Publisher Health

In the UK parents only qualify for treatment on the NHS if they have had three miscarriages in a row.EastEnders actress Lacey Turner has has two miscarriages and believes the current system needs reforming. New research published in The Lancet reveals that miscarriage doubles the risk of depression and quadruples the risk of suicide.

Fixing traumatic injuries to the skin and bones of the face and skull is difficult because of the many layers of different types of tissues involved, but now, researchers have repaired such defects in a rat model using bioprinting during surgery, and their work may lead to faster and better methods of healing skin and bones.
“This work is clinically significant,” said Ibrahim T. Ozbolat, Hartz Family Career Development Associate Professor of Engineering Science and Mechanics, Biomedical Engineering and Neurosurgery, Penn State. “Dealing with composite defects, fixing hard and soft tissues at once, is difficult. And for the craniofacial area, the results have to be esthetically pleasing.”
Currently, fixing a hole in the skull involving both bone and soft tissue requires using bone from another part of the patient’s body or a cadaver. The bone must be covered by soft tissue with blood flow, also harvested from somewhere else, or the bone will die. Then surgeons need to repair the soft tissue and skin.
Ozbolat and his team used extrusion bioprinting and droplet bioprinting of mixtures of cells and carrier materials to print both bone and soft tissue. They report their results in Advanced Functional Materials.
“There is no surgical method for repairing soft and hard tissue at once,” said Ozbolat. “This is why we aimed to demonstrate a technology where we can reconstruct the whole defect — bone to epidermis — at once.”
The researchers attacked the problem of bone replacement first, beginning in the laboratory and moving to an animal model. They needed something that was printable and nontoxic and could repair a 5-millimeter hole in the skull. The “hard tissue ink” consisted of collagen, chitosan, nano-hydroxyapatite and other compounds and mesenchymal stem cells — multipotent cells found in bone marrow that create bone, cartilage and bone marrow fat.

In an effort to determine the potential for COVID-19 to begin in a person’s gut, and to better understand how human cells respond to SARS-CoV-2, the scientists used human intestinal cells to create organoids — 3D tissue cultures derived from human cells, which mimic the tissue or organ from which the cells originate. Their conclusions, published in the journal Molecular Systems Biology, indicate the potential for infection to be harboured in a host’s intestines and reveal intricacies in the immune response to SARS-CoV-2.
“Previous research had shown that SARS-CoV-2 can infect the gut,” says Theodore Alexandrov, who leads one of the two EMBL groups involved. “However, it remained unclear how intestinal cells mount their immune response to the infection.”
In fact, the researchers were able to determine the cell type most severely infected by the virus, how infected cells trigger an immune response, and — most interestingly — that SARS-CoV-2 silences the immune response in infected cells. These findings may shed light on the pathogenesis of SARS-CoV-2 infection in the gut, and indicate why the gut should be considered to fully understand how COVID-19 develops and spreads.
According to Sergio Triana, lead author and a doctoral candidate in EMBL’s Alexandrov team, the researchers observed how infected cells seem to start a cascade of events that produce a signalling molecule called interferon.
“Interestingly, although most cells in our mini guts had a strong immune response triggered by interferon, SARS-CoV-2-infected cells did not react in the same way and instead presented a strong pro-inflammatory response,” Sergio says. “This suggests that SARS-CoV-2 interferes with the host signalling to disrupt an immune response at the cellular level.”
Coronaviruses, including SARS-CoV-2, cause infection by latching on to specific protein receptors found on the surface of certain cell types. Among these receptors is the protein ACE2. Interestingly, the researchers showed that the infection is not explained solely by the presence of ACE2 on the surface of the cells, highlighting our still limited knowledge about COVID-19, even after a year of tremendous research efforts worldwide.
As the disease progressed in the organoids, the researchers used single-cell RNA sequencing, which involves several techniques to amplify and detect RNA. Among these single-cell technologies, Targeted Perturb-seq (TAP-seq) provided sensitive detection of SARS-CoV-2 in infected organoids. Lars Steinmetz’s research group at EMBL recently developed TAP-seq, which the researchers combined with powerful computational tools, enabling them to detect, quantify, and compare expression of thousands of genes in single cells within the organoids.
“This finding could offer insights into how SARS-CoV-2 protects itself from the immune system and offer alternative ways to treat it,” Lars says. “Further study can help us understand how the virus grows and the various ways it impacts the human immune system.”
Story Source:
Materials provided by European Molecular Biology Laboratory. Original written by Ivy Kupec. Note: Content may be edited for style and length.

On a wrinkled sheet of lined paper tucked in my mom’s purse was a list of places we had jotted down, memories to visit. It was January 2020, and my mother and I were on a trip to Chicago, to see the places from her past and my early childhood in and around the Englewood section of the city, where she was born and raised, and where I was, too, before we moved to Denver in 1969. As we drove south in our rental car, from Roosevelt University on South Michigan Avenue, where Mom attended college in the 1950s, toward what was called the Black Belt, I imagined myself as a 7-year-old sitting on the second-floor balcony of my great-aunt’s brick building on South Vernon Avenue, watching people bustle below. I would strain to hear my mother soaking in news and gossip from her aunties, their voices soft and Southern, before I was shooed away, warned to stay out of grown folks’ business.I was most excited to revisit Brice’s, the liquor shop on South Vernon Avenue owned by my dad’s close friend. Most Saturdays, while my mother visited her family a few blocks away, my father would stop in to hang out and talk about fishing with Mr. Brice, whom I remember giving my sister and me free candy and ice cream sandwiches. His store served as a welcoming kind of community center for the neighborhood, and the oaky smell of any liquor shop still brings back that memory. Thinking of the sheltering arms and safe embrace of family and neighbors in that community, a line from the Chicago poet Gwendolyn Brooks came to mind: “that we are each other’s harvest:/we are each other’s business:/we are each other’s magnitude and bond.”But the mixed-income, largely working-class Black neighborhood we remembered was mostly gone. My mother’s childhood apartment had been razed, reduced to a garbage-strewn vacant lot. The home she and my father lived in after they married was boarded up, as was her elementary school, Betsy Ross. Harvard Elementary, where I went, was still there, now known as the John Harvard Elementary School of Excellence, but many of the houses across the street were abandoned, as were several nearby storefronts. Englewood High School was closed in 2008 because of poor performance. Mr. Brice’s was long gone, and the corner looked seedy enough that I refused to let my fearless 89-year-old mother get out of the car.Englewood — near the middle of the country’s third-largest city — reminded me of the rural Mississippi my grandmother and her siblings left behind for safety and greater opportunities nearly a hundred years ago during the Great