Covid vaccines ‘saved far fewer lives than first thought'
In 2024, the World Health Organisation (WHO) claimed that jabs prevented the deaths of 14.4 million globally in the first year alone, with some estimates putting the figure closer to 20 million.
However, new modelling by Stanford University and Italian researchers suggests that while the vaccine did undoubtedly save lives, the true figure is 'substantially more conservative' and closer to 2.5 million worldwide over the course of the entire pandemic.
The team estimated that nine of 10 prevented deaths were in the over-60s, with jabs saving just 299 youngsters aged under 20, and 1,808 people aged between 20 and 30 globally.
Overall 5,400 people needed to be vaccinated to save one life but in the under-30s this figure rose to 100,000 jabs, the paper suggests.
Researchers criticised 'aggressive mandates and the zealotry to vaccinate everyone at all cost', adding that the findings had implications for how future vaccine rollouts are handled.
John Ioannidis, Professor of Medicine at Stanford University and the first author, said: 'I think early estimates were based on many parameters having values that are incompatible with our current understanding.
'In principle, targeting the populations who would get the vast majority of the benefit and letting alone those with questionable risk-benefit and cost-benefit makes a lot of sense.
'Aggressive mandates and the zealotry to vaccinate everyone at all cost were probably a bad idea.'
Since 2021, more than 13 billion Covid-19 vaccine doses have been administered.
But there have been mounting concerns that vaccines could be harmful for some people, particularly the young, and that the risk was not worth the benefit for a population at little risk from Covid.
More than 17,500 Britons have applied to the Government's vaccine damage payment scheme believing they or loved ones were injured by the jab.
In June, manufacturers added warnings for myocarditis and pericarditis to Covid-19 messenger RNA (mRNA) vaccines' prescribing information.
For the new study, experts used worldwide population data, alongside vaccine effectiveness and infection fatality rates, to estimate how many people died from a Covid infection before or after the periods of vaccination.
The team believes earlier modelling may have used overly pessimistic infection fatality rates and overly optimistic vaccine effectiveness, while failing to consider how quickly protection waned.
Based on fewer assumptions
Earlier studies may also have underestimated how many people had already been unknowingly infected by the time they had the vaccine.
Dr Angelo Maria Pezzullo, researcher in general and applied hygiene at the Catholic University of the Sacred Heart, in Milan, said: 'Before ours, several studies tried to estimate lives saved by vaccines with different models and in different periods or parts of the world, but this one is the most comprehensive because it is based on worldwide data. it also covers the omicron period.
'It also calculates the number of years of life that was saved, and it is based on fewer assumptions about the pandemic trend.'
The team calculated that around 14.8 million life-years were saved, one life-year saved per 900 vaccine doses administered.
Researchers concluded that although vaccines had a 'substantial benefit' on global mortality, it was 'mostly limited' to older people.
The over-70s made up nearly 70 per cent of the lives saved, while the 60 to 70s accounted for a further 20 per cent. In contrast, under-20s made up just 0.01 per cent of lives saved and 20 to 30s were 0.07 per cent.
Professor Stefania Boccia, of the Catholic University of the Sacred Heart, added: 'These estimates are substantially more conservative than previous calculations that focused mainly on the first year of vaccination, but clearly demonstrate an important overall benefit from Covid-19 vaccination over the period 2020-2024.
'Most of the benefits, in terms of lives and life-years saved, have been secured for a portion of the global population who is typically more fragile, the elderly.'
Sir David Davis, the former Brexit secretary who fought against vaccine mandates, said: 'Frankly it's a good cautionary tale that if we have another pandemic we should be far more clinical about the risk-benefit ratio.
'We knew pretty quickly who the most susceptible groups were and we should have focused very strictly on them, rather than placing people who were at little risk in hazard's way.
'The level of aggression of trying to force people to become vaccinated and shutting down people who were raising concerns, the reasons for those concerns are all validated in this report.'
Hashtags
Try Our AI Features
Explore what Daily8 AI can do for you:
Comments
No comments yet...
