Is It Healthy to Study in Bed?

With extracurriculars, academics and a social life to maintain, goal-oriented students have to squeeze time from their hectic schedules to get homework done. The result? Lots of studying, writing and reading happens while lying or lounging in bed. Though many parents insist children study only at a desk, they may be surprised to hear what experts think about where and when it’s best to review and learn. We gathered informed opinions from experts in education psychology, sleep medicine and ergonomics.

Doing the Homework

As a debate about homework escalates nationwide, a perhaps less-discussed issue is where this home-studying takes place. Among those who recognize that much of it happens in bed are industrial engineers and furniture designers. Over the years they have come up with across-the-bed tables that angle laptops for proper typing, reading pillows that cradle the neck, back and arms, even hard-sided lap pillows for resting a laptop on.

These can all help bed-studiers be more comfortable. However, Atul Malhotra, a physician and professor of medicine at the University of California, San Diego, with a focus on sleep medicine, notes: “Lying down or sitting upright doesn’t impact your brain function—your posture doesn’t matter.”

The only widely known study specifically on students doing homework in bed versus at a desk was published in May 1968. Of the 100 or so college students they surveyed—admittedly at a time when studying was quite different than the screen-based work now—the researchers at the University of California, Davis, found no difference in grade-point average between those who worked at their desk and those who studied in bed.

“The assumption that there is a single type of study environment optimal for all students appears unwarranted,” the authors concluded.

One concern is that being cozy in bed typically brings on sleepiness, which may compromise a student’s ability to retain information, says Harris Cooper, a social psychologist with a specialty in education at Duke University. But he adds that figuring out how you learn and study most effectively at a young age isn’t a bad thing.

“If they are getting their work done and it is of quality, then knowing what environments work for them will prepare them to be lifelong learners in various locations,” Dr. Cooper says. The professor of psychology and neuroscience suggests parents and students track progress over time to see if they are, indeed, producing as good work in bed as at a desk.

Losing the Last Page

When someone reads a book just before falling asleep, and puts the bookmark on page 89, it’s common not to recall in the morning what happened on page 88, Dr. Malhotra says.

“That which happened right before you sleep doesn’t register, so many people have to re-read page 88—but they will remember page 87,” he says. He doesn’t take issue with one of his daughters who studies in bed with music on. But he suggests that anyone who does homework on the comforter at night go back a few pages or at least 10 minutes’ worth of work in the morning and redo and review it. Also, if you have to read and retain something important, don’t read it just before sleeping, as the few minutes just before sleep aren’t optimal for memory retention.

“Read it, then brush your teeth, then go to sleep,” he says. He also doesn’t mind a little morning lie-in coupled with studying. “You’re often free from distractions in bed in the morning, before the day’s chaos begins,” he says. If you find comfort in bed when the sun comes up, that might be a good opportunity to learn and retain new information.

Getting to Neutral

Standing with arms relaxed at your side is considered the “neutral” posture, with no stress put on any particular part of your body, says ergonomics specialist Janice Fletcher at UC San Diego Health, an academic medical center.

She makes sure people get close to neutral while working at their desks, adjusting keyboards so that the elbows are slightly wider than at right angles, and wrists are either straight or slightly bent downward, “never flexed in the ‘tell it to the hand’ position,” she says. She also places monitors so the neck is neither flexed nor extended. Perhaps surprisingly, the second-most neutral posture is lying in bed flat on your back, though not much studying can be accomplished in that position, she admits.

Ms. Fletcher is fine with people studying in bed, though she suggests that rather than just plopping onto a mattress to do homework, students should plan a little.

The best posture for reading in bed, she says, is sitting up with your back against the headboard and pillows under your arms to raise the reading material to eye level.

“That way you don’t have to bend your neck to view the book or device,” she says. Find a flat surface for writing or supporting a computer on your lap, and use a soft light to prevent a glare that may harm the eyes. For homework involving lots of paper and books, a desk might be a better choice, but bed-studying can be done effectively. “Make yourself as neutral as possible” by sitting similarly to the way you would if you were at a desk, with the help of cushioning, she says.

