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Published12 hours agoShareclose panelShare pageCopy linkAbout sharingThis video can not be playedTo play this video you need to enable JavaScript in your browser.By Chris MasonPolitical editor, BBC NewsBoris Johnson’s evidence was, for the most part, shorn of his usual performative theatrics. Sitting on the press bench in the hearing room, the contempt in which Mr Johnson was held by many of the families of the bereaved sitting metres away was obvious; sniggers of derision from some of them punctuated his early testimony. The thrust of Mr Johnson’s case – contrition, with hindsight, at his tardiness in clocking the imminent scale of the pandemic in early 2020 – was mixed with his best effort to take on the cavalry of his former colleagues who have questioned his competence and the culture of his Downing Street operation. Crude WhatsApp exchanges were framed as entirely typical of the style of many on the messaging service; indulging in the “ephemeral, pejorative, hyperbolical” as he put it. Private, internal anger at his failings was a good thing, he claimed, a “disputatious culture” better than a “quietly acquiescent” one. Two sentence siblings appeared frequently: “I can’t remember” and “I don’t know.” Claims to this end may be judged individually plausible. But their volume stood out. More on Covid and the Covid InquiryLIVE: Follow the latest updates from the Covid inquiryWhat is the UK Covid inquiry and how does it work? How inquiry is exposing deep flaws in Covid decision-making’Moronic’: Vicious Covid WhatsApps reveal No 10 battlesWhat to do if you have Covid: Can you go to work or school?The UK’s governance structures – the wiring of where power lies and who takes decisions – also featured, and there was a parallel here with what the former health secretary Matt Hancock said last week. Mr Johnson felt devolution didn’t work during the pandemic because mixed messages were sent, depending on where you were in the UK, because devolved governments did different things, at different times, from the government at Westminster.He suggested the Public Health Act 1984 had a consequence unforeseen at the time of its passing nearly 40 years ago, because the devolution that was to follow meant lots of pandemic powers rested away from Westminster.What should now happen, he argued, was that this act should be amended to discount pandemics from it.Some will see this as a self-serving argument for a former prime minister to make, perhaps keen on hoarding power at the centre. Others will insist at a time of emergency clarity is key and it was absent during Covid.In big picture terms, Mr Johnson sought to remind the inquiry of his central role as a pandemic prime minister; judging trade offs of a colossal nature; confronting a scenario without modern precedent. The question not asked explicitly but hanging over the inquiry is this: would the UK have coped better had there been a different prime minister? Mr Johnson will fear evidence is already accumulating to suggest the answer to that is yes. We have now seen and heard his first stab at trying to take on that hunch. He is back on Thursday morning to face more questions.More on this storyI should have twigged Covid threat earlier – JohnsonPublished16 hours agoWhat is the UK Covid inquiry and how does it work?Published37 minutes ago

A protein in the immune system programmed to protect the body from fungal infections is also responsible for exacerbating the severity of certain autoimmune diseases such as irritable bowel disease (IBS), type 1 diabetes, eczema and other chronic disorders, new research from The Australian National University (ANU) has found.
The discovery could pave the way for new and more effective drugs, without the nasty side effects of existing treatments. In addition to helping to manage severe autoimmune conditions, the breakthrough could also help treat all types of cancer.
The scientists have discovered a previously unknown function of the protein, known as DECTIN-1, which in its mutated state limits the production of T regulatory cells or so-called ‘guardian’ cells in the immune system.
These guardian cells are crucial to preventing autoimmune disease because they suppress the effects of a hyperactive immune system, which can be extremely dangerous if not properly regulated.
The immune system is designed to protect the body from infection, but in severe cases it becomes overactivated and turns the body’s natural defences against itself.
“When this happens, the immune system wrongly perceives healthy cells as a threat, causing it to attack the body and promote the onset of autoimmune disease,” lead author Dr Cynthia Turnbull, from ANU, said.
“Although the DECTIN-1 protein helps to fight fungal infections, in its mutated state it’s also responsible for exacerbating severe autoimmune disease.

“Understanding how and why the mutated version of this protein causes autoimmunity in patients brings us a step closer to developing more effective drugs and offers new hope to more than one million Australians who suffer from some form of autoimmune disease.”
The scientists believe they can control the immune system by turning the DECTIN-1 protein on and off, like a light switch.
“Turning on the protein would lower the intensity of the immune system’s defensive response which would help to treat conditions such as autoimmune disease,” Professor Carola Vinuesa, from the Francis Crick Institute, said.
“On the other hand, turning off the protein could give the immune system a boost, sending its defensive mechanisms into overdrive and allowing the body to treat an entirely different set of diseases.
“The findings are exciting because there haven’t been many discoveries of so-called modifier proteins such as DECTIN-1, which can change the way the immune system behaves to the extent it can either cause a disease or prevent it.”
According to Dr Turnbull, this means DECTIN-1 could play a key role in treating cancer.