Related Articles
The Guardian
26 minutes ago
- The Guardian
Science could enable a fascist future. Especially if we don't learn from the past
Science is in crisis. Funding infrastructures for both basic and applied research are being systematically decimated, while in places of great power, science's influence on decision making is waning. Long-term and far-reaching studies are being shuttered, and thousands of scientists' livelihoods are uncertain, to say nothing of the incalculable casualties resulting from the abrupt removal of life-saving medical and environmental interventions. Understandably, the scientific community is working hard to weather this storm and restore funding to whatever extent possible. In times like these, it may be tempting to settle for the status quo of six months ago, wanting everything simply to go back to what it was (no doubt an improvement for science, compared to the present). But equally, such moments of crisis offer an opportunity to rebuild differently. As Arundhati Roy wrote about Covid-19 in April 2020, 'Historically, pandemics have forced humans to break with the past and imagine their world anew. This one is no different. It is a portal, a gateway between one world and the next.' What could science look like, and what good could science bring, if we moved through the portal of the present moment into a different world? At worst, science will play its part in accelerating us toward a tech-obsessed end-times-fascist future. At best, science will broaden its power as a positive force, serving the wellbeing of humans and nature alike. Imagining this latter vision in exquisite detail is essential, and we argue here that to first envision and then work towards the best version of science, we need to reckon honestly with science's past and present. Most crucially, we need to confront the commonplace claim that science is – or ought to be – objective and apolitical, uninfluenced by human culture, norms, or values. The current moment has rudely awakened many scientists to the fact that research is indeed political, and further makes clear that scientists' attempts to distance themselves from politics will backfire. Denying the inherent entanglements of science and politics leaves scientists lacking the capacity and tools to mount effective defenses against bad-faith political attacks. This denial also allows science to go unquestioned when it undermines the needs and rights of marginalized beings and places. As much as scientists might wish for science to be cleanly separable from politics, decades of research demonstrates that this has never been true, and never could be. The field of science studies examines the inherently human processes of science – who defines what science is, who gets to conduct scientific research, who pays for it, who benefits from it, who is harmed by it – and how these human dynamics shape scientific knowledge. Feminist science studies in particular documents how power and oppression shape scientific findings and applications, demonstrating that even 'science at its most basic' is in fact inextricable from politics. Some of the most compelling, and consequential, examples of such entanglement can be found in human and animal biology. Consider an analysis of 19th-century science on human race and sex from Sally Markowitz, which clearly reveals the influence of white supremacism on basic biology. Markowitz shows how 19th-century scientists not only asserted that human races are biological categories, but also that the so-called white race is evolutionarily superior. To 'prove' this politically-motivated claim, these scientists first decided that the degree of distinction between men's and women's bodies (or 'sexual dimorphism') was proof of evolutionary superiority, and then claimed, on the basis of selective measurements, that sexual dimorphism is supposedly greater in Europeans than in Africans. Women of African descent were thus mismeasured as both less female and less human than their white counterparts – rendering all people of African descent more 'animal-like'. This 19th-century research has had far-reaching consequences, from justifying enslavement, to supporting eugenic sterilization practices well into the 20th century, to contemporary controversy around the 'femaleness' of elite Black and brown female athletes, among other examples. It may be tempting to relegate such blatant instances to the past, and claim that scientists have since corrected such mistakes. But in fact these ghosts continue to haunt us. In our new book, Feminism in the Wild, we – an evolutionary biologist and a science studies scholar – dive deep into how contemporary scientists describe and understand animal behavior, and find the dominant political perspectives of the last 200 years reflected back to us. Scientific research on mating behavior in species ranging from fruit flies to primates is entangled with patriarchal expectations of masculinity and femininity. Scientists' understanding of animals' foraging behavior mirrors a capitalist theory of economics, based upon assumptions of scarcity and optimization, and expectations of individualism are pervasive throughout scientific research on how