“If you’re at neutral, you’re more comfortable,” Ms. Fletcher says, “and I would guess you’d be less distracted because you wouldn’t be thinking about your discomfort.”

 

 

This article was originally published in The Wall Street Journal. Read the original article.

H.I.V. Is Reported Cured in a Second Patient, a Milestone in the Global AIDS Epidemic

For just the second time since the global epidemic began, a patient appears to have been cured of infection with H.I.V., the virus that causes AIDS.

The news comes nearly 12 years to the day after the first patient known to be cured, a feat that researchers have long tried, and failed, to duplicate. The surprise success now confirms that a cure for H.I.V. infection is possible, if difficult, researchers said.

The investigators are to publish their report on Tuesday in the journal Nature and to present some of the details at the Conference on Retroviruses and Opportunistic Infections in Seattle.

Publicly, the scientists are describing the case as a long-term remission. In interviews, most experts are calling it a cure, with the caveat that it is hard to know how to define the word when there are only two known instances.

Both milestones resulted from bone-marrow transplants given to infected patients. But the transplants were intended to treat cancer in the patients, not H.I.V.

Bone-marrow transplantation is unlikely to be a realistic treatment option in the near future. Powerful drugs are now available to control H.I.V. infection, while the transplants are risky, with harsh side effects that can last for years.

But rearming the body with immune cells similarly modified to resist H.I.V. might well succeed as a practical treatment, experts said.

“This will inspire people that cure is not a dream,” said Dr. Annemarie Wensing, a virologist at the University Medical Center Utrecht in the Netherlands. “It’s reachable.”

Dr. Wensing is co-leader of IciStem, a consortium of European scientists studying stem cell transplants to treat H.I.V. infection. The consortium is supported by AMFAR, the American AIDS research organization.

The new patient has chosen to remain anonymous, and the scientists referred to him only as the “London patient.”

“I feel a sense of responsibility to help the doctors understand how it happened so they can develop the science,” he told The New York Times in an email.

Learning that he could be cured of both cancer and H.I.V. infection was “surreal” and “overwhelming,” he added. “I never thought that there would be a cure during my lifetime.”

At the same conference in 2007, a German doctor described the first such cure in the “Berlin patient,” later identified as Timothy Ray Brown, 52, who now lives in Palm Springs, Calif.

That news, displayed on a poster at the back of a conference room, initially gained little attention. Once it became clear that Mr. Brown was cured, scientists set out to duplicate his result with other cancer patients infected with H.I.V.

In case after case, the virus came roaring back, often around nine months after the patients stopped taking antiretroviral drugs, or else the patients died of cancer. The failures left scientists wondering whether Mr. Brown’s cure would remain a fluke.

Mr. Brown had had leukemia, and after chemotherapy failed to stop it, needed two bone-marrow transplants.

The transplants were from a donor with a mutation in a protein called CCR5, which rests on the surface of certain immune cells. H.I.V. uses the protein to enter those cells but cannot latch on to the mutated version.

Mr. Brown was given harsh immunosuppressive drugs of a kind that are no longer used, and suffered intense complications for months after the transplant. He was placed in an induced coma at one point and nearly died.

Timothy Ray Brown, the first person to be cured of H.I.V., almost died during the treatment.CreditGrant Hindsley for The New York Times
Image
Timothy Ray Brown, the first person to be cured of H.I.V., almost died during the treatment.CreditGrant Hindsley for The New York Times

“He was really beaten up by the whole procedure,” said Dr. Steven Deeks, an AIDS expert at the University of California, San Francisco, who has treated Mr. Brown. “And so we’ve always wondered whether all that conditioning, a massive amount of destruction to his immune system, explained why Timothy was cured but no one else.”

The London patient has answered that question: A near-death experience is not required for the procedure to work.

He had Hodgkin’s lymphoma and received a bone-marrow transplant from a donor with the CCR5 mutation in May 2016. He, too, received immunosuppressive drugs, but the treatment was much less intense, in line with current standards for transplant patients.

He quit taking anti-H.I.V. drugs in September 2017, making him the first patient since Mr. Brown known to remain virus-free for more than a year after stopping.

