Posts Tagged ‘medicine’



Researchers found that a black-box algorithm predicted patient death better than humans.

They used ECG results to sort historical patient data into groups based on who would die within a year.

Although the algorithm performed better, scientists don’t understand how or why it did.

Albert Einstein’s famous expression “spooky action at a distance” refers to quantum entanglement, a phenomenon seen on the most micro of scales. But machine learning seems to grow more mysterious and powerful every day, and scientists don’t always understand how it works. The spookiest action yet is a new study of heart patients where a machine-learning algorithm decided who was most likely to die within a year based on echocardiogram (ECG) results, reported by New Scientist.

The algorithm performed better than the traditional measures used by cardiologists. The study was done by researchers in Pennsylvania’s Geisinger regional healthcare group, a low-cost and not-for-profit provider.

Much of machine learning involves feeding complex data into computers that are better able to examine it really closely. To analogize to calculus, if human reasoning is a Riemann sum, machine learning may be the integral that results as the Riemann calculation approaches infinity. Human doctors do the best they can with what they have, but whatever the ECG algorithm is finding in the data, those studying the algorithm can’t reverse engineer what it is.

The most surprising axis may be the number of people cardiologists believed were healthy based on normal ECG results: “The AI accurately predicted risk of death even in people deemed by cardiologists to have a normal ECG,” New Scientist reports.

To imitate the decision-making of individual cardiologists, the Geisinger team made a parallel algorithm out of the factors that cardiologists use to calculate risk in the accepted way. It’s not practical to record the individual impressions of 400,000 real human doctors instead of the results of the algorithm, but that level of granularity could show that cardiologists are more able to predict poor outcomes than the algorithm indicates.

It could also show they perform worse than the algorithm—we just don’t know. Head to head, having a better algorithm could add to doctors’ human skillset and lead to even better outcomes for at-risk patients.

Machine learning experts use a metric called area under the curve (AUC) to measure how well their algorithm can sort people into different groups. In this case, researchers programmed the algorithm to decide which people would survive and which would die within the year, and its success was measured in how many people it placed in the correct groups. This is why future action is so complicated: People can be misplaced in both directions, leading to false positives and false negatives that could impact treatment. The algorithm did show an improvement, scoring 85 percent versus the 65 to 80 percent success rate of the traditional calculus.

As in other studies, one flaw in this research is that the scientists used past data where the one-year window had finished. The data set is closed and scientists can directly compare their results to a certain outcome. There’s a difference—and in medicine it’s an ethical one—between studying closed data and using a mysterious, unstudied mechanism to change how we treat patients today.

Medical research faces the same ethical hurdles across the board. What if intervening based on machine learning changes outcomes and saves lives? Is it ever right to treat one group of patients better than a control group that receives less effective care? These obstacles make a big difference in how future studies will pursue the results of this study. If the phenomenon of better prediction holds up, it may be decades before patients are treated differently.

https://www.popularmechanics.com/science/health/a29762613/ai-predict-death-health/

By Steven Reinberg

Loneliness can take a heavy toll on heart patients — including a higher risk of death in the year after hospitalization, researchers found.

“This study confirms what has also been indicated in previous research regarding the serious health consequences of loneliness,” said lead researcher Anne Vinggaard Christensen, of Copenhagen University Hospital in Denmark.

“Loneliness should be considered a serious risk factor in patients with cardiac disease and should be included in risk evaluation of patients,” added Christensen, who is with the hospital’s heart center.

The Danish researchers cautioned, however, that their findings can’t prove that loneliness caused people to die, only that loneliness and the risk of death appear to be connected. But the differences in mortality between those who felt lonely and those who didn’t can’t be explained by their medical condition alone, they said.

Loneliness is a subjective experience, one that is distressing and unpleasant, the researchers noted.

The connection between loneliness and health is complex, Christensen said.

People who are lonely or socially isolated tend to have more unhealthy lifestyles. They smoke more, are less likely to be physically active and don’t take their medication, she said.

“Having a social network helps motivate people to make healthier choices,” Christensen said. “A social network can act as a buffer for stress.”

