DR MICHAEL MOSLEY: Should doctors prescribe dummy pills to ease pain?

DR MICHAEL MOSLEY: Should doctors now prescribe dummy pills to ease pain? (…and tell you they’re fake)

How would you feel if you went to see your GP with severe pain caused by a bad back or irritable bowel syndrome (IBS), and you were told they had just the thing to help — a placebo; a pill containing nothing but rice flour or sugar.

That possibility has come closer, thanks to a new study showing that giving patients an ‘honest’ placebo, one where they know they are getting a dummy pill, can be extremely effective at reducing pain.

And with a recent report from the Office of National Statistics showing that deaths from taking high-strength painkillers, such as tramadol and codeine, have doubled over the past ten years, there is clearly a need for safe and effective alternatives.

I’ve been involved in studies of the placebo effect, including one where we recruited more than 100 patients with chronic back pain and told them they were either getting a powerful new painkiller or a placebo. In fact, they were all given a placebo

But if the placebo effect is so effective, why don’t doctors make more use of it?

I’m a huge fan of the placebo effect. I think it’s remarkable that you can give someone a bright-coloured pill, which contains no active ingredient, and this will reduce their pain.

But it is also misunderstood. The assumption is that people who respond either weren’t ill in the first place or are credulous. Neither is true.

I’ve been involved in studies of the placebo effect, including one where we recruited more than 100 patients with chronic back pain and told them they were either getting a powerful new painkiller or a placebo. In fact, they were all given a placebo.

In this study, which was published last July in the European Journal for Person Centred Healthcare, nearly half the patients reported significant pain relief, despite swallowing dummy pills.

As I was told by Dr Jeremy Howick, an expert from Oxford University who designed our study, people who respond best to a placebo are not gullible; they are simply more open minded, especially when it comes to new experiences.

So how does it work? Well, a couple of years ago I watched an intriguing experiment carried out by Manchester University’s Human Pain Research Group. They started by attaching electrodes to a volunteer, Jack, so they could measure his brainwave activity. Then he was given two identical-looking creams and told one was a normal moisturiser, and the other may or may not contain an anaesthetic.

In reality, they were both just moisturisers. He was asked to rub cream from one tub into his left arm, the other into his right.

Next, they heated Jack’s arms with a laser, which he had to rate for painfulness on a scale from one to ten. What they didn’t tell him was that while his left arm got a full blast, his right arm had a weaker zap. They did this several times until Jack was convinced the cream he’d rubbed on his right arm contained an anaesthetic.

Finally, they gave his right arm a full blast with the laser. Amazingly, when that happened, part of Jack’s brain, the frontal cortex, began producing large amounts of brainwaves called alpha waves and this immediately moderated the pain signals reaching the brain.

This, and other research they’ve done, suggests the placebo effect works by ‘persuading’ your brain to express more alpha waves, thereby dialling down the pain, although no one knows why the waves work in this way.

But if the placebo effect is so effective, why don’t doctors make more use of it?

My sister, Susie Stead, has just published a book, Stephen From The Inside Out, about a friend who, when young, was labelled ‘schizophrenic’ and spent more than 25 years in psychiatric wards. Stephen wasn’t diagnosed with autism until his late 40s 

Well, there is a belief among doctors that a placebo treatment works only if patients think they are getting a ‘real’ pill. And that would mean lying to patients, which is unethical. A new study, however, involving people with IBS suggests the placebo effect can work even when you know you are taking a placebo. IBS affects around 20 per cent of adults in the UK and can cause crippling stomach cramps, as well as bloating, diarrhoea and constipation.

There is no known cure, though lifestyle changes can help.

To see whether giving patients an ‘honest’ placebo can help, researchers from the Beth Israel Deaconess Medical Centre in the U.S. recruited 262 people with IBS.

The patients were randomly allocated to three different groups. One group was told it would be getting placebo pills, containing no active ingredient, though the patients were also told that taking the pills could improve their symptoms. The second group was told it would get either a placebo or a pill containing peppermint oil (which can help with IBS), but didn’t know which.

A third group acted as a control and received nothing.

Those given a pill were asked to take it three times a day, 30 minutes before meals, for six weeks. At the end of the study, the patients in both of the pill groups reported a much bigger improvement in their symptoms than the control group.

Seventy per cent of those swallowing pills reported at least a 50-point improvement in their symptom score, while 30 per cent reported their score had increased by at least 150 points, which was considered a ‘very strong’ response.

I wasn’t surprised. In our back- pain study, most of the patients who got relief from taking our placebo pills said they wanted to continue taking them, despite knowing that they were swallowing nothing but ground up rice.

It seems you don’t have to deceive people to tap into the power of the placebo, at least for certain conditions. If you trust the doctor prescribing them, then simply taking pills which you have been told might do you good, really can help.