animals behave in groups. Contemporary researchers express surprise, for instance, at elephants who alter their eating habits to accommodate a fellow herd member disabled by poachers, at ravens who alert one another to the presence of food in the dead of winter, or at female dolphins who begin lactating without having given birth in order to nurse calves whose mothers have died. Dominant evolutionary theories do not explain such instances of care on their own terms, but instead insist that these behaviors must ultimately be self-interested. Not coincidentally, these theories rooted in individualism only rose to dominance in the last 50 years or so, alongside the rise of neoliberalism. Meanwhile, eugenic perspectives, rooted in racism, classism, and ableism, constrain how scientists understand sex, intelligence, performance and more, in humans and animals alike. For example, today's scientists are still somewhat shocked by lizards who successfully navigate tree trunks and branches with missing limbs, as these agile lizards undermine the presumed correlation between an animal's appearance, performance, and survival that's captured in the phrase 'survival of the fittest'. Other scientists continue to argue that peahens (for instance) choose to mate with the most beautiful peacock, despite his expansive tail's costly impediments, because beauty is a 'favorable' trait even if it doesn't promote survival. Such arguments about female mate choice are rooted in a theory developed decades ago by mathematician and evolutionary biologist Ronald A Fisher, a vocal advocate of 'positive eugenics', which means encouraging only people with 'favorable' traits to reproduce. Leonard Darwin (son of Charles Darwin), in his 1923 presidential address to the Eugenics Education Society, made this connection between Fisher's theories and eugenics explicit, stating: 'Wonderful results have been produced…by the action of sexual selection in all kinds of organisms…and if this be so, ought we not to enquire whether this same agency cannot be utilized in our efforts to improve the human race?' Leonard Darwin then went on to deliver an astoundingly modern-sounding description of sexual selection before considering its implications for effective eugenics propaganda. We offer these examples (and many more, in our book), to show that scientific research on the evolution of animal behavior remains thoroughly and undeniably political. But the moral of our story is not that scientists must root out all politics and strive for pure neutrality. Rather, feminist science studies illustrates how science has always been shaped by politics, and always will be. It is therefore incumbent upon scientists to confront this reality rather than deny it. Thankfully, for as long as science has been aligned with systems of oppression, there have been scientists and other scholars resisting this alignment, both explicitly and implicitly. In Feminism in the Wild, we detail the work of scientists developing new mathematical models about female mating behavior that discard old assumptions aligned with patriarchy and eugenics, instead demonstrating that it's possible and even likely that female animals are not necessarily concerned with mating with the 'best' males and that mate choice can be a more flexible and variable affair. We discuss a rich history of theories about animals' behavior in groups that take both individual and collective well-being seriously. And we explore alternatives rooted in queer, Indigenous, and Marxist standpoints, which counter the dominant view that animal behavior is all about maximizing survival and reproduction. Ultimately, we show that it is possible—and even desirable—to fold political analysis into scientific inquiry in a way that makes science more multifaceted and more honest, bringing us closer to the truth than a science which denies its politics ever could. In this historical moment scientists must embrace, rather than avoid, the political underpinnings and implications of scientific inquiry. As Science's editor-in-chief Holden Thorp put it in 2020, 'science thrives when its advocates are shrewd politicians but suffers when its opponents are better at politics.' We agree, and further insist: scientists must reckon honestly and explicitly with the ways in which the knowledge they produce, and the processes by which they produce it, are already and unavoidably political. In doing so, scientists may lose the shallow authority they have harbored by pretending to be above the political fray. They will instead have to grapple with their own political perspectives constantly, as part of the scientific process—a rougher road, no doubt, but one that will lead us to a stronger science, both more empirically rigorous and more politically resilient. Imagine if scientists seized this moment to remake science even while fighting for it. As MacArthur Genius and feminist science studies scholar Ruha Benjamin recently stated: imagination is '[not] an ephemeral afterthought that we have the luxury to dismiss or romanticize, but a resource, a battleground.' And, she continues: 'most people are forced to live inside someone else's imagination.' United in the goal of building a stronger science, we call upon scientists to put our imaginations to work differently, in ways that move us through this nightmare portal into a dreamier world, where justice is not cropped out of scientific endeavors but rather centered and celebrated. Ambika Kamath is trained as a behavioral ecologist and evolutionary biologist. She lives, works, and grows community in Oakland, California, on Ohlone land Melina Packer is Assistant Professor of Race, Gender, and Sexuality Studies at the University of Wisconsin, La Crosse, on Ho-Chunk Nation land. She is the author of Toxic Sexual Politics: Economic Poisons and Endocrine Disruptions