Also, lonely people have been found to have higher levels of stress hormones and lower immune function, she added.

“These different pathways are interconnected and help us understand why people feeling lonely or socially isolated experience worse health,” Christensen said.

James Maddux is a professor emeritus in the department of psychology at George Mason University in Fairfax, Va. Reviewing the findings, he took issue with the study’s methodology.

“My major concern about the methodology is that their measure of loneliness is rather weak and is not consistent with most studies about loneliness that I am familiar with,” Maddux said. He explained that the question used to measure loneliness failed to capture loneliness “as a profound sense of isolation and disconnected from others, accompanied by sadness and a longing to be with others. In other words, loneliness is painful.”

Still, even in its flawed state, the new study “adds to the growing research on the perils of social isolation among people in general and among older adults over 60 in particular,” said Maddux. “These results help reaffirm what we’ve learned so far about how unhealthy social isolation can be.”

For the study, Christensen and her colleagues collected data on more than 13,400 heart patients after they left the hospital from 2013 to 2014. Their average age was in the mid-60s.

Participants completed questionnaires on their health, psychological well-being, quality of life and levels of anxiety and depression.

Compared to people who didn’t feel lonely, those who said they were lonely were nearly three times more likely to be anxious and depressed and have a lower quality of life, the researchers found.

A year later, Christensen’s team found that feeling lonely had a significant impact on participants’ health.

Regardless of other factors, lonely women were nearly three times more likely to die than women who weren’t lonely, and lonely men were more than twice as likely to die, the researchers found.

Living alone, however, is not necessarily equal to feeling lonely, and it was linked to a lower risk of depression and anxiety than living with others.

But among men, living alone was tied with a 39% greater risk for poor heart health. This may be because men tend not to have an extensive support network after divorce or death of a spouse, compared with women, the researchers noted.

“Loneliness can have many causes and can occur even if you have people around you,” Christensen said.

For some, it would help to have a family member who remembers to ask how they are doing and is ready to listen, she said.

“For others, help with practical things might be what they need, and for some, the opportunity to talk to other patients who have gone through the same thing is helpful,” Christensen said.

She also stressed that the effects of loneliness are not confined to heart disease. “It’s also [detrimental] for individuals who do not suffer from an illness. Loneliness seems to be damaging to your health no matter what,” Christensen said.

The report was published online Nov. 4 in the journal Heart.

https://consumer.healthday.com/cardiovascular-health-information-20/misc-stroke-related-heart-news-360/risks-mount-for-lonely-hearts-after-cardiac-surgery-751879.html

Our thinking skills in childhood could offer a glimpse into how our minds might work at the age of 70, according to a study spanning decades.

The research started in 1946, when 502 8-year-olds, who were born in the U.K. in the same week, took tests to measure their thinking and memory skills. The participants took cognitive tests again between the ages of 69 and 71.

The participants also had scans, including a positron emission tomography (PET) scan that detects amyloid-beta plaques in the brain. These sticky collections of protein are linked to Alzheimer’s disease.

The study, published in the journal Neurology, shows those with the highest test scores in childhood were more likely to have high scores later in life. Kids in the top 25 percent had a greater chance of being in that same quartile at 70.

Educational attainment and socioeconomic status also appeared to make a difference. Those who were college-educated scored around 16 percent better in tests than those who left school before they hit 16. Participants who had a white-collar job were able to remember, on average, 12 details from a short story, versus 11 if they had a manual job. Overall, women did better than men when their memory and thinking speed were tested.

Participants who were found to have amyloid-beta plaques in their brains, meanwhile, scored lower on cognitive tests. In one assessment where participants had to find the missing pieces in five geometric shapes, those with the plaque got 23 out of 32 problems correct, versus 25 for those without the plaques.

Dr. Jonathan M. Schott of University College London commented: “Finding these predictors is important because if we can understand what influences an individual’s cognitive performance in later life, we can determine which aspects might be modifiable by education or lifestyle changes like exercise, diet or sleep, which may, in turn, slow the development of cognitive decline.

“Our study found that small differences in thinking and memory associated with amyloid plaques in the brain are detectable in older adults even at an age when those who are destined to develop dementia are still likely to be many years away from having symptoms.”