There’s a powerful connection between the microbes living in your gut, known as the microbiome, and your brain. Not only does your microbiome influence your mood, but there is evidence that children with severe autism can be helped by changing their gut bacteria. More on that in a moment.

The popular image of autism is either of a child rocking to and fro, barely able to speak, or someone who is brilliant at science but bad at human relationships. The truth is more complicated. Autistic spectrum disorder (ASD), can range from those who are severely affected to those who simply find it hard to communicate and interact with other people.

A recent study by the University of Cambridge suggests that around 1.76 per cent of children in England are on the autism spectrum, a higher figure than previously thought.

What’s tragic is that so many people with ASD have been misunderstood or misdiagnosed. My sister, Susie Stead, has just published a book, Stephen From The Inside Out, about a friend who, when young, was labelled ‘schizophrenic’ and spent more than 25 years in psychiatric wards. Stephen wasn’t diagnosed with autism until his late 40s, and none of his talents, including his extraordinary memory and aptitude for poetry, was celebrated in his lifetime.

While autism can’t be ‘cured’, speech and social therapy can help. There is also research that suggests changing the gut microbiome with a faecal transplant (using a treated sample from a donor) can improve some of the symptoms and behavioural problems associated with severe autism.

Evidence for this comes from a small study by researchers at Arizona State University in the U.S. At the start of the study, 83 per cent of the children were rated as having ‘severe’ autism, but two years after the transplant, only 17 per cent were rated ‘severe’. The parents also reported significant improvements in their language, interactions and behaviour.

The researchers are now carrying out a bigger, placebo-controlled trial in adults.

Sleeping well? This is not a rhetorical question, I really want to know. So much so that I recently launched, with the help of researchers from Oxford University, what we are hoping will be the UK’s largest ever sleep study.

If you fill in our questionnaire — find it by googling ‘BBC2 Horizon Sleep Census’ — you will get your own personalised sleep score and discover where you are on the owl-lark spectrum, i.e. the extent to which you’re better suited to late nights or early mornings. We’ll be using the anonymous data to build a detailed picture of what we all do to get a good night’s sleep, as well as the impact that sleep has on how we think and feel.

I will report back on our findings later in the year.

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EMA Reviewing GSK’s Monoclonal Antibody to Treat COVID Patients

(Reuters) – The European Medicines Agency said on Thursday it is reviewing available data on the use of GlaxoSmithKline’s monoclonal antibody to treat COVID-19 patients.

The agency said its review of VIR-7831, which GSK is developing with Vir Biotechnology Inc, will include data from a study comparing its effect with that of a placebo in patients with mild to moderate COVID-19 who were at high risk of progressing to a more severe condition.

While a more comprehensive rolling review is expected to start at a later time, the agency said the current review will provide European Union-wide recommendations for national authorities who may take decisions on early use of the medicine.

The companies reported in March that VIR-7831 reduced the risk of hospitalisation and deaths among patients by 85%, based on interim data from a study.

VIR-7831 has not been granted a marketing authorisation anywhere in the world. The companies said in a statement on Thursday they planned to submit a full marketing authorisation application to the EMA, and talks with global regulators were on to make VIR-7831 available to patients with COVID-19.

In late March, the companies filed an application to U.S. regulators for emergency use authorization of VIR-7831 to treat early-stage COVID-19 infections.

The United States has already recommended similar therapies from Eli Lilly and Co and Regeneron Pharmaceuticals Inc.

European health regulators are reviewing treatments from this class of medicines called monoclonal antibodies, which are synthetically manufactured copies of the human body’s natural infection-fighting proteins and are already being used to treat some types of cancers.

GSK and Vir announced a partnership in 2020 to research COVID-19 treatments, and earlier this year said they will expand that partnership to develop monoclonal antibody treatments for influenza and other respiratory illnesses.

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Cerebral venous sinus thrombosis: What to know about rare blood clot condition

blood

Cerebral venous sinus thrombosis was reported in six American women after they were injected with the Johnson & Johnson COVID-19 vaccine, prompting federal officials to recommend a pause Tuesday in giving doses of the one-shot vaccine until an investigation can be completed.

But what is cerebral venous sinus thrombosis, and why are the U.S. Food & Drug Administration and the Centers for Disease Control and Prevention so concerned about it?

Dr. Geoffrey Barnes, a cardiologist and vascular medicine specialist at the Michigan Medicine Frankel Cardiovascular Center, told the Free Press Tuesday that the condition is an extremely rare form of stroke.

“This is a blood clot that forms in one of the veins that helps to drain blood from your head back down to your heart,” Barnes said. “It’s an uncommon place for blood clots to form, and when it forms up there, patients tend to have sort of a collection of symptoms.”