The Independent
4 hours ago
- The Independent
This fuzzy animal friend may be the key to treating schizophrenia
Llamas – likely without red pajamas – may hold the key to treating schizophrenia. The serious brain disorder causes people to interpret reality abnormally, and affects approximately 3.7 million U.S. adults between the ages of 18 to 65 years old, according to the nonprofit RTI International. But the domesticated South American woolly animal might be be able to help. French researchers said this week that they had used llama antibodies, or proteins that help to protect the immune system, to design a tiny fragment of an antibody known as a 'nanobody' that will trigger a neurotransmitter in the brain involved in regulating neural activity. Neurotransmitters are chemical molecules that carry messages or signals from one nerve cell to the next target cell, according to the Cleveland Clinic. No llamas were harmed in the study and researchers can identify nanobodies in a petri dish. In the past, llama antibodies have also proven effective in fighting Covid and other 'SARS-like' viruses. When scientists at the Institute of Functional Genomics injected the molecule into the veins or the muscles, it was able to break the blood-brain barrier and effectively reach brain receptors. The barrier is a a tightly locked layer of cells that defend your brain from harmful substances. Studying the impact of the nanobodies in two tests using mice, the researchers found that they corrected cognitive deficits that were observed. There was an improvement of cognitive function with just one shot, and a prolonged effect over one week. Clinical studies are now required to show that their findings could be a new avenue of treatment for schizophrenia. "In humans obviously we don't know [yet], but in mice yes, it is sufficient to treat most deficits of schizophrenia," molecular biologist Jean-Philippe Pin told Newsweek.. He was a co-author of the research which was published in the journal Nature. Pin said that medications currently given to schizophrenia patients "treat the symptoms well, but less the cognitive deficits." The cause of the chronic condition remains unknown, but the World Health Organization says it is thought that an interaction between genes and a range of environmental factors may be the reason. The exact prevalence of schizophrenia is difficult to measure. Some have tied cases in Canada to cannabis use. Although schizophrenia can occur at any age, people are typically diagnosed between the ages of 16 and 30. Symptoms vary from person to person. There is no cure, but it can be treated through antipsychotic medications, talk therapy, and self-management strategies, the National Alliance on Mental Illness says. The study's authors hope to add this strategy to the list. 'This research confirms the potential of nanobodies as a new therapeutic strategy for acting on the brain, with their use eventually being broadened to include the treatment of other neurological illnesses,' the institute said in a statement.
The Independent
5 hours ago
- The Independent
Millions of people are suffering from brain fog. A new study will find out why
Millions of people who recover from infections like COVID-19, influenza and glandular fever are affected by long-lasting symptoms. These include chronic fatigue, brain fog, exercise intolerance, dizziness, muscle or joint pain and gut problems. And many of these symptoms worsen after exercise, a phenomenon known as post-exertional malaise. Medically the symptoms are known as myalgic encephalomyelitis or chronic fatigue syndrome (ME/CFS). The World Health Organization classifies this as a post viral fatigue syndrome, and it is recognised by both the WHO and the United States Centers for Disease Control and Prevention as a brain disorder. Experiencing illness long after contracting an infection is not new, as patients have reported these symptoms for decades. But COVID-19 has amplified the problem worldwide. Nearly half of people with ongoing post-COVID symptoms – a condition known as long-COVID – now meet the criteria for ME/CFS. Since the start of the pandemic in 2020, it is estimated that more than 400 million people have developed long-COVID. To date, no widely accepted and testable mechanism has fully explained the biological processes underlying long-COVID and ME/CFS. Our work offers a new perspective that may help close this gap. Our research group studies blood and the cardiovascular system in inflammatory diseases, as well as post-viral conditions. We focus on