“Cancer cells can disguise themselves by releasing certain proteins and chemicals into the body that essentially render them invisible from the immune system’s natural defences,” she said.
“We think that by using drugs to turn off the DECTIN-1 protein, in combination with existing therapies, we can activate the immune system and help it identify and attack the cancerous cells.”
Current treatments for autoimmune?disease aren’t very effective and have a lot of damaging side effects. This is because the majority of existing treatments suppress the entire immune system rather than targeting a specific area.
“That means it might not fix the exact problem behind the patient’s disease and could inadvertently make them vulnerable to infections. Many people on these kinds of treatments also get bacterial, fungal and viral infections which can make their autoimmunity worse,” Professor Vinuesa said.
By examining the DNA of a Spanish family, the researchers discovered the DECTIN-1 mutation was responsible for exacerbating the severity of a chronic autoimmune disease suffered by the family’s only child.
“We found the family was also carrying a mutated version of another immune system protein known as CTLA-4. The CTLA-4 mutation prevents guardian cells from working properly and is known to cause severe autoimmune disease in about 60 to 70 per cent of people who carry it in their DNA,” Dr Pablo Canete, from the University of Queensland, said.
“Strangely, the remaining 30 to 40 per cent of the population who carry this mutated protein don’t develop disease.
“We discovered?the family’s only child had both the DECTIN-1 mutation and the CTLA4 mutation, while his parents had only one of each. This helped us identify why the child, who is now in his twenties, was the only person in the family to develop severe autoimmunity, ending a 20-year-long mystery behind the cause of his disease.
“By discovering the existence of mutated versions of modifier proteins such as DECTIN-1, we finally have an explanation for why some people develop severe autoimmune diseases while others don’t, even if they inherit gene mutations passed down from family members.”

Light therapy leads to significant improvements in sleep and psycho-behavioral symptoms for patients with Alzheimer’s disease, according to a new study published this week in the open-access journal PLOS ONE by Qinghui Meng of Weifang Medical University, China, and colleagues.
The cognitive decline associated with Alzheimer’s disease is often accompanied by sleep disturbances and psycho-behavioral symptoms including apathetic and depressive behavior, agitation and aggression. Photobiomodulation is a non-pharmacological therapy that uses light energy to stimulate the suprachiasmic nucleus (SCN), a sleep modulator in the brain. Despite light therapy receiving increased attention as a potential intervention for Alzheimer’s, a systematic evaluation of its efficacy and safety has been unavailable.
In the new study, researchers searched multiple research databases to identify all randomized controlled trials related to light therapy intervention for Alzheimer’s disease or dementia. Fifteen high-quality trials with available methods and relevant outcomes were selected for further analysis. The included trials were written in English, published between 2005 and 2022, and performed in seven countries. They included a combined 598 patients.
The meta-analysis of all fifteen trials found that light therapy significantly improved sleep efficiency, increased interdaily stability (a measure of the strength of circadian rhythms), and reduced intradaily variability (a measure of how frequently someone transitions between rest and activity during the day). In patients with Alzheimer’s disease, light therapy also alleviated depression and reduced patient agitation and caregiver burden.
Given the limited sample sizes in studies included in this meta-analysis, the authors advocate for larger future studies, which could also explore if bright light exposure could cause any adverse behavior in patients. They conclude that light therapy is a promising treatment option for some symptoms of Alzheimer’s disease.
The authors add: “Light therapy improves sleep and psycho-behavioral symptoms in patients with Alzheimer’s disease and has relatively few side effects, suggesting that it may be a promising treatment option for patients with Alzheimer’s disease.”

In a new study of more than 50,000 Korean adolescents, those who used a smartphone for more than 4 hours per day had higher rates of adverse mental health and substance use. Jin-Hwa Moon and Jong Ho Cha of Hanyang University Medical Center, Korea, and colleagues present these findings in the open-access journal PLOS ONE on December 6, 2023.
Prior research has shown that smartphone use among adolescents has increased in recent years, and that this usage may be associated with higher risk of adverse health — such as psychiatric disorders, sleep issues, eye-related problems, and musculoskeletal disorders. However, growing evidence suggests that at least some daily internet usage may be associated with better physical and mental health for adolescents.
To deepen understanding of the relationship between adolescents’ use of smartphones and health, Moon, Cha and colleagues analyzed data on more than 50,000 adolescent participants in the ongoing Korea Youth Risk Behavior Web-based Survey collected in 2017 and in 2020. The data included the approximate number of daily hours each participant spent on a smartphone as well as various health measures. The statistical analysis employed propensity score matching to help account for other factors that could be linked to health outcomes, such as age, sex, and socioeconomic status.
The researchers found that in 2020, the percentage of adolescents in the study who used a smartphone more than 2 hours per day was 85.7 percent — up from 64.3 percent in 2017. Adolescents who used a smartphone for more than 4 hours per day had higher rates of stress, thoughts of suicide, and substance use than those with usage below 4 hours per day. However, adolescents that used a smartphone 1-2 hours per day encountered fewer problems than adolescents who did not use a smartphone at all.
The authors note that this study does not confirm a causal relationship between smartphone use and adverse health outcomes. Nonetheless, the findings could help inform usage guidelines for adolescents — especially if daily usage continues to rise.
The authors add: “This research shows the impact of using smart devices for more than 4 hours a day on adolescent health.”