Migration. But it is Chicago, not the rural South, that has the country’s widest racial gap in life expectancy: In the Streeterville neighborhood, nine miles north, which is 73 percent white, residents live, on average, to 90 years old; in Englewood, where nearly 95 percent of residents are Black, people live to an average of only 60.Over this past year, Black lives have been cut even shorter by Covid-19, which strikes marginalized communities disproportionately, creeping into the fault lines of our society. Black Americans have been hospitalized with Covid-19 at nearly three times the rate of white Americans, and the death rate is twice as high. The deaths have taken a toll: In the first six months of the pandemic, the average life span of an American declined by a full year: from 78.8 years in 2019 to 77.8 years in the first half of 2020. But Black life expectancy plummeted more, declining by nearly three years in the same time frame.One in 379 Black Chicagoans have died due to Covid-19. In Englewood’s 60621 ZIP code, 1 in 363 people have died due to Covid, compared with 1 in 2,162 people in Streeterville’s 60611 ZIP code. That same Streeterville ZIP code had one of the highest Covid vaccination rates in the city, with 42.6 percent of residents having received a full series and 60.7 percent one dose by late April. Englewood’s 60621 ZIP code had one of the lowest vaccination rates in the city, with 14.2 percent having received a full series and only 22.1 percent at least one dose.But long before the pandemic, the story of Chicago’s yawning disparity between Black and white life spans was written through my own family history. How did a Promised Land to generations of Black families become a community of lost lives?The author’s family in Chicago in 1962; the author at her family’s home on South Wentworth; her great-aunt and -uncle’s former home on 62nd and South Vernon in January 2020.Photo illustration by Mark HarrisMy seven great-aunts and -uncles, the Clement family, left Mississippi in the mid-1920s. Like so many African-Americans, they fled the South to escape the indignities and menace of Jim Crow laws and the epidemic of lynchings and other forms of racial terrorism, and to pursue the chance to work in a thriving economy fueled by rapidly growing factories, mills and packinghouses. One sister went to New York City, one to Cleveland and another to Detroit. The other four siblings chose Chicago. They had read articles about the city in The Chicago Defender, the Black newspaper that was circulated widely throughout the South, and boarded the Illinois Central together. My grandmother Mollie Dee, still a teenager, stayed behind on the farm that their parents, Charles and Mahalia, owned in Iuka, a city in the northeastern part of Mississippi.My great-aunts and -uncles settled on the South Side in the area where most of the Black population resided, which stretched from 22nd Street to 31st Street along State Street and later expanded south. Beginning in 1916, as Black Southerners poured into the city, the Chicago Real Estate Board promoted a set of racially restrictive covenants that allowed property owners to keep certain communities white by preventing Black people from occupying, renting or buying housing. Increasing numbers of newly arrived Black residents were hemmed into specific neighborhoods, including the area where my family put down roots.My mother’s classmate Lorraine Hansberry used what happened to her family as inspiration for her 1959 play, “A Raisin in the Sun.” The Hansberrys bought their home in 1937, in an area whiter than where our family lived, just south of the University of Chicago. Mobs confronted the family, and a white neighbor sued the Hansberrys, contending that a restrictive agreement prevented Black people from buying homes in the neighborhood. Carl Hansberry, Lorraine’s father, challenged the case, and in 1940 Hansberry v. Lee reached the U.S. Supreme Court. He won, and that suit laid the groundwork for a later case that struck down the racist covenants in 1948.‘Now you drive through communities like Englewood and see empty lot after empty lot after empty lot.’My Aunt Sweetie, who could barely read or write, managed to scrimp and save the money she earned as a maid and bought a two-story brick home on 62nd and South Vernon Avenue, big enough to house several family members. My Aunt Lottie and her husband, Brother Harry, opened a grocery store nearby on South Parkway. My grandmother, the youngest of the Clement children, made her way to Chicago several years after her older siblings, in 1928. She moved into the home on South Vernon and also worked as a maid. Shortly after she arrived, she met my grandfather, Homer Alexander, at a dance. He was also from Mississippi and was captivated by her free spirit and flouncy flapper dress. They married in 1929.By then, the Black population of Chicago had ballooned to about 7 percent from 2 percent in 1910. White residents had fled from the area known as Bronzeville on the South Side, which had become home to a vast majority of African-American Chicagoans — about a quarter million by 1930. The stark segregation would be reflected in dramatically different statistics for disease and death.While race affects health outcomes regardless of income and education, and longstanding discrimination in the institutions and structures of American society erodes the health and well-being of all Black Americans, health most directly correlates with the resources a community has to offer. From the beginning of life to the end, the environment where people make their homes, work, attend school, play and worship has a profound influence on health outcomes. Wealthy communities tend to be safer and have adequate health care services, outdoor space, clean air and water, public transportation and affordable healthful food, as well as opportunities for education, employment and social support that all contribute to longer, healthier lives. Poorer communities generally lack a healthful environment and basic services and support, which makes the lives of residents more difficult and ultimately shorter. Violence, too, is harder to keep at bay in neighborhoods that lack options, services and hope.In Englewood, about 60 percent of the residents have a high school diploma or equivalency or less, and 57 percent of households earn less than $25,000 a year. Streeterville, on the other side of Chicago’s chasm, has a median income of $125,000. The vast majority of residents there have at least a college degree; 44 percent have a master’s degree or higher. And, predictably, Englewood has long shouldered an unequal burden of disease. It has among the city’s highest rates of deaths from heart disease and diabetes, as well as rates of infant mortality and children living with elevated blood-lead levels, according to the Chicago Department of Public Health. These differences all lead up to that irrefutable racial gap in life spans.