Earlier this year, Schott and his team published a separate study in the journal The Lancet Neurology that showed having high blood pressure in a person’s mid-30s was linked to higher levels of blood vessel damage in the brain, as well as shrinkage of the organ.

Professor Tara Spires-Jones from the UK Dementia Research Institute at the University of Edinburgh, who did not work on the new study, told Newsweek the findings add to other studies that suggest our genetics, as well as environmental factors, play a role in how we maintain our thinking skills as we age.

“However, this does not mean that all of your brain power during aging is determined during childhood,” she said. “There is good scientific evidence from this study and many others that keeping your brain and body active are likely to reduce your risk of developing Alzheimer’s disease, even as adults.”

Learning, socializing and exercise can all help, she said.

“One way this works is by building new connections between brain cells, called synapses. Synapses are the building blocks of memory, so building up a robust network of synapses, sometimes called ‘brain reserve’ is thought to be the biology behind the finding that more education is associated with a lower risk of dementia and age-related cognitive decline,” explained Spires-Jones.

Spires-Jones suggested amyloid-beta plaques might be linked with lower tests scores in the study because they build up and damage the connections between brain cells, called synapses, impairing brain function.

“Amyloid plaques are also widely thought to initiate a toxic cascade that leads to dementia in Alzheimer’s disease, including the build-up and spread of another pathology called ‘tangles,'” she said.

She said the study was “very strong” but limited because observational studies can’t explain the links that emerge, and the participants were all white so the results might not relate to other populations.

“It will be important in future work to try and understand the biological underpinnings for the associations between childhood intelligence and better cognitive ability during aging,” she said.

https://www.newsweek.com/dementia-aging-study-brains-tests-1468657


Dr. Jean-Jacques Muyembe first encountered Ebola in 1976, before it had been identified. Since then, from his post at the Congo National Institute for Biomedical Research, he has led the global search for a cure.

by EYDER PERALTA

Dr. Jean-Jacques Muyembe says his story starts in 1973. He had just gotten his Ph.D. at the Rega Institute in Belgium. He could have stayed in Europe, but he decided to return to Congo, or what was then known as Zaire, which had only recently attained independence from Belgium.

If he had stayed in Belgium, he says, he would have been doing routine lab work. But in Congo, he would be responsible for the “health of my people.”

“But when I arrived here the conditions of work were not good,” he says. “I had no lab; I had no mice for the experimentation, so it was very difficult to work here.”

Being a microbiologist without mice or a lab was useless, so he took a job as a field epidemiologist. In 1976, he was called to an outbreak of a mysterious disease in central Congo.

Lots of people had died of something that presented like yellow fever, typhoid or malaria. Muyembe arrived to a nearly empty hospital. He says people thought the infection was coming from the hospital, and he found only a mother and her baby.

“I thought that it was malaria or something like this,” he says. “But in the night the baby died, so the hospital was completely empty.”

By morning, as the people of Yambuku heard Muyembe had been sent by the central government in Kinshasa, they started lining up at the hospital hoping he had medicine for them.

“I started to make physical exam,” he says. “But at that time we had no gloves in the whole hospital.”

And, of course, he had to draw blood, but when he removed the syringes, the puncture would gush blood.

“It was the first time for me to see this phenomenon,” he says. “And also my fingers were soiled with blood.”

Muyembe says he washed his hands, but it was really luck that kept him from contracting an infection. He knew immediately this was something he’d never seen before. Some of the Belgian nuns in the village had been vaccinated against yellow fever and typhoid, but this disease was different. It was killing people fast. When he took liver samples with a long needle, the same thing would happen — blood would continue to gush.

He persuaded one of the nuns who had the disease to fly with him to Kinshasa. He took blood samples before she died and sent them to Belgium, where they had an electron microscope to try to identify the culprit. Scientists there and in the United States saw this was a new virus that caused hemorrhagic fever.

They named it Ebola, after a river near the village.

The discovery, says Muyembe, was thanks to a “consortium of research.”