The proposal has elicited mounting opposition from tobacco companies, Black activists worried about police enforcement and small businesses, as President Biden moves into an election year.The Biden administration is delaying a decision on whether to ban menthol cigarettes amid intense lobbying from tobacco companies, convenience stores and industry-backed groups that contend that billions of dollars in sales and jobs will be lost, a senior administration official confirmed on Wednesday.The proposal has also generated concerns that Black smokers will become the targets of aggressive police tactics, although some Black leaders, top lawmakers and government officials dispute that and say that tobacco companies are financing and fueling those fears.The plan to eliminate menthol cigarettes has been years in the making. The Food and Drug Administration formally proposed an official rule last year, aimed at reducing health disparities, citing statistics that an estimated 85 percent of Black smokers prefer menthol brands. Black men especially face outsize health risks, including high rates of smoking-related lung cancer and death.In recent months, dozens of groups have had appointments with administration officials to discuss the proposal. Tobacco companies and convenience store groups fighting the ban have aligned with the National Action Network, founded by the Rev. Al Sharpton, to advance the argument about the potential for racial targeting by the police. The group attended a large meeting with tobacco lobbyists and top administration officials on Nov. 20.Many other Black organizations, including a majority of the Congressional Black Caucus, have dismissed the policing argument, calling it a cynical attempt to exploit trauma and distract from the harm of cigarettes.“What we’re seeing now,” said Patrice Willoughby, vice president of policy and legislative affairs at the N.A.A.C.P., “is the reaction of a very well-organized industry that has been peddling death to the Black community.”The F.D.A. has said it would like to see the proposal finalized this year, and Michael Felberbaum, an agency spokesman, said on Wednesday that it remained committed to issuing the rule “as expeditiously as possible.” The White House timetable for a decision on the ban had been shifting as months passed, against the backdrop of President Biden’s tough re-election bid next year.President Biden returned to the White House after pardoning a turkey on Nov. 20, when tobacco lobbyists, Black civil rights leaders, senior White House officials and the heads of the F.D.A. and U.S. Health and Human Services department all met.Erin Schaff/The New York Times In recent weeks, public health groups have increasingly expressed concerns about the delays, urging administration officials to act quickly. The Washington Post earlier reported that the Biden administration would postpone any action on the proposal until the spring.Senator Richard J. Durbin, the Democratic majority whip from Illinois, addressed the rumors of political motivations for the delay on the Senate floor on Wednesday, saying concerns that Black people would vote against the president in the next election because of the ban were “greatly exaggerated.”“And I want to make it clear,” he said, “they’re peddling stories — Big Tobacco is — that we’re going to go out and arrest African Americans if they use menthol cigarettes. But that’s not the case at all.”The F.D.A. has said that the ban will be enforced at the manufacturers’ level, and not against individuals.The largest U.S. tobacco companies have considerable financial stakes in the menthol cigarette market, which the Federal Trade Commission estimates is a little more than one-third of all U.S. cigarette sales. Menthol cigarette sales for Reynolds American, which makes the top-selling Newport brand, total about $7 billion a year, research by Goldman Sachs shows.Reynolds has vowed to fight the ban all the way to the Supreme Court, a battle that could postpone implementation of the final prohibition rule for years. Both Altria, which makes menthol Marlboros, and Reynolds have attempted to soften their public image in recent years with pledges of a smoke-free future, marketing e-cigarettes like NJOY and the popular Vuse products. Yet cigarettes still make up three-quarters of the $76 billion U.S. tobacco market, with alternatives like vapes trailing far behind, according to Goldman Sachs estimates.Convenience store, gas station and wholesaler groups have stacked the White House meeting calendar, too, predicting a loss of $34 billion in sales from menthol cigarettes and snacks and drinks purchased by customers, and from flavored cigars that would be banned under a companion proposal. The menthol ban would not cover the sale of menthol e-cigarettes.The old R.J. Reynolds Tobacco Company factory sits just blocks away from its current headquarters in Winston Salem, N.C.Caitlin Penna for The New York TimesMr. Biden’s administration has called the effort a “critical piece” of his Cancer Moonshot initiative, noting that about 30 percent of all cancer deaths are caused by smoking. The F.D.A. has estimated that the menthol ban could reduce smoking by 15 percent in 40 years. Studies project that as many as 650,000 smoking-related deaths could be avoided.The agency proposed the ban more than a year ago and forwarded it to the White House in October. Public health groups have been at the edge of their seats watching the White House calendar fill with meetings, mostly from opponents of the ban.“Each day we wait is another day for Big Tobacco to hook new users and target communities with menthol cigarettes and flavored cigars,” Nancy Brown, chief executive of the American Heart Association, said in a statement. “By prohibiting the sale of menthol cigarettes and flavored cigars, the administration would make historic progress in saving lives from tobacco use.”About 18.5 million smokers choose a menthol brand. Researchers say the cooling sensation of the menthol flavor makes it easier to start smoking and harder to quit. Public opinion polls have shown that about 60 percent of Americans favor banning menthol cigarettes.Tobacco companies have been criticized for decades for targeting Black communities, with studies documenting industry marketing for menthol cigarettes in magazines like Essence and Ebony, and with billboards and discounts targeted at Black neighborhoods.Researchers have documented decades of tobacco industry marketing for menthol cigarettes in magazines like Essence and Ebony, and with billboards and discounts targeted at Black neighborhoods.via American Heart AssociationLobbying over the ban has been intense, with Reynolds and Altria donating millions of dollars in recent years to Republican-controlled super PACs and also spending millions lobbying in Congress.Some Republican lawmakers have opposed the ban, including Senator Marco Rubio of Florida, who is supported by a PAC that received $10,000 from Reynolds late in 2022. He wrote letters in July warning that the ban could give Mexican drug cartels a new illegal substance to traffic.A spokesman for Mr. Rubio said two Democrats signed a similar letter and that supporters backed the senator because they agreed with his agenda, not the other way around.Some House Republicans have also sent letters to the administration warning that the ban could have a disastrous effect on small businesses and that it could encourage cigarette smuggling that would benefit terrorist groups.In June, a House appropriations bill included a provision that would have prohibited any spending on imposing the ban. Representative Andy Harris, a Republican and doctor from Maryland, argued that a ban would “take products out of the legal system and put them into illicit markets,” helping criminals and straining law enforcement.Representative Debbie Wasserman Schultz, Democrat of Florida, introduced a measure to protect the ban, telling fellow House members that they had “succumbed to Big Tobacco yet again” and urging them to protect future generations. “We have to prevent more death,” she said.The bill stalled on the House floor and is said to have little chance of passing.Opponents of the ban demonstrated last month in front of the Manhattan office of Senator Chuck Schumer, the Democratic majority leader.Gwen Carr, the mother of Eric Garner, who died after a police officer placed him in a chokehold, warned at the protest that a menthol ban would increase police encounters. “This will create more havoc in the Black and brown communities,” she said.In an interview, Ms. Carr said she had not received money from tobacco companies. “I can’t be bought,” she said.Gwen Carr, the mother of Eric Garner, at a rally outside New York City Hall in March, calling in part for legislators to oppose a menthol ban.Michael M. Santiago/Getty ImagesEbonie Riley, a senior vice president at the National Action Network, acknowledged the group had received money from tobacco companies but declined to say how much. She said the group’s opposition to the menthol ban was not related to those donations.“We don’t endorse smoking of any kind, but we do endorse adult decisions,” Ms. Riley said.Ms. Riley also attended one of the largest White House meetings about the ban late last month. Attendees included senior White House officials; Dr. Robert Califf, the F.D.A. commissioner; and Xavier Becerra, the secretary of Health and Human Services. The National Organization of Black Law Enforcement Executives, which for years listed Reynolds as a sponsor and has received funding from Altria, was also there.Opponents to the ban supplied White House officials with a report issued by a task force in Massachusetts, where flavored tobacco has been banned for years, that recommended criminal charges for possession or sale of banned products. Tobacco companies have argued that such a provision would lead to the use of more force by the police in minority communities.Reynolds representatives also met twice with White House officials in November, said Luis Pinto, a company spokesman. He said the company argued that bans were not effective and that the F.D.A. had vastly underestimated the cost of keeping illegal menthol cigarettes out of the country.Mr. Pinto said White House officials had inquired about the matter, and Reynolds followed up with an F.D.A. report estimating that enforcement would cost about $659,000 a year for the work of five employees.“The illicit cigarette market is already thriving; and a menthol ban will only fuel the size, scope and span of that market, as millions of menthol cigarette smokers will look for a replacement,” according to a follow-up letter Reynolds sent on Nov. 14. David Sutton, an Altria spokesman, said the company was also concerned about illicit sales as well as lost tax revenue and jobs.“We believe equitable harm reduction, not prohibition, is the better path forward, and that the F.D.A. should authorize smoke-free products and encourage adult smokers to transition to a smoke-free future,” Mr. Sutton said in an email.David A. Fahrenthold