“It is very clear that life expectancy is most influenced by geography,” said Dr. Judith L. Singleton, a medical and cultural anthropologist who is conducting an ongoing study at Northwestern University about life expectancy inequality across Chicago neighborhoods. Her father came to Chicago from New Orleans in the 1930s and settled in Bronzeville. In 1960, her parents bought a home on the far South Side. After her mother died, she finally moved her dad out of his home after 40 years because of a lack of services, including nearby grocery stores, and fear for his safety. “If you live in a neighborhood with lots of resources and higher incomes, your chances of a longer life are better — and the opposite is true if your community has few resources,” she said. “There’s something really wrong with that.”Historically, there has been a damning explanation of why poor communities have crumbling conditions and a dearth of services: not that something is wrong that needs to be fixed, but that something is wrong with the people and the community themselves. It’s their fault; they did this to themselves by not eating right, by avoiding medical care, by being uneducated. Nearly every time former President Donald Trump opened his mouth to speak about Black communities in Detroit, Baltimore, Atlanta and, yes, Chicago, he parroted the underlying assumption that Black communities in America are solely to blame for their own problems. In 2019, during sworn testimony before Congress, Trump’s former lawyer Michael Cohen claimed that his boss had characterized Black Chicago with disdain and blame: “While we were once driving through a struggling neighborhood in Chicago,” Trump “commented that only Black people could live that way.” In 2018, the American Values Survey found that 45 percent of white Americans believed that socioeconomic disparities are really a matter of not trying hard enough — and that if Black people put in more effort, they could be just as well off as white people.What really happened was more sinister. On the South Side of Chicago, a pattern of intentional, government-sanctioned policies systematically extracted the wealth from Black neighborhoods, bringing an erosion of health for generations of people, leaving them to live sick and die young.Like mine, Dr. Eric E. Whitaker’s family traveled a path up North from Mississippi to the South Side of Chicago. I met Whitaker, a physician and former director of the Illinois Department of Public Health, in 1991, when I was a health-communications fellow at what is now known as the Harvard T.H. Chan School of Public Health. He was in medical school at the University of Chicago Pritzker School of Medicine, taking a year off to earn his master’s in public health. After we became friends, we discovered that his maternal grandparents had owned a three-flat building around the corner from our family home on South Vernon Avenue.He recalls the area as a thriving mixed-income neighborhood, a place of comfort, full of life and energy, though all that remains of his grandparents’ building is a memory and a pile of rubble. “What I remember of my grandparents’ home was the vitality,” said Whitaker, who would meet his close friend Barack Obama during the year he spent at Harvard, when Obama was at Harvard Law School. “There would be people on porches, kids playing in the streets. It was aspirational. Now you drive through communities like Englewood and see empty lot after empty lot after empty lot. Every once in a while I take my kids to see where Dad came from. When I show them the vacant lot where Grandma’s house used to be, they think, Wow, this is sad.”But what Whitaker and I remember with a warm glow wasn’t the whole story. Even as our relatives were starting their hopeful new lives in the 1930s, the government-sanctioned practice of redlining arose in response, enforcing segregation, lowering land and property values and seeding disinvestment and decay for more than 30 years.When my grandmother became pregnant with my mom in 1929, my grandparents rented a house on the same block as Brother Harry’s grocery store. My mom was born at home in 1930, my Uncle Homer the following year. My grandfather worked as a bellhop at a downtown hotel on Michigan Avenue, while my grandmother, who had gone to beauty school, was doing hair out of a salon not far from the house on South Vernon. During the Depression, my grandfather left Chicago to find work. My grandmother couldn’t hold onto their rental apartment and moved with her children to 59th and South Prairie, next to the L tracks. My mother remembers sitting in front of the window in the room she shared with her brother, watching the trains rumble by full of white people on the way to and from work and hoping her father would return home soon. When we visited last year, my mother pointed to a desolate patch of land. “It used to be right there,” she said.‘Our own federal policies actually created a lot of the conditions that people now are faced with.’A few years later, after my grandfather returned, he was hired as a Pullman porter, one of the best jobs available to Black men at the time. Though hauling suitcases and serving white folks traveling on trains in sleeping cars was backbreaking, sometimes demeaning work, it provided a firm financial footing for my grandparents and a toehold into middle class that allowed them to put money aside. In the early 1940s, they bought a solid two-flat building on East 64th Place. They lived on the first floor and rented the second floor and the basement. I asked my mother how Grandfather could afford the down payment, and she told me he didn’t have a mortgage; he bought the house on some kind of contract.Beginning in the 1940s, speculators created home-sale contracts to trap African-American families who were eager to purchase homes but whose housing choices were restricted by racial segregation and redlining. These contracts offered Black buyers the false impression of a mortgage but without the protections. Instead, buyers made monthly installments at high interest rates toward bloated purchase prices, but never gained ownership until the contract was paid in full and all conditions met. That meant that contract sellers held the deed of the home and were able to evict the buyers for any missed payments. Black contract buyers accumulated no equity in their homes. Though activists fought this housing injustice, in the 1950s and 1960s more than 75 percent of Black home buyers in Chicago bought on contract, like my grandparents did.According to the 2019 report “The Plunder of Black Wealth in Chicago,” released by the Samuel DuBois Cook Center on Social Equity at Duke University, this practice extracted between $3.2 billion and $4 billion from Chicago’s Black community. “The curse of contract sales still reverberates through Chicago’s Black neighborhoods (and their urban counterparts nationwide),” the report’s authors wrote, “and helps explain the vast wealth divide between Blacks and whites.” My mother recalls that her father was always terrified about missing a payment because he knew he could lose his building — and their home — at any time.In 1953, my mother was attending the graduate school of social work at Loyola University, and doing her fieldwork in the psychiatric unit at Edward Hines Jr. V.A. Hospital. My dad, Andres Villarosa, was working as a bacteriologist at the same hospital and gave my mother a ride to work one day. They were married in 1954 and moved into a two-bedroom apartment on 64th and South Vernon, in a building owned by a friend of my grandmother’s not far from where my mother’s aunts and uncles lived. She couldn’t find the house when we visited. I pointed to a building with boarded-up windows, peeling paint on the trim and splintered steps leading to the doorway. “Mom, is that it?” She nodded.My grandparents managed to hold onto their building, and in 1958 my grandmother persuaded my grandfather to buy another one; but this time they were able to get a real mortgage. In the early 1960s, after my sister and I were born, our family moved into the building on 75th and South Wentworth with our grandparents.But by the time I was in third grade at Harvard Elementary School, the toxic combination of housing covenants, redlining and contract buying had sapped the life out of many of the neighborhoods on the South Side. The city’s deliberate placement of high-rise public-housing projects in Black communities effectively concentrated poverty and limited economic opportunity for public-housing residents. The unemployment rate for Black Chicagoans was 12.8 percent, compared with 6.7 percent for their white counterparts. By that year, the city’s homicide rate had more than doubled from a decade before, and nearly one-third of all Black residents lived below the poverty level.