“I think this does change the game a little bit,” said Dr. Ravindra Gupta, a virologist at University College London who presented the findings at the Seattle meeting. “Everybody believed after the Berlin patient that you needed to nearly die basically to cure H.I.V., but now maybe you don’t.”

Although the London patient was not as ill as Mr. Brown had been after the transplant, the procedure worked about as well: The transplant destroyed the cancer without harmful side effects. The transplanted immune cells, now resistant to H.I.V., seem to have fully replaced his vulnerable cells.

Most people with the H.I.V.-resistant mutation, called delta 32, are of Northern European descent. IciStem maintains a database of about 22,000 such donors.

So far, its scientists are tracking 38 H.I.V.-infected people who have received bone-marrow transplants, including six from donors without the mutation.

The London patient is 36 on this list. Another one, number 19 on the list and referred to as the “Düsseldorf patient,” has been off anti-H.I.V. drugs for four months. Details of that case will be presented at the Seattle conference later this week.

The consortium’s scientists have repeatedly analyzed the London patient’s blood for signs of the virus. They saw a weak indication of continued infection in one of 24 tests, but say this may be the result of contamination in the sample.

The most sensitive test did not find any circulating virus. Antibodies to H.I.V. were still present in his blood, but their levels declined over time, in a trajectory similar to that seen in Mr. Brown.

None of this guarantees that the London patient is forever out of the woods, but the similarities to Mr. Brown’s recovery offer reason for optimism, Dr. Gupta said.

“In a way, the only person to compare with directly is the Berlin patient,” he said. “That’s kind of the only standard we have at the moment.”

Most experts who know the details agree that the new case seems like a legitimate cure, but some are uncertain of its relevance for AIDS treatment overall.

“I’m not sure what this tells us,” said Dr. Anthony Fauci, director of the National Institute of Allergy and Infectious Diseases. “It was done with Timothy Ray Brown, and now here’s another case — ok, so now what? Now where do we go with it?”

One possibility, said Dr. Deeks and others, is to develop gene-therapy approaches to knock out CCR5 on immune cells or their predecessor stem cells. Resistant to H.I.V. infection, these modified cells should eventually clear the body of the virus.

(CCR5 is the protein that He Jiankui, a scientist in China, claimed to have modified with gene editing in at least two children, in an attempt to make them resistant to H.I.V. — an experiment that set off international condemnation.)

Several companies are pursuing gene therapies but have not yet been successful. The modification must target the right number of cells, in the right place — only the bone marrow, for example, and not the brain— and tweak only the genes directing production of CCR5.

“There are a number of levels of precision that must be reached,” said Dr. Mike McCune, a senior adviser on global health to the Bill and Melinda Gates Foundation. “There are also concerns that you might do something untoward, and if so you might wish to have a kill switch.”

Several teams are working on all of these obstacles, Dr. McCune said. Eventually, they may be able to develop a viral delivery system that, when injected into the body, seeks out all CCR5 receptors and deletes them, or even a donor stem cell that is resistant to H.I.V. but could be given to any patient.

“These are dreams, right? Things on the drawing table,” Dr. McCune said. “These dreams are motivated by cases like this — it helps us to imagine what might be done in the future.”

One important caveat to any such approach is that the patient would still be vulnerable to a form of H.I.V. called X4, which employs a different protein, CXCR4, to enter cells.

“This is only going to work if someone has a virus that really only uses CCR5 for entry — and that’s actually probably about 50 percent of the people who are living with H.I.V., if not less,” said Dr. Timothy J. Henrich, an AIDS specialist at the University of California, San Francisco.

Even if a person harbors only a small number of X4 viruses, they may multiply in the absence of competition from their viral cousins. There is at least one reported case of an individual who got a transplant from a delta 32 donor but later rebounded with the X4 virus. (As a precaution against X4, Mr. Brown is taking a daily pill to prevent H.I.V. infection.)

Mr. Brown says he is hopeful that the London patient’s cure proves as durable as his own. “If something has happened once in medical science, it can happen again,” Mr. Brown said. “I’ve been waiting for company for a long time.”

This article was originally published in The New York Times. Read the original article.