Published15 hours agoShareclose panelShare pageCopy linkAbout sharingBy Dawn Limbu & Paul BarltropBBC News, LondonTwo women whose mothers died in care homes from Covid said they want to hear why “thousands of people died needlessly on Boris Johnson’s watch”.Jane Wier, from Cirencester, attended the Covid inquiry in London with the Covid-19 Families campaign group.Former Prime Minister Mr Johnson is the latest political figure to give evidence to the public inquiry examining the response to the pandemic.He apologised for the pain, loss and suffering during the pandemic.But Ms Wier said answers were needed so that lessons could be learned for the future.”I’m not sure that what we heard today is going to be sufficient to enable that to happen,” she addedLast week, the former health secretary Matt Hancock told the inquiry that entering lockdown three weeks earlier would have cut deaths in the first Covid wave by 90%.In the first of two days of testimony, Mr Johnson said he should have “twigged” the seriousness of Covid sooner, conceding earlier action could have been taken against the virus.He said he had underestimated the “scale and the pace of the challenge” posed but that this was also true of scientists and the “entire Whitehall establishment”.Image source, PA MediaMr Johnson insisted ministers did their “level best” in the circumstances and defended his record in office.The enquiry asked Mr Johnson about the weeks before the first lockdown, including the controversial decision to let Cheltenham Festival go ahead in March 2020.He said that, with hindsight, mass gatherings should have been stopped earlier and admitted mistakes were made.The former PM added that “there were unquestionably things we should have done differently” and said he took “personal responsibility for all decisions made”.Image source, ReutersMs Wier was joined at the enquiry by fellow campaigner Nicola, who asked not to disclose her surname. She also lost her mother to Covid.”She has no voice now and we need to know that lessons have been learnt so that in future, people won’t have to go through the same as we’ve been through,” she said.Nicola said she was “shocked” by today’s inquiry, saying she felt Mr Johnson had not explained where he thought he went wrong.Dr Kit Yates, senior lecturer at the Department of Mathematical Sciences at University of Bath criticised the government’s actions during the pandemic.”Many decisions were taken that probably weren’t in the country’s best interest,” he said.”Things like if we had stopped to think about the mathematical implications of the forecast and we’d believed them – we might have operated differently,” added Dr Yates.Mr Johnson will return for a second day of questioning on Thursday at 10:00 GMTFollow BBC West on Facebook, X and Instagram. Send your story ideas to: bristol@bbc.co.uk More on this storyBoris Johnson returns for day two of evidence at Covid inquiryPublished1 day agoWhat is the UK Covid inquiry and how does it work?Published37 minutes agoEight tough questions facing Johnson on CovidPublished1 day agoLockdown should have been weeks earlier – HancockPublished6 days agoRelated Internet LinksUK Covid-19 InquiryThe BBC is not responsible for the content of external sites.