“The neighborhoods that we’re talking about are the way they are largely because of social and public policies that really so destroyed many cities, and particularly Black and brown neighborhoods,” said Dr. Helene Gayle, a physician who spent 20 years at the Centers for Disease Control and Prevention and is now the president and C.E.O. of the Chicago Community Trust, a philanthropic community organization focused on addressing the racial and ethnic wealth gap. “These are not about choices,” Gayle continued. “These are about the reality of options that people have in their lives or don’t have in their lives and how our own federal policies actually created a lot of the conditions that people now are faced with.”I remember my parents’ complaints about Chicago and whisper-hiss conversations about how they needed to get out of the city. They looked in a mostly white suburb near my father’s job at Hines Hospital. While house hunting, my mother asked a police officer if the area would be safe for a Black family, and he told her, “I can’t guarantee that we could protect you and your family.” My mom later told me, “That was all I needed to know; we couldn’t move there. If someone hurt my baby girls, your father would kill them, he would go to jail and I’d be a single mother.”Mollie Dee Alexander, the author’s grandmother; the author’s parents in the 1970s; the author’s mother at Betsy Ross Elementary School, January 2020.Photo illustration by Mark HarrisIn 1969, my father applied for a transfer to Denver, and my parents packed up our Rambler station wagon and moved the family to the suburb of Lakewood, Colo. We were part of a larger trend of Black suburbanization: In the 1970s, the overall Black population in American suburbs increased by 70 percent as families like mine left the city, taking advantage of a world newly expanded by civil rights legislation that finally dismantled some of the institutional discrimination in housing and education.Leaving Chicago, the only city she had ever known, and moving far away from her parents and extended family was especially wrenching for my mother. But my parents wanted to get out of a rapidly decomposing Black Chicago and give my sister and me a better childhood than the one they had. To them it meant we would grow up in a house with a backyard, not an apartment near the Dan Ryan Expressway; go to a school with a cafeteria, not run to the church across the street at noon to eat a free lunch served by volunteers in the basement. We would learn alongside the white children, play outside with them in the safe streets of our suburban community and get all the privileges reserved for them that weren’t available in the resource-starved Black neighborhoods of Chicago.Around the time we left, many other Black working- and middle-class families left Chicago, too. Englewood hemorrhaged Black people: According to data gathered by the Great Cities Institute at the University of Illinois, Chicago, between 1970 and 2019, almost 65,000 Black residents relocated, a decrease of 75 percent, even though the neighborhood remains almost all Black. Between 1980 and 2019, the overall Black population of Chicago fell by more than 33 percent, a loss of some 400,000 residents.As middle-class families departed and wealth shrank, so did services and support. For the first half of the 20th century, Englewood was home to the city’s largest shopping district outside of the Loop. But as the neighborhood declined, several large department stores and many small businesses left or closed shop. A 2013 investigation by the WBEZ radio station found that since 2002, about 200 Chicago public schools had either shut down or been radically shaken up, with 50 schools closing in 2013 alone; of the more than 70,000 students who experienced a school closure or complete restaffing, 88 percent were Black. Between 1970 and 1991, 36 percent of Chicago’s hospitals closed, many of them serving communities of color. Michael Reese, the hospital on South Ellis Avenue where Eric Whitaker’s mother worked as a nurse for more than 30 years, and where Whitaker and his two brothers were born, closed in 2008; demolition began the next year. As these trends drained the lifeblood from communities, a 2010 analysis published in the American Journal of Public Health found that virtually no progress was made in the previous 15 years to close the city’s racial health gap. “You can take a map of poverty,” Whitaker said, “overlay with every class of disease and it’d be the same place.”In 1997, Whitaker helped found Project Brotherhood, a weekly clinic for Black men, in the Woodlawn neighborhood. Though a full-service clinic supported by the Cook County health system was already in place, Whitaker and his colleagues noticed that Black men rarely used it. “We ended up going to do focus groups with men from the community to ask them the question: ‘You have a resource here, why don’t you use it?’” he said. “And the answer was that men felt disrespected by the health care system. Others said they didn’t want people to see them going to the center or they just didn’t find it a place of comfort. That meant they were delaying care they absolutely needed to get.”But according to a 2016 study published in the American Journal of Preventive Medicine, access to medical care accounts for only 20 percent of the contributors to healthy outcomes; socioeconomic and environmental factors of the community, at 50 percent, are far more important. “My ideas over time have evolved as I’ve gotten more exposed to the explicit tie between health and wealth,” said Whitaker, who now runs Zing Health, which offers Medicare Advantage health plans for underserved seniors. “I feel you can make more of an impact by having job and economic development, rather than putting another clinic or any kind of health services out in the community.”My mother and I were relieved when we saw the family home on South Vernon still standing, and the building on South Wentworth perfectly intact. But a few relics and memories won’t save these communities that were the dream of generations of our ancestors who found their way out of the horrors of the Jim Crow South and hoped to start better lives — only now to have them cut short by longstanding discrimination, neglect and disinvestment.My mother turned 90 last year after our trip, and I am grateful for her long life — bolstered by leaving Chicago and spending her later years in more healthful environments. I looked back at the picture I took of her, standing in front of her elementary school on 60th and South Wabash Avenue, the building sagging with decay, and thought of not just what we left, but also what was lost.As my mother points to the stained bricks on the facade of her school building, the January wind churning dead leaves at her feet, I notice she’s standing under a towering and sturdy tree. Though it is stripped bare by the winter, its roots run deep in front of the faded school where Mom’s little-girl self roamed the halls sharing secrets with her friend Lorraine. I think of the people who remained, including my great-aunts and -uncles, and who still live in and around Bronzeville — and the hard effort and resilience it takes to survive and thrive in an environment that has been intentionally robbed of the resources our ancestors worked so hard to produce. I am reminded of the lines of another poem by Gwendolyn Brooks, who attended Englewood High School some years before my mother and Hansberry. In “The Second Sermon on the Warpland,” she writes: “It is lonesome, yes. For we are the last of the loud./Nevertheless, live./Conduct your blooming in the noise and whip of the whirlwind.”Top photograph in opening photo illustration from the Chicago Housing Authority. Other photographs courtesy of the author.Linda Villarosa is a contributing writer for the magazine whose work focuses on race and health. She teaches journalism and Black studies at the City College of New York in Harlem.