An H.I.V. Cure: Answers to 4 Key Questions

At a scientific conference in Seattle on Tuesday, researchers reckoned with a day that many thought might never arrive. A patient appears to have been cured of H.I.V., the virus that causes AIDS, for only the second time since the epidemic began.

A sort of electric hope hangs in the air, said Dr. Steve Deeks, an AIDS specialist at the University of California, San Francisco, who is attending the gathering: “The whole approach to a cure is shifting more from aspiration to something that people are realizing could be feasible.”

It is a hope that must be tempered with realism: H.I.V. is a wily adversary, and scientists and patients living with the virus are all too well acquainted with past failures in the fight against the epidemic.

Here’s what the news means right now.

Not yet. The second case does provide “proof of concept,” shining a light on a potential path to an H.I.V. cure. Scientists intend to pursue it with vigor.

But this apparent success does not mean that an easy cure is around the corner, and certainly not that infected patients should stop taking their pills.

“Sometimes the amount of desperation for a cure is driven by the stigma that’s still out there,” said Richard Jefferys, a director at Treatment Action Group, an advocacy organization. “But while two or three people is a drop in the ocean compared to the 35 million H.I.V.-positive people in the world, it’s a whole lot better than zero.”

Both men believed to have been cured so far had H.I.V. and cancer. Both received bone-marrow transplants to treat the cancer, not the H.I.V. In each case, the bone-marrow donors carried a key genetic mutation, called delta 32, that hampers H.I.V.’s entry into certain blood cells.

Bone-marrow transplants are risky procedures, so this is not likely to be a treatment option for the majority of people with H.I.V. And it is worth noting that until now, most other attempts to repeat the first cure had also failed.

Whatever the path to a cure turns out to be, it will not be simple.

Cure means the virus seems to be gone forever. Remission is a more conservative term: The virus is under control in the body, but maybe not forever.

After his case, there were many failed attempts to duplicate this success. Each time, the virus came back after the patient stopped taking anti-H.I.V. drugs.

The newly reported case, in a man described only as the “London patient,” has been H.I.V.-free for 18 months since stopping the drugs. Extraordinarily sensitive tests cannot find the virus in his body. To some scientists, that’s a cure. Others are more skeptical.

“We don’t have any international agreement on what time without viral rebound is necessary to speak about cure,” said Dr. Annemarie Wensing, a virologist at the University Medical Center Utrecht in the Netherlands.

It is worth noting that there have been patients who went into remission without a bone-marrow transplant. In these cases, the immune system seems able to maintain tight control over the virus, even without drugs. For years, researchers have been trying to figure out how it happens.

A transplant from a delta 32 donor essentially wipes out the immune cells that are vulnerable to H.I.V., replacing them with cells that are resistant to the virus. Already many groups of scientists are trying to mimic the benefits of a bone-marrow transplant without the risks of the actual procedure.

The delta 32 mutation occurs in a gene that directs production of a protein called CCR5, which sits on the surface of certain immune cells. A common type of H.I.V. needs this protein, among others, to enter cells in order to reproduce.

The gene that directs production of CCR5 may be modified with newer gene therapy techniques, similar to treatments developed for hemophilia and sickle-cell disease. And scientists have tried to edit CCR5 from a person’s immune cells in the lab and to infuse the modified cells back into the body.

But so far the numbers of cells derived with this method do not seem to be enough to make anyone resistant to H.I.V.

In one trial funded by Sangamo Therapeutics, however, researchers reported a curious finding: Although the infusion did not cure H.I.V. infection, the amount of virus in the body seemed to decline by a thousandfold. The company is planning a follow-up study to explore this further.

Another approach would be to deliver enzymes that edit the genes directly into the body. The real challenge is in targeting the enzymes: Many teams are looking into delivery via nanoparticles, for example, but this strategy is years from success, Dr. Deeks said.

An even more intriguing option is to design a predecessor stem cell that would produce a steady stream of H.I.V.-resistant immune cells in the body. At least one group in China is trying to edit CCR5 from stem cells that can be infused into patients with both cancer and H.I.V.

Early studies at the University of Pennsylvania suggest that something like this might work, noted Dr. Mike McCune, a global health adviser to the Bill and Melinda Gates Foundation.