Published16 minutes agoShareclose panelShare pageCopy linkAbout sharingThis video can not be playedTo play this video you need to enable JavaScript in your browser.By Paul SeddonPolitics reporterBoris Johnson has said he should have “twigged” the seriousness of Covid sooner, conceding earlier action could have been taken against the virus.Giving evidence to the Covid inquiry, the former prime minister said he had underestimated the “scale and the pace of the challenge” posed.But he said this was also true of scientists and the “entire Whitehall establishment”.And he insisted ministers did their “level best” in the circumstances.In the first of two days of testimony, Mr Johnson sought to defend his record in office, which has come in for criticism from other witnesses who have given evidence to the inquiry.He defended the timing of the first lockdown, saying that modelling had been incorrect and he had been advised not to impose measures too early.He admitted to a “certain amount of incoherence in our thinking,” but added: “Once we decided to act, I think it was pretty fast from flash to bang.”Lockdown should have been weeks earlier – HancockWhat is the UK Covid inquiry and how does it work? Eight tough questions facing Johnson on CovidHe began his testimony by saying he was sorry for the “pain and the loss and the suffering” people experienced during the pandemic.His comments were interrupted by protesters, who were ordered to leave the inquiry room. Some members of bereaved families stood up holding pieces of paper, spelling out the message: “The dead can’t hear your apologies.”Mr Johnson has been criticised for being slow to make decisions during the pandemic and being unable to make up his mind about what to do.Over several hours of questioning by lead inquiry lawyer Hugo Keith KC he put in a measured performance, which largely lacked the tetchy exchanges seen during his grilling over Partygate by a committee of MPs earlier this year.But the former prime minister had to take back an accusation that Mr Keith had suggested he “put his feet up” at his official country retreat during the 2020 February half-term, adding he had confused it with comments from someone else.And he choked up when he described the return of the virus after the first national lockdown, describing 2020 as a “tragic, tragic year”.Image source, ReutersMr Johnson defended his overall approach to the pandemic, adding that Covid had required “completely novel” measures and it was his job to “go through the arguments”.He added that people within government had collectively been reluctant to believe worse-case predictions about the impact of the virus, given the experience of previous diseases.”It would certainly be fair to say of me, the entire Whitehall establishment, scientific community included, that we underestimated the scale and the pace of the challenge,” he said.He added that he was subsequently “rattled” by scenes of chaos in northern Italy in mid-February, when pictures of swamped hospitals hit the world’s media.”We should have collectively twigged much sooner. I should have twigged,” he added.Over more than five hours of testimony, he also:Said the gender balance of his team should have been better and “too many meetings were male-dominated”Admitted he had been unable to retrieve around 5,000 WhatsApp messages from his old phone between January and June 2020, blaming technical problems Denied deleting any messages, adding he had done “his best” to hand over all relevant evidence to the inquirySaid he regretted describing long Covid as “bollocks” in a handwritten note on a document from October 2020Conceded he should not have shaken hands with patients during a hospital visit in March 2020, adding he should have been more “precautionary”He added, however, that given what is known now, mass gatherings should have been stopped earlier than they were.”With hindsight, as a symbol of government earnestness rather than just being guided by the science, we should perhaps have done that,” he said.He also defended his decision to keep Matt Hancock as health secretary, despite being urged to sack him by his former adviser Dominic Cummings, telling the inquiry he considered him a “good communicator”.WhatsApp messages He rejected suggestions that expletive-laden WhatsApp messages between his advisers revealed by the inquiry showed a “toxic” culture in his Downing Street operation.The language in the messages reflected the “deep anxiety” of people doing their best, he said.He added it also showed that the people around him were “naturally self-critical, and critical of others,” adding that this was “creatively useful” when it came to making decisions.And he revealed that he had spoken to former civil servant Helen MacNamara, who has previously accused him of failing to tackle “misogynistic language” used about her in a WhatsApp group by Mr Cummings.”I don’t remember seeing it at the time, but I must have seen it because I was on the group,” he told the inquiry.”I have rang Helen MacNamara to apologise to her for not having called it out.”More on this storyLockdown should have been weeks earlier – HancockPublished5 days agoCovid inquiry: Key points from Cummings evidencePublished31 October