Moderate drinking is unlikely to impair the immune response to the Covid vaccine, but heavy drinking might.After a long year and a lot of anticipation, getting the Covid-19 vaccine can be cause for celebration, which for some might mean pouring a drink and toasting to their new immunity. But can alcohol interfere with your immune response?The short answer is that it depends on how much you drink.There is no evidence that having a drink or two can render any of the current Covid vaccines less effective. Some studies have even found that over the longer term, small or moderate amounts of alcohol might actually benefit the immune system by reducing inflammation.Heavy alcohol consumption, on the other hand, particularly over the long term, can suppress the immune system and potentially interfere with your vaccine response, experts say. Since it can take weeks after a Covid shot for the body to generate protective levels of antibodies against the novel coronavirus, anything that interferes with the immune response would be cause for concern.“If you are truly a moderate drinker, then there’s no risk of having a drink around the time of your vaccine,” said Ilhem Messaoudi, director of the Center for Virus Research at the University of California, Irvine, who has conducted research on the effects of alcohol on the immune response. “But be very cognizant of what moderate drinking really means. It’s dangerous to drink large amounts of alcohol because the effects on all biological systems, including the immune system, are pretty severe and they occur pretty quickly after you get out of that moderate zone.”Moderate drinking is generally defined as no more than two drinks a day for men and a maximum of one drink a day for women, whereas heavy drinking is defined as four or more drinks on any day for men and three or more drinks for women. Keep in mind that one “standard” drink is considered five ounces of wine, 1.5 ounces of distilled spirits, or 12 ounces of beer.Some of the first concerns about alcohol and Covid vaccination began circulating after a Russian health official who warned in December that people should avoid alcohol for two weeks before getting vaccinated and then abstain for another 42 days afterward. According to a Reuters report, the official claimed that alcohol could hamper the body’s ability to develop immunity against the novel coronavirus. Her warning sparked a fierce backlash in Russia, which has one of the world’s highest drinking rates.In the United States, some experts say they have heard similar concerns about whether it is safe to drink around the time of vaccination. “We’ve been getting a lot of questions from our patients about this,” said Dr. Angela Hewlett, an associate professor of infectious diseases who directs the Covid infectious diseases team at the University of Nebraska Medical Center. “Understandably, people who are receiving these vaccines want to make sure they’re doing all the right things to maximize their immune response.”Clinical trials of the Covid vaccines that are currently approved for use by the Food and Drug Administration did not specifically look at whether alcohol had any impact on the effectiveness of the vaccines, Dr. Hewlett said. It’s possible that there will be more information on that in the future. But for now, most of what is known comes from previous research, including studies that examined how alcohol affects the immune system in humans and whether it hinders the immune response in animals that received other vaccines.One thing that is clear from studies is that heavy alcohol consumption impairs the immune response and increases your susceptibility to bacterial and viral infections. It prevents immune cells from traveling to sites of infection and carrying out their duties, like destroying viruses, bacteria and infected cells; makes it easier for pathogens to invade your cells, and causes a host of other problems.In contrast, moderate drinking does not seem to have this effect. In one study, scientists exposed 391 people to five different respiratory viruses and found that moderate drinkers were less likely to develop colds, but not if they were smokers.In another study, Dr. Messaoudi and colleagues provided rhesus monkeys access to alcoholic beverages for seven months and then looked at how their bodies responded to a vaccine against poxvirus. Much like humans, some rhesus monkeys enjoy alcohol and will drink a lot, while others show less interest and will limit themselves to small amounts. The researchers found that the animals that were chronically heavy drinkers had a weak response to the vaccine. “They had almost a nonexistent immune response,” Dr. Messaoudi said.The animals that consumed only moderate amounts of alcohol, however, generated the strongest response to the vaccine, even compared to the teetotalers that consumed no alcohol at all. Studies in rats have found a similar pattern: Those consuming large amounts of alcohol have only a weak immune response to infections compared to animals given moderate amounts of alcohol or none at all. Other studies have found that when people drink moderately, it seems to lower inflammatory markers in their blood.Another reason to moderate your alcohol intake is that heavy drinking — along with the hangover that can ensue — can potentially amplify any side effects you might have from the Covid vaccine, including fever, malaise or body aches, and make you feel worse, said Dr. Hewlett of the University of Nebraska Medical Center. Dr. Hewlett chose not to drink after getting the Covid vaccine. But she said that people should feel free to imbibe so long as they drink within reason.“Having a glass of champagne probably won’t inhibit any immune response,” she said. “I think having a celebratory beverage in moderation is fine.”Do you have a health question? Ask Well

SharecloseShare pageCopy linkAbout sharingimage copyrightEPAMedical supplies from the UK arrived in India on Tuesday – the first international shipment aimed at stemming a devastating Covid-19 surge.Ventilators and oxygen equipment landed in Delhi, but far more will be needed, with India recording 320,000 new infections on Tuesday, and deaths rising close to 200,000 overall.Hospitals are overwhelmed, with people waiting in the streets outside.The US, France and Germany are among nations sending desperately needed aid.Covid-19 in India: Visual guide to the crisisThe messages deciding between life and deathThe UK shipment, including ventilators and oxygen concentrators – which will help hospitals manage oxygen supplies – was unloaded at Delhi airport.Foreign ministry spokesman Arindam Bagchi said it was “international co-operation at work”, but it is just the first trickle in what needs to be a flood of supplies.US President Joe Biden said on Monday he would send up to 60 million doses of the AstraZeneca Covid-19 vaccine abroad and, although the destinations were not given, India could be a prime recipient.The World Health Organization chief, Tedros Adhanom Ghebreyesus, said it was “doing everything we can, providing critical equipment and supplies”.France is sending oxygen production units, as well as oxygen containers and respirators.And India has stepped up its own efforts – the first “Oxygen Express” train, which aims to transport 70 tonnes of the gas, arrived in Delhi.But around many Indian cities, images still show people waiting outside hospitals in ambulances or lying on makeshift beds, while elsewhere flames rise from the funeral pyres of victims.