In addition, some scientists are trying to force the virus into remission with broadly neutralizing antibodies, immune molecules that can disable various types of H.I.V.

Five to 10 years at the earliest. And that covers only types of H.I.V. that rely on CCR5 to infect cells. Another form of H.I.V., called X4, relies on a different protein to enter cells; none of these theoretical treatments would guard against infection with that form of the virus.

“Nobody should really be anticipating a cure or a remission is around the corner,” Dr. McCune said.

But gene therapy and gene editing are moving at a lightning pace, and it is not unreasonable to think that some researcher somewhere will find a way to do for the immune system what these bone-marrow transplants did for these two patients.

“We need to push on multiple fronts at once,” Dr. McCune said.

 

This article was originally published in The New York Times. Read the original article.

A second person has probably been cured of HIV

ESTABLISHED HIV infection is easy to control but impossible to cure. Or almost impossible. The exception seems to be Timothy Brown, a man often referred to as the Berlin patient. In 2006, after a decade of successfully suppressing his infection with anti-retroviral drugs, Mr Brown developed an unrelated blood cancer, acute myeloid leukaemia. To treat this life-threatening condition he opted, the following year, for a blood-stem-cell transplant. And, at the same time, he volunteered as a guinea pig for an experimental anti-HIV treatment, which worked. Now, a team of doctors in London have reported a similar case.

Blood-stem-cell transplantation is a normal, though radical, treatment for various sorts of blood cancer. Stem cells are the precursors from which particular tissues grow. Blood-stem-cell transplantation involves using drugs (backed up, in Mr Brown’s case, by radiotherapy) to kill a patient’s natural blood-producing tissue, the bone marrow, and then transfusing in new stem cells from a donor.

So far, so normal. But Mr Brown, at the suggestion of his doctors, chose from among the 267 possible tissue-matched donors one who had inherited from both parents a mutation that, in healthy people, prevents HIV infection in the first place. (The mutation in question alters one of the proteins the virus attaches itself to when entering a cell.) After two such transplants Mr Brown was cleared of the leukaemia and, as far as it is possible to tell, HIV had stopped replicating in his body.

The newly reported patient, treated by Ravindra Gupta of University College, London, and his colleagues, had Hodgkin’s lymphoma and underwent a stem-cell transplant for this in 2016. As in Mr Brown’s case, the cell donor had inherited the protective mutation from both parents. Sixteen months later, as they describe in Nature, the patient’s doctors withdrew the HIV-controlling drugs and watched. There was no resurgence of the virus, as would be usual if those drugs were withdrawn from any other HIV patient. Nor has there been any change in the patient’s HIV status in the 18 months since the drugs’ withdrawal.

In cases like this doctors are loth to use the word “cured”, since the future is unpredictable and the mechanism involved serves only to break HIV’s reproductive chain, not to purge the virus from the body entirely. They talk instead of patients being “in remission”. Nevertheless, the experience of the person who will probably come to be known as the London patient is important. It shows Mr Brown’s case was not a fluke. Which gives comfort to those working on the idea of editing protective mutations into stem cells drawn from people with HIV, and then returning the edited cells to the patient. This would avoid the risks of rejection that come with transplants from donors.

Most researchers in the field are proceeding cautiously, testing their results on mice, and with some success. But this is an area that can encourage over-reach. The gene-edited-baby scandal which happened in China late last year was, according to those involved, an attempt to engineer the relevant mutation into people from birth.

Such over-reach aside, even if the editing of blood stem cells could be made to work reliably, transplanting them back into people would probably remain a rare procedure—for the methods used to kill a patient’s existing bone marrow make such transplantation dangerous in and of itself. But it would at least be available as a treatment of last resort for those with forms of HIV that have developed resistance to drugs. And that would save some lives.

 

This article was originally published in The Economist. Read the original article.

Growing Pains for Field of Epigenetics as Some Call for Overhaul

Our genes are not just naked stretches of DNA.

They’re coiled into intricate three-dimensional tangles, their lengths decorated with tiny molecular “caps.” These so-called epigenetic marks are crucial to the workings of the genome: They can silence some genes and activate others.