Like any typical car or house or society, the pace at which parts of our bodies fall apart varies from part to part.
A study of 5,678 people, led by Stanford Medicine investigators, has shown that our organs age at different rates — and when an organ’s age is especially advanced in comparison with its counterpart in other people of the same age, the person carrying it is at heightened risk both for diseases associated with that organ and for dying.
According to the study, about 1 in every 5 reasonably healthy adults 50 or older is walking around with at least one organ aging at a strongly accelerated rate.
The silver lining: It may be possible that a simple blood test can tell which, if any, organs in a person’s body are aging rapidly, guiding therapeutic interventions well before clinical symptoms manifest.
“We can estimate the biological age of an organ in an apparently healthy person,” said the study’s senior author, Tony Wyss-Coray, PhD, a professor of neurology and the D. H. Chen Professor II. “That, in turn, predicts a person’s risk for disease related to that organ.”
Hamilton Oh and Jarod Rutledge, graduate students in Wyss-Coray’s lab, are lead authors of the study, which will be published online Dec. 6 in Nature.
Biological versus chronological age
“Numerous studies have come up with single numbers representing individuals’ biological age — the age implied by a sophisticated array of biomarkers — as opposed to their chronical age, the actual numbers of years that have passed since their birth,” said Wyss-Coray, who is also the director of the Phil and Penny Knight Initiative for Brain Resilience.

The new study went a step further, coming up with distinct numbers for each of 11 key organs, organ systems or tissues: heart, fat, lung, immune system, kidney, liver, muscle, pancreas, brain, vasculature and intestine.
“When we compared each of these organs’ biological age for each individual with its counterparts among a large group of people without obvious severe diseases, we found that18.4% of those age 50 or older had at least one organ aging significantly more rapidly than the average,” Wyss-Coray said. “And we found that these individuals are at heightened risk for disease in that particular organ in the next 15 years.”
Only about 1 in 60 people in the study had two organs undergoing aging at that fast clip. But, Wyss-Coray said, “They had 6.5 times the mortality risk of somebody without anypronouncedly aged organ.”
Using commercially available technologies and an algorithm of their own design, the researchers assessed the levels of thousands of proteins in people’s blood, determined that nearly 1,000 of those proteins originated within one or another single organ, and tied aberrant levels of those proteins to corresponding organs’ accelerated aging and susceptibility to disease and mortality.
They started by checking the levels of nearly 5,000 proteins in the blood of just under 1,400 healthy people ages 20 to 90 but mostly in mid- to late stages of life, and flagging all proteins whose genes were four times more highly activated in one organ compared with any other organ. They found nearly 900 such organ-specific proteins, which they whittled down to 858 for purposes of reliability.
To do this, they trained a machine-learning algorithm to guess people’s age based on the levels of those nearly 5,000 proteins. The algorithm tries to pick proteins that best correlate with a trait of interest (in this case, accelerated biological aging in a person or in a particular organ) by asking, one by one, “Does this protein enhance the correlation?”
The scientists verified the algorithm’s accuracy by assessing the ages of another 4,000 or so people who were somewhat representative of the U.S. population.

Then they used the proteins they’d identified to zero in on each of the 11 organs they’d selected for analysis, measuring levels of organ-specific proteins within each individual’s blood.
While there was some modest aging synchrony among separate organs within any person’s body, that person’s individual organs largely went their separate ways along the aging path.
Organ age gap
For each of the 11 organs, Wyss-Coray’s team came up with an “age gap”: the difference between an organ’s actual age and its estimated age based on the algorithm’s organ-specific-protein-driven calculations. The researchers found that the identified age gaps for 10 of the 11 organs studied (the only exception being intestine) were significantly associated with future risk of death from all causes over 15 years of follow-up.
Having an accelerated-aging organ (defined as having a 1-standard-deviation higher algorithm-scored biological age of the organ than the group average for that organ among people of the same chronological age) carried a 15% to 50% higher mortality risk over the next 15 years, depending on which organ was affected.
People with accelerated heart aging but initially exhibiting no active disease or clinically abnormal biomarkers were at 2.5 times as high a risk of heart failure as people with normally aging hearts, the study showed.
Those with “older” brains were 1.8 times as likely to show cognitive decline over five years as those with “young” brains. Accelerated brain or vasculature aging — either one — predicted risk for Alzheimer’s disease progression as well as the best currently used clinical biomarkers do.
There were likewise strong associations between an extreme-aging (more than 2 standard deviations above the norm) kidney score and both hypertension and diabetes, as well as between an extreme-aging heart score and both atrial fibrillation and heart attack.
“If we can reproduce this finding in 50,000 or 100,000 individuals,” Wyss-Coray said, “it will mean that by monitoring the health of individual organs in apparently healthy people, we might be able to find organs that are undergoing accelerated aging in people’s bodies, and we might be able to treat people before they get sick.”
Identifying the organ-specific proteins that best indicate excessive organ aging and,consequently, elevated disease risk could also lead to new drug targets, he said.
Wyss-Coray, Oh and Rutledge have co-founded a company, Teal Omics Inc., to explore the commercialization of their findings. Stanford University’s Office of Technology Licensing has filed a patent application related to this work.
Researchers from Washington University; the University of California, San Francisco; the Albert Einstein College of Medicine; and Montefiore Medical Center contributed to the work.
The study was funded by the National Institutes of Health (grants P50AG047366, P30AG066515, AG072255, AG057909, AG061155, AG044829, AG066206 R01AG044546, RF1SH053303, RF1AG058501, UQ1AG058922, P01AG003991, RF1AG074007 and T32AG047126), the Stanford Alzheimer’s Disease Research Center, the Michael J. Fox Foundation, the Alzheimer’s Association, the Milky Way Research Foundation and Nan Fung Life Sciences.