coagulation, inflammation and endothelial cells. Endothelial cells make up the inner layer of blood vessels and serve many important functions, like regulating blood clotting, blood vessel dilation and constriction, and inflammation. Our latest review aims to explain how ME/CFS and long-COVID start and progress, and how symptoms show up in the body and its systems. By pinpointing and explaining the underlying disease mechanisms, we can pave the way for better clinical tools to diagnose and treat people living with ME/CFS and long-COVID. What is endothelial senescence? In our review, our international team proposes that certain viruses drive endothelial cells into a half-alive, 'zombie-like' state called cellular senescence. Senescent endothelial cells stop dividing, but continue to release molecules that awaken and confuse the immune system. This prompts the blood to form clots and, at the same time, prevent clot breakdown, which could lead to the constriction of blood vessels and limited blood flow. By placing 'zombie' blood-vessel cells at the centre of these post-viral diseases, our hypothesis weaves together microclots, oxygen debt (the extra oxygen your body needs after strenuous exercise to restore balance), brain-fog, dizziness, gut leakiness (a digestive condition where the intestinal lining allows toxins into the bloodstream) and immune dysfunction into a single, testable narrative. From acute viral infection to 'zombie' vessels Viruses like SARS-CoV-2, Epstein–Barr virus, HHV-6, influenza A, and enteroviruses (a group of viruses that cause a number of infectious illnesses which are usually mild) can all infect endothelial cells. They enable a direct attack on the cells that line the inside of blood vessels. Some of these viruses have been shown to trigger endothelial senescence. Multiple studies show that SARS-CoV-2 (the virus which causes COVID-19 disease) has the ability to induce senescence in a variety of cell types, including endothelial cells. Viral proteins from SARS-CoV-2, for example, sabotage DNA-repair pathways and push the host cell towards a senescent state, while senescent cells in turn become even more susceptible to viral entry. This reciprocity helps explain why different pathogens can result in the same chronic illness. Influenza A, too, has shown the ability to drive endothelial cells into a senescent, zombie-like state. What we think is happening We propose that when blood-vessel cells turn into 'zombies', they pump out substances that make blood thicker and prone to forming tiny clots. These clots slow down circulation, so less oxygen reaches muscles and organs. This is one reason people feel drained. During exercise, the problem worsens. Instead of the vessels relaxing to allow adequate bloodflow, they tighten further. This means that muscles are starved of oxygen and patients experience a crash the day after exercise. In the brain, the same faulty cells let blood flow drop and leak, bringing on brain fog and dizziness. In the gut, they weaken the lining, allowing bits of bacteria to slip into the bloodstream and trigger more inflammation. Because blood vessels reach every corner of the body, even scattered patches of these 'zombie' cells found in the blood vessels can create the mix of symptoms seen in long-COVID and ME/CFS. Immune exhaustion locks in the damage Some parts of the immune system kill senescent cells. They are natural-killer cells, macrophages and complement proteins, which are immune molecules capable of tagging and killing pathogens. But long-COVID and ME/CFS frequently have impaired natural-killer cell function, sluggish macrophages and complement dysfunction. Senescent endothelial cells may also send out a chemical signal to repel immune attack. So the 'zombie cells' actively evade the immune system. This creates a self-sustaining loop of vascular and immune dysfunction, where senescent endothelial cells persist. In a healthy person with an optimally functioning immune system, these senescent endothelial cells will normally be cleared. But there is significant immune dysfunction in ME/CFS and long-COVID, and this may enable the 'zombie cells' to survive and the disease to progress. Where the research goes next There is a registered clinical trial in the US that is investigating senescence in long-COVID. Our consortium is testing new ways to spot signs of ageing in the cells that line our blood vessels. First, we expose healthy endothelial cells in the lab to blood from patients to see whether it pushes the cells into a senescent, or 'zombie,' state. At the same time, we are trialling non‑invasive imaging and fluorescent probes that could one day reveal these ageing cells inside the body. In selected cases, tissue biopsies may later confirm what the scans show. Together, these approaches aim to pinpoint how substances circulating in the blood drive cellular ageing and how that, in turn, fuels disease. Our aim is simple: find these ageing endothelial cells in real patients. Pinpointing them will inform the next round of clinical trials and open the door to therapies that target senescent cells directly, offering a route to healthier blood vessels and, ultimately, lighter disease loads.