Those symptoms, he said, can include:

  • Severe headache
  • Vision changes
  • Severe nausea
  • Vomiting
  • Rarely, some people will have seizures

With these strokes, the blood clot forms in the cerebral spinal vein, he said.

“It is a pretty uncommon location,” Barnes said. “The two most common places in the body where people develop blood clots are either in the veins of the legs, or in the lungs; those are overwhelmingly where most blood clots form.”

Peter Marks, director of the Center for Biologics Evaluation and Research at the FDA, said in the general population, this occurs in between 2 and 14 people per million population.

What’s different about the six U.S. women who developed this condition within 6 and 13 days of getting a COVID-19 vaccine is that they also had a low platelet count, also known as thrombocytopenia.

“The combination here—the real thing that is so notable here—is not just the cerebral venous sinus thrombosis or the thrombocytopenia,” Marks said. “Those two things can occur. It’s their occurrence together that makes a pattern, and that pattern is very, very similar to what was seen in Europe with another vaccine.”

The vaccine Marks was referencing is AstraZeneca’s, which is similar to Johnson & Johnson’s in that it’s a recombinant vector vaccine using the adenovirus, which causes the common cold, that’s modified with the genetic spike protein found in SARS-CoV-2.

While Johnson & Johnson’s vaccine was developed using human adenovirus, there have been reports of blood clots in people in other countries who received AstraZeneca’s vaccine. It uses chimpanzee adenovirus.

“We don’t have a definitive cause,” Marks said. “But the probable cause that we believe may be involved here … is a similar mechanism that may be going on with other the other adeno-viral vector vaccine. That is that this is an immune response that occurs very, very rarely after some people receive the vaccine, and that immune response leads to activation of the platelets and these extremely rare blood clots.”

For most people who are having a stroke or are treated for blood clots, the standard therapy in hospitals is to give them heparin, a blood thinner, Barnes said.

But for people who have a CVST following a COVID-19 vaccine, that’s not the recommendation.

“What we are learning about these blood clots and how they might be associated with the use of the AstraZeneca vaccine in Canada and Europe and now it sounds like potentially with the Johnson & Johnson Johnson vaccine here,” Barnes said, “is we actually need … to use a different form of a blood thinner. That’s sort of the critical piece for doctors to know about.

“Doctors need to be aware that if this very rare blood clot occurs within three weeks of somebody getting the J&J vaccine, then there’s some routine lab tests that they need to do, and they would want to start them on a non-heparin blood thinner.”

Two important studies were published Monday in the New England Journal of Medicine, Barnes said, that suggest that after getting one of these COVID-19 vaccines, the body can form an immune response that binds heparin with platelets, which is one of the things in the blood that helps people form blood clots.

“We see patients who get this sort of allergic reaction, you might call it, to heparin all the time,” Barnes said. “But what’s interesting here is it seems to have developed in people who never got heparin before. And so because we’re aware of this, now we know how to immediately jump in and use some non-heparin blood thinners.”

Barnes said people who’ve recently gotten a Johnson & Johnson vaccine shouldn’t be all that concerned.

“I want to reassure people that this is an exceedingly rare event,” he said. “We’re talking about six cases that have been reported from the CDC and the FDA despite millions and millions of doses of the J&J vaccine.

“We’re talking a fairly tiny percentage of people who have developed the rare blood clot. The second thing I would say is what we’ve learned from Europe and Canada, is that there does not seem to be any role for taking aspirin or a blood thinner, you know, shortly after getting your vaccine. Again, the risk of this blood clot is so exceedingly low. that we don’t want people to have other harms from taking medicines, things like that.

“The third thing I would say is that it’s really important to understand the time course. If you just got your vaccine yesterday or the day before, it’s pretty common that you might feel for muscle aches, maybe chills, fever, headache, flu-like symptoms. That’s a sign that your body’s reacting to the vaccine as we would expect—that’s not something to be concerned about.”

For anyone who got a Johnson & Johnson vaccine a month or two ago, “you’re also out of the window where we’re not concerned about any blood-clotting risk,” Barnes said.

“But if you fall in this window of about four to five days up to three weeks (post-vaccination), that’s where we’ve heard about these very rare blood clot events and so those are the people for whom we just want to keep our antenna up.

“We want to be aware of it in case they develop these new severe symptoms.”

Those people, he explained, should go to the hospital for an evaluation if they develop symptoms of CVST, such as severe headache, vision changes, severe nausea and vomiting or seizures.

“You can be reassured that every hospital in the region has the tools needed to do this evaluation,” Barnes said. “In the rare case where this is found, we have the tools necessary to treat it, but it’s pretty unlikely this is not going to be a common event that people will experience.”

He said it’s also not a reason to avoid getting a COVID-19 vaccine.