But Google “Who discovered Ebola?” and you get a bunch of names — all of them white Western males. Dr. Jean Jacques Muyembe has been written out of history.

“Yes, but it is …” he pauses. He takes a breath and laughs, looking for the right way to respond.

“Yes. It is not correct,” he says. “It is not correct.”

The man who gets the bulk of the credit for discovering Ebola is Dr. Peter Piot. At the time, he was a young microbiologist at the Institute for Tropical Medicine in Belgium. He was the one to receive the blood samples sent by Muyembe.

He describes his experience in No Time to Lose, a book about his professional life, including his vast work on HIV.

But Ebola was his big break. In the book, he describes how vials of blood had arrived in melting ice, some of them broken.

He describes how the World Health Organization ordered them to give up the samples, to send them to England and eventually the Centers for Disease Control and Prevention in the United States, which was one of the only labs equipped to handle a deadly virus like Ebola.

He describes how angry that made him and Dr. Stefaan Pattyn, the man running the lab at the time, who died in 2008.

“[Pattyn] claimed that we needed a few more days to ready it for transport,” Piot wrote. “So we kept a few tubes of VERO cells, as well as some of the newborn mice, which were dying. Perhaps it was a stubborn rebellion against the whole Belgian history of constantly being forced to grovel to a greater power. That material was just too valuable, too glorious to let it go.”

Almost simultaneously, scientists at the CDC and Piot looked at the samples under an electron microscope and saw a snakelike filament — huge in comparison to other viruses and very similar to the Marburg virus. The CDC, which kept the world’s reference lab for hemorrhagic viruses, confirmed this was something new. This was Ebola.

The Congo National Institute for Biomedical Research sits in the middle of Kinshasa.

There are ragged couches along the corridors and goats feeding in the courtyard. But this is where the bulk of the science is being done on the second largest Ebola outbreak in history.

Tucked in corners around the building, there are high-tech labs. Scientists in full biohazard suits run Ebola samples through sophisticated machines that spit out DNA sequences. On the bulletin boards outside the offices, scientists have pinned papers published in international journals about the science done right here.

Workers are constantly dragging in boxes of brand-new scientific gear. On this day, almost all of them are stamped with the American flag.

It’s no secret there is resentment among scientists here about what many believe is a marginalization of their work by the West.

Joel Lamika, who runs an Ebola smartphone app at the institute, says many foreign governments want to stamp their flags on the work Congolese have done.

“They want to claim like it’s theirs,” he says. “But it is theft.”

Lamika says perhaps one good thing that has come out of this latest Ebola outbreak is that it is giving the world a chance to rewrite history.

Muyembe, he says, is a national hero. His picture is on a huge banner in front of this institute. During previous Ebola outbreaks, and especially the huge one in West Africa that killed more than 11,000 people, the the scientific community used Muyembe as an example of someone who had gotten it right. Under his leadership, Congo had managed to quickly quell nine previous outbreaks.

Maybe this outbreak, he says, will give the world an opportunity to know who Muyembe is.

“It’s time for the world to learn that Ebola was discovered by a Congolese,” he said. “By Dr. Jean-Jacques Muyembe.”

Today, Peter Piot is the director of the prestigious London School of Hygiene and Tropical Medicine. He’s friends with Muyembe and expresses nothing but admiration for not only his scientific prowess, but the way he has managed public health emergencies.

But in his book, he mentions Muyembe only in passing, as a bright scientist constantly pressuring Piot for more resources.

When asked if he feels responsible for writing Muyembe out of history, Piot pauses.

“I think that’s a fair comment,” he says. “But my book was not an attempt to write the history of Ebola, but more my personal experience.”

Piot says at the time of that first Ebola outbreak, African scientists were simply excluded. White scientists — with a colonial mentality — parachuted in, took samples, wrote papers that were published in the West and took all of the credit.

But things are changing, he says. Muyembe, for example, is finally starting to get his due. He was recently given a patent for pioneering the first treatment for Ebola and he has received several international awards, including the Royal Society Africa Prize and, just this year, the Hideyo Noguchi Africa Prize.

“That reflects, I think, the [change in] power relations in global health and science in general,” he said.

