-controlled case series study methods observed a greater increase in the risk of myocarditis or myopericarditis 1 to 28 days after mRNA-1273 (adjusted hazard ratio, 3.92 [95% CI, 2.30–6.68]) than after BNT162b2 (adjusted hazard ratio, 1.34 [95% CI, 0.90–2.00]).7 They also observed the risk was largely confined to those younger than 40 years and was present for both younger men and women for mRNA-1273. The reasons for male predominance in myocarditis is not known but may relate to sex hormone differences in both the immune response and myocarditis, or to the underdiagnosis of cardiac dis-ease in women.15,16This study has several strengths. First, the United Kingdom offered an ideal place to carry out this study given that 3 types of COVID-19 vaccination have been rolled out at the same speed and scale as each other. Second, this was a population-based study of data recorded prospectively and avoided recall and selection biases linked to case reports. Third, the large sample size provided sufficient power to investigate these rare outcomes, which could not be assessed through clini-cal trials. Fourth, the self-controlled case series study design removes potential confounding from fixed char-acteristics, and the breakdown of our study period into weekly blocks accounted for temporal confounding. Of note, the estimated IRRs were consistently <1 in the pre-exposure period before vaccination and >1 in the pre-risk period before a SARS-CoV-2–positive test. This was expected because events are unlikely to happen shortly before vaccination (relatively healthy people are receiving the vaccine) and more likely to happen before a SARS-CoV-2–positive test (as a standard procedure, patients admitted to the hospital are tested for SARS-CoV-2). We also assessed the robustness of our results through several sensitivity analyses.There are some limitations to consider. First, the number of people receiving a booster dose of ChAdOx1 or mRNA-1273 vaccine was too small to evaluate the risk of myocar-ditis. Second, we relied on hospital admission codes and death certification to define myocarditis, and it is possible that we might have over- or underestimated risk because of misclassification. Third, although we were able to include 2 230 058 children age 13 to 17 years in this analysis, the number of myocarditis events was small (56 events in all periods and 16 events in the 1 to 28 days after vac-cination) in this subpopulation and precluded a separate evaluation of risk. It should also be noted that only the first occurrence of myocarditis in the study period is used in this analysis. Therefore, the results found for the risk of myo-carditis after a third dose do not include repeated instances of myocarditis in the same individual. A comparison of rates of death with myocarditis between those infected with SARS-CoV-2 or vaccinated was not possible, given that for this analysis, we have included only people who had been vaccinated. Therefore, a patient with COVID-19 who died after myocarditis before receiving a vaccination will not be included, and rates of myocarditis death after SARS-CoV-2 will be under estimated.In summary, the risk of hospital admission or death from myocarditis is greater after SARS- CoV2 infection than COVID-19 vaccination and remains modest after sequential doses including a booster dose of BNT162b2 mRNA vaccine. However, the risk of myocarditis after vaccination is higher in younger men, particularly after a second dose of the mRNA-1273 vaccine.

ARTICLE INFORMATIONReceived March 10, 2022; accepted June 7, 2022.AffiliationsNuffield Department of Primary Health Care Sciences (M.P., X.W.M., S.D., A.H., C.A.C.C., J.H.-C.), Wellcome Centre for Human Genetics (L.H.), British Heart Foundation Centre of Research Excellence, National Institute for Health Research, Oxford Biomedical Research Centre, Radcliffe Department of Medicine, John Rad-cliffe Hospital (K.M.C.): National Institute for Health Research Biomedical Research Centre, Oxford University Hospitals National Health Service Trust (P.W.); University of Oxford. School of Immunology and Microbial Sciences, King’s College London, Centre for Inflammation Research (M.S.-H.). Leicester Real World Evidence Unit, Diabetes Research Centre (F.Z., K.K.), University of Leicester. Usher Institute (M.S.-H., N.L.M., A.S.), British Heart Foundation University Centre for Cardiovascular Sci-ence (N.L.M.), University of Edinburgh. Centre for Academic Primary Care, School of Medicine, University of Nottingham (C.A.C.C.)

UK Govt Denies ‘Safe Use’ Recommendation for Pfizer Vaccine In Pregnant Women, Says Those Breastfeeding Should NOT Be Vaccinated.

FURTHER STUDIES ARE BEING CONDUCTED TO ASCERTAIN MORE DETAILS ABOUT THE IMPACT OF THE VACCINES.

Authors:  NATALIE WINTERS AUGUST 30, 2022 The National Pulse

The British government has recommended against pregnant and breastfeeding women receiving the Pfizer COVID-19 vaccine, admitting that “sufficient reassurance of safe use of the vaccine” for the demographic “cannot be provided at the present time.”

The findings were revealed in a comprehensive report from the country’s Department of Health and Social Care, “Summary of the Public Assessment Report for COVID-19 Vaccine Pfizer/BioNTech,” last updated on August 16th. The report was published through the government’s Medicines & Healthcare products Regulatory Agency.

The report’s “Toxicity Conclusions” section outlines why the department recommends against pregnant and breastfeeding women receiving the vaccine, noting:

“In the context of supply under Regulation 174, it is considered that sufficient reassurance of safe use of the vaccine in pregnant women cannot be provided at the present time: however, use in women of childbearing potential could be supported provided healthcare professionals are advised to rule out known or suspected pregnancy prior to vaccination. Women who are breastfeeding should also not be vaccinated.

“The absence of reproductive toxicity data is a reflection of the speed of development to first identify and select COVID-19 mRNA Vaccine BNT162b2 for clinical testing and its rapid development to meet the ongoing urgent health need. In principle, a decision on Licensing a vaccine could be taken in these circumstances without data from reproductive toxicity studies animals, but there are studies ongoing and these will be provided when available,” continued the report.

The admission follows controversy over several Western governments’ hasty approvals and, in some cases, mandates of COVID-19 vaccines.

In the U.S., following a massive lobbying campaign by pharmaceutical giants including Pfizer, many jobs, businesses, and schools required COVID-19 vaccination for entry. As a result, companies including Pfizer have enjoyed record-breaking profits throughout the COVID-19 pandemic.

The British government’s report also follows U.S. health agencies such as the Food and Drug Administration (FDA) appearing to slow roll the release of data relevant to the efficacy and long-term health implications of the COVID-19 vaccine.