CAMBRIDGE, Mass. — Most labs devoted to women’s diseases are accompanied by obvious symbols of womanhood: a rose, a tulip, an hourglass silhouette. Not Linda Griffith’s. Tucked away in the building for biological engineering, the M.I.T. Center for Gynepathology Research is marked only by the letters CGR in red and black, the G formed from a curved arrow representing the hand of the engineer.“We needed something that wasn’t all pink and flowers,” said Dr. Griffith, the lab’s director. “We really thought it should be, like, ‘This is science.’”Dr. Griffith founded the lab in 2009 with the goal of helping researchers solve endometriosis, a chronic disorder in which tissue similar to that which normally lines the uterus instead grows outside it. The disease strikes one in 10 women, as well as trans men and nonbinary people who menstruate. Its hallmarks are extreme pain and, in some cases, infertility.Yet it suffers from a branding problem: It falls into the abyss of “women’s diseases” (overlooked), diseases that don’t kill you (unimportant) and menstrual problems (taboo). Researchers often call endometriosis “benign,” as in noncancerous — but doing so, Dr. Griffith believes, lessens the seriousness of a common, painful disease.Her mission is to change the conversation, from one of women’s pain to one of biomarkers, genetics and molecular networks. “I don’t want to make endometriosis a women’s issue,” she told the M.I.T. Tech Review in 2014. “I want to make it an M.I.T. issue.”Dr. Griffith, spry at 60, with a fringe of blonde hair and a slight Georgia drawl, is uniquely poised to help effect that transition. She started her career in bioengineering, sculpting organs like liver and bone from scratch by seeding polymer scaffolds with living cells. In 1997, she helped create an iconic creature called the “earmouse” by injecting a human ear-shaped scaffold with cartilage from a cow’s knee, and growing it on the back of a lab mouse.Now she brings those skills to the task of better understanding the uterus. In her lab, she has begun growing uterine organoids — tiny domed droplets, with glands that look like swirling craters — from the uterine cells of endometriosis patients. These “patient avatars” are ideal tools for testing potential new treatments for the disease: Biologically, they are closer to human uterine cells than those of mice (which don’t naturally menstruate). And they enable researchers to sidestep the ethical issues that would arise with human trials.“That’s really the power of this,” Dr. Griffith said. “You can take patients who we know how they respond or do not respond to therapies, and compare and start to understand and tease apart why that is.”Her research highlights what a remarkable organ the uterus truly is — and not just during its signature function, pregnancy. Humans, unlike almost every other mammal, shed their entire endometrium — the womb’s inner lining — once a month and grow it back, whether or not a fertilized egg takes hold.Dynamic, resilient and prone to reinvention, the uterus offers a window into some of biology’s greatest secrets: tissue regeneration, scarless wound healing and immune function. “The endometrium is inherently regenerative,” Dr. Griffith said. “So studying it, you’re studying a regenerative process — and how it goes wrong, in cases.”Now, her work “is drawing the interest of those who have never worked on or never thought about endometriosis,” said Dr. Stacey Missmer, a reproductive biologist at Michigan State University and co-director of the Boston Center for Endometriosis. Essentially, Dr. Missmer said, Dr. Griffith is saying: “All you cool kids in the other disciplines, this is a really interesting area to ask questions.”A name for the painAlex Brown, a postdoctoral researcher in tissue engineering, holds an isolated patient biopsy suspended in culture media.Duncan Allison O’BoyleBefore Dr. Griffith turned her scientific lens on the womb, she spent years trying to avoid thinking about the pain it caused her. For nearly three decades doctors dismissed her symptoms — stomach-turning nausea, stabbing pelvic pain and alarming levels of blood loss during her period — as just part of being a woman.“I felt like I was being gaslighted,” she said.She grew up fearless, a tree-climbing Girl Scout in Valdosta, Ga. In high school, she sewed her own clothes, earned a black belt in karate and fixed her family’s car radiator. “There was nothing we couldn’t do, whether we were male, female, whatever,” said her younger sister, Susan Berthelot. “We had a lot of confidence, and a lot of love, and a lot of freedom.”But when Dr. Griffith hit puberty, her body began imposing limitations. Her period was so agonizing it would leave her curled in the fetal position for days. When she was 13, a gynecologist prescribed birth control pills, a scandalous proposition. “In the South especially, it was not done,” she said. Her mother, at a loss, gave her gin.Unable to control what was going on inside her body, she focused on what she could control: math, and building things. She went to Georgia Tech on a scholarship to study chemical engineering. But she found herself failing tests when she was on her period, and going to the infirmary to get monthly shots of the opioid Demerol.By the time she began graduate studies at the University of California, Berkeley, she had developed an elaborate period regimen: She wore all-black outfits, inserted three Super Plus tampons and swallowed upward of 30 Advil tablets a day. But her pain kept increasing. When she consulted a male doctor, he took one look at her black leather jacket, pixie cut and Bugatti motorcycle and diagnosed her as “rejecting her femininity.”Her real diagnosis came by accident. In November 1988, soon after she went to M.I.T. as a postdoc, she checked into the Brigham and Women’s Hospital in Boston to drain a small cyst on her left ovary. She woke up the next day to find a row of staples along her midriff, holding together a six-inch incision.Her gynecologist told her she had a disease called endometriosis, which had fused her pelvic organs together with a sticky, speckled tissue that resembled the lining of her uterus. This rogue tissue responded to her monthly hormone cycle, swelling, shedding and attempting to bleed; that was the origin of the pain.Images taken during a laparoscopic exam following one of Dr. Linda Griffith’s several endometriosis surgeries. The disease she is studying one in 10 women, as well as trans men and nonbinary people who menstruate. Its hallmarks are extreme pain and, in some cases, infertility.Ilana Panich-Linsman for The New York TimesSurgeons had burned or scraped off as much of the tissue as possible; there was little else they could do. In 1940, the gynecologist who gave endometriosis its name, Dr. John Sampson, deemed the disease “tantalizingly alluring and elusive.” A half-century later, not much had changed. There was no cure, and researchers still didn’t know exactly how endometriosis took root.Still, Dr. Griffith treated the diagnosis as good news. “To have someone tell me something was wrong with me, it was a huge relief,” she said.Her gynecologist presented two options: She could go on Danazol, a hormone-blocking drug that would halt the growth of the disease but would also send her body into a menopause-like state; or she could get pregnant, a common recommendation in the 1980s, and not uncommon today.The medical reasoning — which has since been questioned — was that by temporarily stopping menstruation, pregnancy could reduce symptoms and slow or reverse the growth of lesions. “It was almost viewed as a two-for-one benefit,” said Dr. Elizabeth Stewart, who performed Dr. Griffith’s first surgery. “It’s clear there was some sexism in the approach to endometriosis then. I think there’s still some now.”Dr. Griffith recalls her then-husband answering for her: “We’ll have a baby.”She opted for the Danazol. Eight years later, she divorced the husband.Soon she was jump-starting the field of biological engineering, developing technologies to 3D-print organ scaffolds and growing artificial human ears on the backs of mice. She was an architect; her medium was the building blocks of life. But it never occurred to her to try to solve her own disease.“Psychologically, it wasn’t something I wanted to think about,” she said. “I just wanted to pretend like it wasn’t happening.”A ‘women’s thing’ worth doingOne of Dr. Griffith’s many motorcycles, circa 1988.Ilana Panich-Linsman for The New York TimesThe turning point came in 2007, when a member of M.I.T.’s board of trustees, Susan Whitehead, asked her to speak at a Women in Science and Engineering luncheon about how her work on tissue engineering could benefit women.Dr. Griffith was annoyed. “I was working on all the things that guys were working on,” she later recalled at a 2018 scientific meeting. “It didn’t ever occur to me to work on a women’s thing.” But Whitehead was a friend, so she agreed.Near the end of the event, the moderator asked her where she saw herself in 10 years. Something welled up inside her. She had just had her eighth surgery for endometriosis, and had helped her 16-year-old niece, Caitlin, receive a diagnosis for endometriosis after years of having doctors attribute her symptoms to stress. Watching Caitlin go through the same ordeal “made lava shoot out of my head,” Dr. Griffith recalled recently.“I have a chronic disease called endometriosis,” she blurted out to the luncheon audience, and mentioned her niece. “There’s no better treatment for her, 30 years younger than me, than there was for me when I was 16.” If a major breakthrough in treatment didn’t come soon, “that’s where I’m going to be in 10 years,” she said. “Maybe it’ll be solved, but I don’t think so.”The audience broke into applause.Dr. Griffith reset her goals. When it came to making liver and bone, “so many other people could do them,” she recalled. “But there was this one thing only I could do.” She had recently been awarded a MacArthur “genius” grant, which came with $500,000 for any research project.In 2009, she used it toward opening the Center for Gynepathology Research, the only engineering lab in the nation to focus on endometriosis. (In October 2020, federal funding for endometriosis research doubled from $13 million to $26 million after Representative Abby Finkenauer of Iowa, 32, shared her own endometriosis journey on the House floor.)At the launch event for the center, Padma Lakshmi, host of Top Chef and co-founder of the Endometriosis Foundation of America, lamented the lack of research on such a devastating disease.