During this outbreak, Muyembe has also made a decision many thought unthinkable even a few years ago. He decided that all of the blood samples collected during this Ebola epidemic will stay in Congo. Anyone who wants to study this outbreak will have to come to his institute.

American scientists, who have led the way in studying Ebola, have privately expressed frustrations. But Piot says the decision was obviously made because of how African scientists have been treated. Western scientists, he says, should get over it.

“We have to wake up to two things,” he says. “One, the world has changed. And two, it’s a matter of fairness.”

Muyembe keeps his office ice cold, and when he talks, he nervously drums a pen against his notebook. He’s terribly serious about his work, but he also offers an easy smile as he remembers his work.

The thing that makes him glow is talking about the treatment he developed.

“It is the most important achievement of my life,” he says.

In 1995, during another outbreak, he wondered whether antibodies developed by Ebola survivors could be siphoned from their blood and used to treat new cases. So he injected Ebola patients with the blood of survivors, taking inspiration from a practice used before sophisticated advances in vaccine-making.

“We did eight patients and seven survived,” he says.

The medical establishment wrote him off. He didn’t have a control group, they told him. But Muyembe knew that in this village, Ebola was killing 81% of people. Just this year, however, that science became the foundation of what is now proven to be the first effective treatment against Ebola, saving about 70% of patients.

“But if this idea was accepted by scientists, we [could have] saved a lot of people, a lot of lives,” he says.

You can tell Muyembe is hurt by all this. Ever since he returned to Congo, he has fought for recognition for his country. His whole life, he has dreamed that big science could come out of his home country.

Just as he announced that samples would not leave Congo, he also got a commitment from Japan to build a state-of-the-art research facility right here. Soon, the goats in the courtyard will be gone, replaced by a facility just as good as those in Belgium or in the United States.

At 77, Muyembe says he doesn’t regret coming back to Congo. And, unlike when he returned in 1973, now he has equipment.

“Now I have mice here,” he says, laughing. “I have mice. I have subculture. Now, everything is here.”

His biggest legacy, he says, won’t be that he helped to discover Ebola or a cure for it. It’ll be that if another young Congolese scientist finds himself with an interesting blood sample, he’ll be able to investigate it right here in Congo.

https://www.npr.org/sections/goatsandsoda/2019/11/04/774863495/this-congolese-doctor-discovered-ebola-but-never-got-credit-for-it-until-now?utm_source=Nature+Briefing&utm_campaign=c9c91341f8-briefing-dy-am-20191105&utm_medium=email&utm_term=0_c9dfd39373-c9c91341f8-44039353

Laura Lewis and her team of researchers have been putting in late nights in their Boston University lab. Lewis ran tests until around 3:00 in the morning, then ended up sleeping in the next day. It was like she had jet lag, she says, without changing time zones. It’s not that Lewis doesn’t appreciate the merits of a good night’s sleep. She does. But when you’re trying to map what’s happening in a slumbering human’s brain, you end up making some sacrifices. “It’s this great irony of sleep research,” she says. “You’re constrained by when people sleep.”

Her results, published last week in the journal Science, show how our bodies clear toxins out of our brains while we sleep and could open new avenues for treating and preventing neurodegenerative diseases like Alzheimer’s.

When we sleep our brains travel through several phases, from a light slumber to a deep sleep that feels like we’ve fallen unconscious, to rapid eye movement (REM) sleep, when we’re more likely to have dreams. Lewis’ work looks at non-REM sleep, that deep phase which generally happens earlier in the night and which has already been associated with memory retention. One important 2013 study on mice showed that while the rodents slept, toxins like beta amyloid, which can contribute to Alzheimer’s disease, got swept away.

Lewis was curious how those toxins were cleared out and why that process only happened during sleep. She suspected that cerebrospinal fluid, a clear, water-like liquid that flows around the brain, might be involved. But she wasn’t sure what was unique about sleep. So her lab designed a study that measured several different variables at the same time.

Study participants had to lie down and fall asleep inside an MRI machine. To get realistic sleep cycles, the researchers had to run the tests at midnight, and they even asked subjects to stay up late the night before so people would be primed to drift off once the test began.