If one spouse or partner in a heterosexual couple has high blood pressure, the other partner often does too, according to new research published today in the Journal of the American Heart Association, an open access, peer-reviewed journal of the American Heart Association.
“Many people know that high blood pressure is common in middle-aged and older adults, yet we were surprised to find that among many older couples, both husband and wife had high blood pressure in the U.S., England, China and India,” said senior author Chihua Li, Dr.P.H., a post-doctoral fellow at the University of Michigan and the study’s corresponding author. “For instance, in the U.S., among more than 35% of couples who were ages 50 or older, both had high blood pressure.”
Researchers investigated whether heterosexual partners in the U.S., England, China and India mirrored each other’s high blood-pressure status. Previous studies have explored the union of high blood pressure and other diseases among couples in a single country setting or used small regional samples.
“Ours is the first study examining the union of high blood pressure within couples from both high- and middle-income countries,” said study co-lead author Jithin Sam Varghese, Ph.D., an assistant research professor at the Emory Global Diabetes Research Center at Emory University in Atlanta. “We wanted to find out if many married couples who often have the same interests, living environment, lifestyle habits and health outcomes may also share high blood pressure.”
The researchers analyzed blood pressure measures for 3,989 U.S. couples, 1,086 English couples, 6,514 Chinese couples and 22,389 Indian couples and found: The prevalence of both spouses or partners having high blood pressure was about 47% in England; 38% in the U.S.; 21% in China and 20% in India. Compared to wives married to husbands without high blood pressure, wives whose husbands had high blood pressure were 9% more likely to have high blood pressure in the U.S. and England, 19% more likely in India and 26% more likely in China. Within each country, similar associations were observed for husbands. The association was consistent when the analyses were stratified by area of residence within each country, household wealth, length of marriage, age groups and education levels.”High blood pressure is more common in the U.S. and England than in China and India, however, the association between couples’ blood pressure status was stronger in China and India than in the U.S and England. One reason might be cultural. In China and India, there’s a strong belief in sticking together as a family, so couples might influence each other’s health more,” said study co-lead author Peiyi Lu, Ph.D., a post-doctoral fellow in epidemiology at Columbia University Mailman School of Public Health. “In collectivist societies in China and India, couples are expected to depend and support each other, emotionally and instrumentally, so health may be more closely entwined.”
These findings highlight the potential of using couple-based approaches for high blood pressure diagnosis and management, such as couple-based screening, skills training or joint participation in programs, Li noted.

Study background and details: The researchers used cross-sectional data — capturing a single point in time — taken from studies of aging that are representative of populations across entire countries, including the 2016-17 Health and Retirement Study in the U.S., the 2016-17 English Longitudinal Study on Ageing, the 2015-16 China Health and Retirement Longitudinal Study, and the 2017-19 Longitudinal Aging Study in India. These four studies have harmonized design and measures, and each adopted a household survey that first recruited a primary participant that met the age eligibility — 50 and older for the studies in the U.S. and England and 45 and older for the studies in China and India — and then invited his or her spouse or partner to participate regardless of their age. Couples were defined as heterosexual participants living in the same household who reported to be married or partnered to one another, and those who were older than legal age for marriage for their country at the time of the survey. The average age of husbands in the study was 65.7 years in the U.S.; 74.2 years in England; 61.5 in China; and 57.2 years in India. The average age of wives in the study was 62.9 years in the U.S; 72.5 years in England; 59.2 years in China and 51.1 years in India. High blood pressure was defined based on measurements at one time point. Participants were noted as having hypertension if they had one of the following: systolic blood pressure higher than 140 mm Hg or diastolic greater than 90 mm Hg, as measured by health professionals; or if they answered yes when asked if they had a history of high blood pressure.Among the study’s limitations were its cross-sectional design, meaning it captured a single point in time and thus only one blood-pressure measurement, and that the surveys included only heterosexual couples.
According to the American Heart Association’s 2023 statistics, in 2020, nearly 120,000 deaths were primarily attributable to high blood pressure, and from 2017 to 2020, 122.4 million (46.7%) U.S. adults had high blood pressure.
“Varghese, Lu and colleagues report an important finding among middle-aged and older adults — if your spouse has hypertension, you are more likely to have hypertension, too.
These findings are important because hypertension is among the most dominant modifiable cardiovascular risk factors and remains highly prevalent and poorly controlled on an increasingly global level. As the authors point out, the current focus of clinical and public health strategies to control hypertension on the individual level is not adequate. The authors suggest that interventions that target spouses may, thus, be especially effective,” said Bethany Barone Gibbs, Ph.D., FAHA, an associate professor and chair of the department of epidemiology and biostatistics at the School of Public Health at West Virginia University, and chair of the writing committee for the Association’s 2021 Statement on Physical Activity as a Critical Component of First-Line Treatment for Elevated Blood Pressure or Cholesterol.
“Following this idea, making lifestyle changes, such as being more active, reducing stress or eating a healthier diet, can all reduce blood pressure; however, these changes may be difficult to achieve and, more importantly, sustain if your spouse or partner (and greater family unit) are not making changes with you,” she said. “These findings also hint at a broader approach — interventions using a socioecological model considering determinants of hypertension across individual, interpersonal, environmental and policy levels are likely going to be necessary to reduce the global public health burden of hypertension.”