“I have to say, I’m really shocked that it’s the first research center of its kind in America,” she said. “That is stunningly bad news on the one hand, that she’s the first one doing it. On the other hand, better late than never. Thank God for Dr. Linda Griffith.”A window into the wombDr. Griffith, Clara Ives, left, and Lauren Baugh entering the tissue culture room of her lab as new patient samples were isolated for future use.Duncan Allison O’BoyleImagine the uterus as an orange, with the lining as the rind: fluffy, living tissue that serves as a plush bedding for a potential embryo. Each month, triggered by a drop in the hormone progesterone, the lining sloughs off and grows anew, complete with delicate, spiraling blood vessels.This process repeats itself swiftly, scarlessly, without a trace of injury, again and again, as many as 500 times in a woman’s life. “How the body can coordinate that is extraordinary,” said Dr. Hilary Critchley, a reproductive biologist at the University of Edinburgh — and still poorly understood.But this remarkable dynamism, some researchers argue, is a double-edged sword. “A little thing gets out of balance, and there you go,” said Dr. Griffith.Dr. Griffith’s models offer a glimpse into what happens when the process goes wrong — for instance, when this growing tissue takes root in places it shouldn’t. Her bits of bioengineered tissue allow researchers to visualize the growth of lesions and systematically parse the role of immune cells, inflammation and hormones in the disease.“You’re actually seeing in three dimensions what’s going on inside the uterus and this gland formation and nerve formation,” said endometriosis specialist Dr. Keith Isaacson, who co-directs her lab. “That is incredibly exciting.” (Dr. Isaacson, who has been Dr. Griffith’s endometriosis surgeon since 2000, and provides the patients’ cells for her models.)With her background in systems engineering, Dr. Griffith sees the uterus not as an island but as an organ that interacts intimately with everything around it. To capture these systemic interactions, her team connects her models to other organs like bone marrow, gut and liver, and hopes one day to seed them with blood vessels, nerve cells and immune cells.The insights from this research transcend the womb. For instance, one enduring mystery about the disease is how lesions can appear in places as far-flung as the lungs, eyes, spine and even the brain. Dr. Hugh Taylor, chair of the department of obstetrics, gynecology and reproductive sciences at Yale School of Medicine, is investigating whether stem cells, which are plentiful in the uterine lining, could contribute to this process by circulating throughout the body.Because uterine stem cells are relatively accessible, they could also be a boon to regenerative medicine. Dr. Taylor has shown that, like other stem cells, they can be grown in vitro into new neurons and insulin-making cells to treat diseases like Parkinson’s and diabetes.Another area ripe for improvement is diagnosis. One of the most frustrating aspects of endometriosis is that women typically wait seven to 10 years or more to learn that they have the disease, a process that requires invasive surgery. Now, researchers are developing a simple test to screen for genetic markers of endometriosis in menstrual blood and return a near-instant diagnosis.Just a few milliliters of this blood, collected on a sponge, provides a wealth of markers of health and disease, said Christine Metz, an immunologist at Northwestern’s Feinstein Institute who is developing the test with Peter Gregersen, a geneticist there. Besides endometriosis, it could also help doctors screen for pelvic inflammation, infertility, fibroids, environmental toxins and early cancer.“We were kind of surprised that it had been neglected as a natural resource,” Dr. Metz said.They soon discovered why. In 2018, Dr. Metz began approaching male gynecologists to ask their patients for menstrual samples, and “some people said we were completely insane,” she recalled. Others, she added, “had never heard of a menstrual cup. Which was also, I’m going to say, disappointing.” They began asking patients directly for samples, and have since enrolled 1,000 patients in their study.One might well ask why more researchers have not focused on the uterus until recently. Bioengineers in particular have always taken an interest in tissues that regenerate and self-heal. “And yet it took them how many decades to recognize that one of the most regenerative tissues is found inside the uterus?” asked Kathryn Clancy, a biological anthropologist who studies reproduction at the University of Illinois.The reason, she believes, is simple: “Because none of the researchers had uteruses.”Lessons from cancerDr. Griffith at home with her husband, Doug Lauffenburger, a systems biologist at M.I.T.Ilana Panich-Linsman for The New York TimesThree stone cherubs form an arc above the doorway to Dr. Griffith’s kitchen in Cambridge, Mass. They were a gift from her mother, to commemorate the embryos that she and her current husband, Doug Lauffenburger, a systems biologist with whom she shares a lab at M.I.T., made in 1997 through in vitro fertilization. Endometriosis prevented the embryos from implanting.She held on to her dream of having children, but in 2001, just after her 40th birthday, the pain in her abdomen grew unbearable. On Sept. 11, as the Twin Towers fell, she rushed to the hospital in a fog of painkillers and underwent a hysterectomy with Dr. Isaacson. (Endometriosis pain is the leading cause of hysterectomies for American women in their 30s.)“There was no decision,” Dr. Griffith recalled. “It was hysterectomy or death.”Even after that, her disease returned, twice. Then in 2009, just after she had pivoted to studying endometriosis, she faced a new obstacle: cancer.Dr. Griffith likes to say that compared to endometriosis, stage 4 breast cancer was a walk in the park. “Not like a super-beautiful day — like a stormy-day walk in the park,” she added. “But it was, like, people understood.” Colleagues wrote her cards, sent her food, extended condolences. Her dean offered her a sabbatical semester.Dr. Griffith soon learned that the way breast cancer research was categorized was far ahead of endometriosis. Doctors used molecular tests to classify patients into subtypes, which dictated which targeted treatment they should receive. With endometriosis, “there’s no metrics,” she said. “This was this huge thing for me that was so crystallizing.”Dr. Griffith knew that her disease, like cancer, was not one disease but many, a medusa of waving tentacles. She began talking to Dr. Lauffenburger, who had been studying breast cancer for over a decade, about how to take a similar approach to classifying endometriosis patients.Together, they identified networks of inflammatory markers that tended to be associated with more painful manifestations of the disease and fertility, and published their findings in Science Translational Medicines in 2014. The work was cited as the first step toward creating subtypes of the disease. “That was really us together, because it was his vision of systems biology but filtered through my practical connection to the clinic,” Dr. Griffith said.For the next year, she held lab meetings from her hospital bed in between chemotherapy sessions. “We transformed our lab meetings, literally,” said Dr. Nicole Doyle, a postdoctoral fellow in Dr. Griffith’s lab at the time. “We just showed up for her chemo treatments and would sit there with her. That diagnosis had to adapt to her life, not the other way around.”Throughout chemo, Dr. Griffith never seemed to waver in her positivity. When she shaved off her hair, she threw a lab party. But Dr. Lauffenburger found it excruciating to watch his wife suffer from this new foe, after battling the old one for so long.When it came to cancer, “I viewed it as a terrible thing,” he said one evening over dinner at their home.Dr. Griffith saw it differently: She took a curse and turned it into a gift.“It was a terrible thing,” she allowed. “But it was a good thing, scientifically.”Ilana Panich-Linsman for The New York Times[Like the Science Times page on Facebook. | Sign up for the Science Times newsletter.]