Lewis outfitted the participants with an EEG cap so she could look at the electrical currents flowing through their brains. Those currents showed her which stage of sleep the person was in. Meanwhile, the MRI measured the blood oxygen levels in their brains and showed how much cerebrospinal fluid was flowing in and out of the brain. “We had a sense each of these metrics was important, but how they change during sleep and how they relate to each other during sleep was uncharted territory for us,” she says.

What she discovered was that during non-REM sleep, large, slow waves of cerebrospinal fluid were washing over the brain. The EEG readings helped show why. During non-REM sleep, neurons start to synchronize, turning on and off at the same time. “First you would see this electrical wave where all the neurons would go quiet,” says Lewis. Because the neurons had all momentarily stopped firing, they didn’t need as much oxygen. That meant less blood would flow to the brain. But Lewis’s team also observed that cerebrospinal fluid would then rush in, filling in the space left behind.

“It’s a fantastic paper,” says Maiken Nedergaard, a neuroscientist at the University of Rochester who led the 2013 study that first described how sleep can clear out toxins in mice. “I don’t think anybody in their wildest fantasy has really shown that the brain’s electrical activity is moving fluid. So that’s really exciting.”

One big contribution of the paper is it helps show that the systems Nedergaard has been studying in mice are present and hugely important for humans too. “It’s telling you sleep is not just to relax,” says Nedergaard. “Sleep is actually a very distinct function.” Neurons don’t all turn off at the same time when we’re awake. So brain blood levels don’t drop enough to allow substantial waves of cerebrospinal fluid to circulate around the brain and clear out all the metabolic byproducts that accumulate, like beta amyloid.

The study also could have clinical applications for treating Alzheimer’s. Recent attempts at developing medications have targeted beta amyloid. But drugs that looked promising at first all failed once they got into clinical trials. “This opens a new avenue,” says Nedergaard. Instead of trying to act on one particular molecule, new interventions might instead focus on increasing the amount of cerebrospinal fluid that washes over the brain.

That would help clear out beta amyloid but also could help with other molecules like tau, a protein that gets tangled in Alzheimer’s patients’ brains and harms the connections between neurons. Finding a way to clear out all of that garbage could be much more powerful than just focusing on one piece of the problem. “Aging is not just about one molecule,” says Nedergaard. “Everything fails.”

These discoveries bring along their own set of questions. Lewis didn’t study what happens during other stages of sleep, and she only looked at healthy young adults. But the methods she used were entirely noninvasive—or as noninvasive as having people sleep in an MRI while hooked up to lots of machines can be. She didn’t even inject any dye. That will make it easier to start studying older participants who may be developing neurodegenerative diseases.

https://www.wired.com/story/scientists-now-know-how-sleep-cleans-toxins-from-the-brain/?bxid=5c48e315fc942d0477abe04c&cndid=50678559&esrc=sign-up-page&source=EDT_WIR_NEWSLETTER_0_DAILY_ZZ&utm_brand=wired&utm_campaign=aud-dev&utm_mailing=WIR_Daily_110119&utm_medium=email&utm_source=nl&utm_term=list1_p4


An infection with a drug-resistant strain of E. coli proved fatal for a man who received a fecal transplant.

The first person known to die as a result of a fecal transplant is a 73-year-old man who developed a fatal infection with antibiotic-resistant bacteria that were in the donor’s stool sample.

News of the man’s death surfaced in June; he was one of two patients in separate clinical trials who became ill after receiving fecal transplants from the same donor.

Both patients developed infections with a strain of Escherichia coli, or E. coli, that demonstrated resistance to different types of antibiotics. Details of the man’s death were described in a new study published online Oct. 30 in The New England Journal of Medicine.

The two patients, who were participants in clinical trials conducted at Massachusetts General Hospital (MGH), received fecal transplants in the form of pills that were made in November 2018.

Fecal microbiota transplantation (FMT) — commonly known as a “poop transplant” or fecal transplant — is emerging as an effective experimental treatment for Clostridium difficile, or C. diff, a potentially life-threatening bacterial gut infection. In guts with depleted microbial diversity, poop transplants boost diversity with microbial infusions from a healthy person’s gut microbiome, distilled from stool samples and delivered as an enema or an oral pill.