Pancreatic cancer is one of the deadliest cancers — only about one in eight patients survives five years after diagnosis. Those dismal statistics are in part due to the thick, nearly impenetrable wall of fibrosis, or scar tissue, that surrounds most pancreatic tumors and makes it hard for drugs to access and destroy the cancer cells.
Now, researchers at the Salk Institute have discovered how a class of anti-cancer drugs called HDAC inhibitors can help treat pancreatic cancer by modulating the activation of fibroblasts — the cells that make up that wall of scar tissue.
The new research was published in Nature Communications on December 6, 2023.
“These drugs turn out to be hitting both the tumor itself as well as the fibrotic tissue around it. This could be a very effective way to treat pancreatic cancers, which have typically been very difficult to reach,” says senior author Professor Ronald Evans, director of Salk’s Gene Expression Laboratory and March of Dimes Chair in Molecular and Developmental Biology.
In response to a new pancreatic tumor, the pancreas typically activates fibroblasts — the connective cells that support the structure of most organs. When flipped from a resting state to an active state, fibroblasts build a thick layer of scar tissue around the cancer. While this normal protective mechanism can help wall off a cancer and prevent its spread, fibroblasts also produce signaling molecules that the tumor itself takes advantage of to grow.
“In the context of most pancreatic cancers, fibroblasts are acting as both good players and bad players,” says Michael Downes, senior staff scientist and co-corresponding author on the paper. “It’s a double-edged sword.”
In the new research, the team probed the effect on fibroblasts of an experimental class of cancer drugs known as histone deacetylase (HDAC) inhibitors. HDACs alter the three-dimensional structure of DNA inside cells, making some stretches of DNA easier or harder for other molecules to access and read. Targeting HDACs can therefore prevent cells from making large changes to their behavior, such as the out-of-control growth of cancer cells. But how the drugs work on all cell types is not well understood.

In experiments on isolated cells, the researchers discovered that HDAC inhibitors prevented fibroblasts from becoming activated and tumor supportive.
“Using HDAC inhibitors actually did two things — it both turned down the growth signals from the fibroblasts to the cancer cells and it reduced the actual activation and accumulation of the fibroblasts,” says Gaoyang Liang, first author and research associate in Evans’ lab.
In mice, the researchers found that one experimental HDAC inhibitor, entinostat, both reduced the activation of fibroblasts around pancreatic tumors and slowed tumor growth. When the researchers analyzed data from humans with pancreatic cancer, they discovered something similar: the higher the levels of HDAC1 in the fibrotic tissue around a patient’s tumor, the worse their outcome.
“This is in agreement with what we saw in cells and in mice,” says Downes. “If you have more HDAC activities in the fibroblasts, you have a worse outcome. On the other hand, if you inhibit the HDACs, you have a better outcome.”
Since HDAC inhibitors work by preventing cells from activating certain genetic programs, the researchers wanted to know which stretches of DNA impacted by the drugs were most relevant for fibroblast activation. They identified several genes that HDAC inhibitors prevent from being expressed — suggesting that new drugs could target those genes to keep fibroblasts from becoming activated and promoting cancer growth and fibrosis.
“There have been some questions in the past about whether targeting fibroblasts is a good thing or a bad thing in pancreatic cancers, because people have shown that if you get rid of fibroblasts altogether it actually makes the cancers more aggressive,” says Annette Atkins, co-author of the study and senior research scientist in Evans’ lab. “But what our results suggest is that we don’t have to get rid of them; just limiting their activation is beneficial.”
More work is needed to pinpoint how to best deliver HDAC inhibitors to the dense fibrotic tissue around pancreatic tumors, as well as how they might be most effectively combined with other cancer treatments.
Other authors of the paper are Tae Gyu Oh, Nasun Hah, Yu Shi, Morgan L. Truitt, Corina E. Antal, Annette R. Atkins, Yuwenbin Li, Antonio F. M. Pinto, Dylan C. Nelson, Gabriela Estepa, Senada Bashi, Ester Banayo, Yang Dai, Ruth T. Yu, Tony Hunter, and Dannielle D. Engle of Salk; Hervé Tiriac of UC San Diego; Cory Fraser of HonorHealth Scottsdale; Serina Ng, Haiyong Han, and Daniel D. Von Hoff of The Translational Genomic Research Institute; and Christopher Liddle of the University of Sydney.
The work was supported by grants from the Lustgarten Foundation (including award 552873), Don and Lorraine Freeberg Foundation, Ipsen Bioscience, a Stand Up To Cancer-Cancer Research UK-Lustgarten Foundation Pancreatic Cancer Dream Team Research Grant (SU2C-AACR-DT-20-16), a Ruth L. Kirschstein National Research Service Award (F32CA217033), a Life Sciences Research Foundation Fellowship, the Damon Runyon Cancer Research Foundation (DRG-2244-16), the National Institutes of Health (CA082683, 5T32CA009370), and the William Isacoff Research Foundation.