SharecloseShare pageCopy linkAbout sharingUS police officers are seen mocking a 73-year-old dementia sufferer as they watch video of her shoulder going “pop” during her forcible arrest, according to footage released by her lawyer.Karen Garner was detained on 26 June last year after she walked out of a Walmart in the state of Colorado without paying for $13 of items.Her elbow was fractured and shoulder dislocated, says her attorney.An investigation has been launched into the Loveland Police Department arrest.In the footage released on Monday from the booking area of the police station on the day of the arrest, officers are seen fist-bumping one another as they review body camera video of the incident.Video from inside Ms Garner’s nearby holding cell shows the frail-looking grandmother slumped handcuffed to a bench while the officers joke about the incident, says her lawyer.”Ready for the pop? Hear the pop?” one of the officers says at one point, referring to Ms Garner’s shoulder.As they continue to watch the footage, the same officer says: “I love it.” Don’t shoot, I’m disabledThe Garner family hired a sound engineer to enhance audio of the officers’ remarks.Their lawyer has filed a federal lawsuit against the department, alleging the officers violated the Americans with Disabilities Act and “violently assaulted” Ms Garner. Attorney Sarah Schielke says her client went six hours without medical help while confused and crying in pain after an arrest that amounted to “torture”.”They failed Karen Garner,” Ms Schielke said in a press release. “They failed the community. And they did it all on camera.” Loveland police said in a statement on Monday they would not be making any comments pending the results of a “criminal investigation” launched last week.The Larimer County district attorney is looking into the department’s use of force during Ms Garner’s arrest. Loveland police chief Robert Ticer has pledged full transparency with the inquiry, which will be led by Fort Collins Police.One officer has been placed on administrative leave and two others moved to administrative duties.The bodycam footage caused public outcry when it was released earlier this month. It shows two police officers stopping Ms Garner as she was picking flowers by the roadside after she left the Walmart store in the town of Loveland, about 50 miles (80km) north of Denver.CCTV from the supermarket shortly beforehand showed members of staff stopping Ms Garner to recover the $13.38 of merchandise, which included cans of soda and laundry detergent. After she walks away from the officers, she is thrown to the ground, handcuffed, shoved face down on the bonnet of the police car and has her legs tied together with a hobble. She was left bleeding.Ms Garner’s daughter-in-law, Shannon Steward, told the Denver Post the arrest had worsened Ms Garner’s dementia.”She hasn’t come back the way she was before,” Ms Steward told the newspaper. “It was too much.”The release of the footage comes amid a nationwide reckoning over police brutality, especially against African Americans, although Ms Garner is white.

SharecloseShare pageCopy linkAbout sharingZaz Hassan survived Covid but, one year on, is still living with the after-effects of the virus. “You live with the hope that you will get better,” Zaz tells me, as he takes a break from his physio class at Croydon University Hospital’s long Covid centre. “For me, the end point would be to get back to work and just play with my kids. It may take time but people are recovering, so there is still the hope that I can come out of this.”The paediatric doctor, 42, has been off work since March 2020, when he fell ill with Covid-19, at the peak of the first wave. And like many other patients, his recovery has been far from straightforward. ‘Shooting pains’After spending two weeks on a ventilator in intensive care, Zaz was discharged from hospital and felt he was slowly making progress. Then, in September, his young children returned to school. He thinks he probably picked up a cold from one of them, which “completely wiped” him out. Since then, he has been dealing with recurring symptoms, from fatigue to back problems to “shooting pain” in his legs. “It’s like when you have the flu where you absolutely can’t move and your whole body aches,” Zaz says.”You are just absolutely exhausted. The fatigue was a big thing and then I started developing the brain fog, which, for me, was not being able to find words, not being able to speak in sentences.”Long Covid: More than a million affected in February’My fatigue was like nothing I’ve experienced before’Middle-aged women ‘worst affected by long Covid”Long Covid’: Why are some people not recovering?Zaz is one of more than 1,000 patients seen by the long Covid clinic in Croydon. Another 500 are on the waiting list for diagnosis and possible referral to a specialist team for physiotherapy or a heart or lung scan. In an exercise class in the bright hospital gym, Zaz and two other long Covid patients switch tentatively from parallel walking bars to a treadmill and free weights. ‘Misjudge distances’Specialist physiotherapists help with the equipment and compare the men’s progress with previous sessions. The mood is determined – but there is frustration at the slow rate of recovery. “A couple of times I’ve felt I am going to tumble,” Zaz tells the physio he’s working with. “I misjudge distances and feel my legs are going to give way.”

BBCThe fatigue was a big thing and then I started developing the brain fog, which, for me, was not being able to find words, not being able to speak in sentencesZaz Hassan Long Covid patientDr Yogini Raste, a consultant respiratory doctor and one of the people running the Croydon clinic, says: “We see a whole spectrum of patients, from those admitted to intensive care who had a prolonged stay [in hospital] for many weeks.”Then, there are those who were never tested in the first wave, who thought they would get better at home but then started to develop a whole host of strange symptoms.”There is no universally agreed definition of “long Covid” – but it can include a broad range of health problems. The most common are fatigue and a cough, followed by a headache and muscle pain.As with any new medical condition, hard evidence about the prevalence of long Covid is difficult to come by. A survey by the Office of National Statistics (ONS) in March found about one in five people infected still had symptoms five weeks later, with one in seven still sick in some way after 12 weeks.

BBCWe can’t tell these patients how long it’s going to last for, so they are on a bit of a rollercoasterDr Yogini RasteConsultant respiratory doctor And the ONS estimates 1.1 million people were affected in the UK in the four weeks from 6 February. “We can’t tell these patients how long it’s going to last for, so they are on a bit of a rollercoaster,” Dr Raste says. “They might have a few weeks where they feel they are getting better and improving. “Then, just as they are coming out of that tunnel, there is another setback, so that in itself can be a great source of anxiety.”Breathing exercisesThere is no drug approved to treat long Covid. Instead, doctors try to treat individual symptoms of the condition through physiotherapy, speech therapy or breathing exercises. And in some cases, patients are referred on to specialists in cardiology, neurology and respiratory care. The NHS is now planning to open 83 long Covid clinics across England by the end of April, costing £24m in 2021, with more likely to be needed in the future. NHS England chief executive Sir Simon Stevens has said people with long-term after-effects need a “clear front-door” to know where they can access help.In Scotland, Wales and Northern Ireland, treatment for long Covid patients tends to be through existing hospital and GP services, with some dedicated clinics for those discharged from intensive care.But some long Covid patients say they are still having to rely on internet sites for support and advice. ‘More support'”Most people and not getting answers and we appreciate that sometimes there are just no answers to give,” Aasim, one of the other patients in the Croydon physiotherapy class, says. “If you look at social-media platforms, you will see the numbers that are on support groups. We are having to speculate and be our own doctors. “Something there needs to change. We need to be taken more seriously and be given more support.”You can contact and follow Jim Reed on Twitter.What has been your experience of the pandemic? Have you had long Covid? Have you been shielding? Share your experiences by emailing haveyoursay@bbc.co.uk.Please include a contact number if you are willing to speak to a BBC journalist. You can also get in touch in the following ways:WhatsApp: +44 7756 165803Tweet: @BBC_HaveYourSayUpload pictures or videoPlease read our terms & conditions and privacy policy

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