Epigenetic marks are crucial for our development. Among other functions, they direct a single egg to produce the many cell types, including blood and brain cells, in our bodies. But some high-profile studies have recently suggested something more: that the environment can change your epigenetic marks later in life, and that those changes can have long-lasting effects on health.

In May, Duke University researchers claimed that epigenetics could explain why people who grow up poor are at greater risk of depression as adults. Even more provocative studies suggest that when epigenetic marks change, people can pass them to their children, reprogramming their genes.

But criticism of these studies has been growing. Some researchers argue that the experiments have been weakly designed: Very often, they say, it’s impossible for scientists to confirm that epigenetics is responsible for the effects they see.

Three prominent researchers recently outlined their skepticism in detail in the journal PLoS Genetics. The field, they say, needs an overhaul.

“We need to get drunk, go home, have a bit of a cry, and then do something about it tomorrow,” said John M. Greally, one of the authors and an epigenetics expert at the Albert Einstein College of Medicine in New York.

Among other criticisms, he and his co-authors — Ewan Birney of the European Bioinformatics Institute and George Davey Smith of the MRC Integrative Epidemiology Unit at the University of Bristol in England — argue that in some cases, changes to epigenetic marks don’t cause disease, but are merely consequences of disease.

Some studies, for example, have found that people with a high body mass index have unusual epigenetic marks on a gene called HIF3A. Some researchers have suggested that those marks change how HIF3A functions, perhaps reprogramming fat cells to store more fat.

If that were true, then drugs that reverse these changes might be able to help obese people lose weight. But Dr. Smith and his colleagues have found that overweight subjects experienced epigenetic changes to HIF3A only after they put on weight.

But these experiments are especially hard to set up, he noted, because scientists have to gather blood or other genetic samples from healthy people and then wait years for some of them to get sick.

In other cases, apparent changes in epigenetic marks may actually be the result of different kinds of cells becoming more or less common in people, Dr. Greally and his colleagues also warned. “That’s where things get hairy,” Dr. Greally said.

Smoking, for example, triggers a boom in immature blood cells, which carry epigenetic marks different from those of other cell types in the blood.

Rafael A. Irizarry, an applied statistician at Dana-Farber Cancer Center and the Harvard School of Public Health, said new methods could help researchers steer clear of this confusion.

Scientists can sort cells into different types before looking at their epigenetic marks, he said. It’s even becoming possible to look at the epigenetics of one cell at a time.

“But it makes the process way more expensive,” Dr. Irizarry said.

Dr. Greally and his colleagues note another source of confusion: Normal genetic variation leads some people to produce different epigenetic marks than others.

If researchers were to find that alcoholics carry an unusual epigenetic mark, for instance, that wouldn’t necessarily mean that it resulted from heavy drinking. These people may have a genetic variation that puts them at risk of alcoholism and, perhaps coincidentally, creates an unusual epigenetic mark on their DNA.

Dr. Greally said these possibilities have been neglected because scientists have been so captivated by the idea that epigenetic marks can reprogram cells.

“Since you don’t talk about anything else, you interpret the results solely through that little sliver of possibility,” he said.

He and his colleagues go so far as to claim that no published results on the links between epigenetic marks and disease “can be said to be fully interpretable.”

Other experts feel that such an indictment is a bit too broad. Dr. Flanagan pointed to several recent studies in which scientists confronted the very challenges that Dr. Greally and his colleagues wrote about. Last year, for example, a team of European scientists investigated how smoking causes lung cancer. They took advantage of large-scale studies in Australia, Norway and Sweden that collected blood from tens of thousands of people and tracked their health for years.

The scientists found that smokers who got lung cancer tended to lose the same epigenetic marks on a pair of genes.

Dr. Greally said that genetic variations the smokers were born with might account for the results. “That’s not tested in the study,” he said. “It could definitely be the case.”

Nevertheless, he added, these reports offer some good starting points for bigger studies in the future.

“There’s nothing wrong with an exploratory study, but call it an exploratory study and acknowledge the fact that it may merely be reporting noise,” Dr. Greally said.

“If you say, ‘Look, I’m finding something that’s intriguing here,’ that’s legit.”

 

This article was originally published in The New York Times. Read the original article.