But FMT is also being tested as a method of restoring gut microbial diversity for conditions not caused by C. diff. The two clinical trials at MGH were testing the impact of FMT on microbiome issues associated with liver disease and the effectiveness of preventive FMT prior to stem cell transplants.

Eight days after the 73-year-old patient received his last FMT dose, he developed a fever and chills, and exhibited “altered mental status,” according to the study. His condition quickly worsened. The man developed sepsis — an extreme immune response to infection causing inflammation throughout the body and organ damage — and died two days later, with evidence of an antibiotic-resistant strain of E. coli in his blood.

The other patient who became ill from the FMT, a 69-year-old man, also tested positive for the drug-resistant strain of E. coli. However, his infection responded to treatment with antibiotics. Eventually, he was pronounced “clinically stable,” the researchers wrote in the study.

Antibiotic resistance in harmful bacteria is a growing concern worldwide. With the emergence of these so-called superbugs — some of which can share their resistance with other bacteria — entire classes of antibiotics are becoming less effective at quelling infections, and health practitioners are losing key weapons in their disease-fighting arsenals.

High-risk patients

In January 2019, a regulatory review by the U.S. Food and Drug Administration (FDA) dictated that stool samples for FMT had to be screened for drug-resistant microbes. But as this E. coli strain is rare in healthy people, the pills that were produced in November were not tested retroactively, the study authors reported.

Both of the FMT-sickened patients were considered at high risk for bacterial infection because of conditions that weakened their immune systems. The man who recovered had advanced cirrhosis — severe scarring of the liver — and the man who died had recently undergone a stem cell transplant and was taking immunosuppressing drugs so that the transplant would not be rejected, the scientists reported. Samples from the same donor were administered to 22 patients in all, and although several other recipients tested positive for the resistant E. coli, the bacteria didn’t make them ill.

On Nov. 4, FDA officials will conduct a 7-hour public hearing at the agency’s Silver Spring, Maryland, campus, “to obtain public input on the state of the science regarding FMT to treat C. difficile infection not responsive to standard therapies,” according to a notice on the FDA website.

The FDA hearing will also review clinical evidence to evaluate the effectiveness and risks of using FMT to combat persistent C. difficile “and to better understand the impact of FDA’s enforcement policy on product development,” agency officials said in the statement.

https://www.livescience.com/fecal-transplant-death.html?utm_source=Selligent&utm_medium=email&utm_campaign=9583&utm_content=20191101_LS_Essentials_Newsletter+-+adhoc+&utm_term=3675605&m_i=uxOuCb14GZ_f_Gtk%2Bp9nsep0qM1OWDMFvl255HddfzLlp4atZ49G7gBQyO3IdDiaYEBisgwkAznzqIBplBPr0oSWQdXtA95quF

By Nicholas Bakalar

Trans fatty acids, known to increase the risk for heart disease, stroke and diabetes, have now been linked to an increased risk for dementia.

Researchers measured blood levels of elaidic acid, the most common trans fats, in 1,628 men and women 60 and older and free of dementia. Over the following 10 years, 377 developed some type of dementia.

Trans fats, which are added to processed food in the form of partially hydrogenated vegetable oils, increase levels of LDL, or “bad” cholesterol. Meat and dairy products naturally contain small amounts of trans fats, but whether these fats raise bad cholesterol is unknown.

After controlling for other factors, the scientists found that compared with those in the lowest one-quarter in blood levels of elaidic acid, those in the highest were 50 percent more likely to develop any form of dementia and 39 percent more likely to develop Alzheimer’s disease in particular. Elaidic acid levels were not associated with vascular dementia considered alone. The study is in Neurology.

The senior author, Dr. Toshiharu Ninomiya, a professor of public health at Kyushu University in Japan, said the study is observational so cannot prove cause and effect. “It is difficult to avoid trans fats completely, and the risk of a small amount of trans fats is unclear,” he said. “But it would be better to try to avoid them as much as possible.”