“We know that the COVID pandemic is the most important health risk out there right now, and especially here in Michigan,” Barnes said. “We are on the front lines of that, and anything we can do to get the COVID pandemic under control is going to be really important.

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Can financial stress lead to physical pain in later years?

financial stress

Financial stress can have an immediate impact on well-being, but can it lead to physical pain nearly 30 years later? The answer is yes, according to new research from University of Georgia scientists.

The study, published in Stress & Health, reveals that family financial stress in midlife is associated with a depleted sense of control, which is related to increased physical pain in later years.

“Physical pain is considered an illness on its own with three major components: biological, psychological and social,” said Kandauda A.S. Wickrama, first author and professor in the College of Family and Consumer Sciences. “In older adults, it co-occurs with other health problems like limited physical functioning, loneliness and cardiovascular disease.”

Most pain research is neurological, but it’s important to also connect it to stressful family experiences, according to the researchers.

“Dr. Wickrama and I are both interested in the context surrounding families and how that context impacts the relational, physical and mental health of the individuals in the family,” said lead author Catherine Walker O’Neal, associate research scientist in the College of Family and Consumer Sciences. “Finances are an important component of our work because it’s such a relevant contextual stressor families face.”

The authors used data from the Iowa Youth and Family Project, a longitudinal study that provides 27 years of data on rural families from a cluster of eight counties in north-central Iowa. The data was collected in real time from husbands and wives in 500 families who experienced financial problems associated with the late 1980s farm crisis. Most of the individuals are now over 65 years old, and the couples are in enduring marriages—some as long as 45 years.

Even after the researchers controlled for concurrent physical illnesses, family income and age, they found a connection between family financial hardship in the early 1990s and physical pain nearly three decades later. Additional findings from their study show it’s more likely that financial strain influences physical pain, though physical pain can in turn influence financial strain through additional health care costs.

Physical pain is a biopsychosocial phenomenon, according to Wickrama. The research suggests that stressful experiences like financial strain erode psychological resources like a sense of control. This depletion of resources activates brain regions that are sensitive to stress, launching pathological, physiological and neurological processes that lead to health conditions like physical pain, physical limitations, loneliness and cardiovascular disease.

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Why women may be better equipped to fight COVID

covid

When it comes to COVID-19, women seem to be the stronger sex, suffering severe disease at about half the rate as men, but the reason for this has been elusive.

Now, a chance experiment by an ophthalmology researcher at Duke Health has led to an insight: Women have more of a certain type of immune cell that fights infections in mucosal tissue, and these immune cells amass in the lungs, poised to attack the COVID virus.

“Better armed with these specialized immune cells, women appear to be more equipped to fight some of the most severe impacts of COVID-19, notably the respiratory infections that can become life-threatening,” said Daniel Saban, Ph.D., an associate professor in Duke’s Department of Ophthalmology and in the Department of Immunology.

Saban, who led the study that appears online in the Cell Press journal Med, said the investigation began last spring as COVID first spread and he was sidelined from his normal caseload studying eye diseases. A piece of equipment in his lab—a device that can perform 36-color flow cytometry—was sitting idle, so he decided to use it to examine blood samples from COVID patients.

“We didn’t start with a hypothesis,” Saban said. “It was a completely unbiased approach, where we asked our colleagues to provide blood and tissue samples from COVID patients as well as healthy people. We had no idea what we would find, if anything.”

Saban and the members of his lab, including Chen Yu, Ph.D. and Sejiro Littleton, quickly saw that a white blood cell called mucosal associated invariant T cells, or MAIT cell, circulated more abundantly in the blood from healthy women compared to healthy men. MAIT cells are highly specialized white blood cells that contribute to immune defenses in mucosal organs and tissues.

Among COVID patients, however, there were few MAIT cells circulating in the blood, even among women, where the population of MAIT cells radically fell off, leading the researchers to question where these cells had gone.

They found their answer in tissue samples from the lungs of COVID patients. Overall, there were an abundance of MAIT cells in the lung tissue of people with COVID, but upon closer inspection, they found night-and-day differences between the sexes.

“We first found this dichotomy in healthy blood,” Saban said. “Circulating MAIT cells in women expressed genes indicative of a robust profile poised for fighting an infection, but this was not the case in males. Then we looked in the tissue and were able to find evidence of this same pattern by sex.”

Saban said there are numerous examples of sexual differences in the immune responses to infections, noting those differences have been prevalent all along with COVID-19.

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Tweaked COVID vaccines in testing aim to fend off variants

Tweaked COVID vaccines in testing aim to fend off variants

Dozens of Americans are rolling up their sleeves for a third dose of COVID-19 vaccine—this time, shots tweaked to guard against a worrisome mutated version of the virus.

Make no mistake: The vaccines currently being rolled out across the U.S. offer strong protection. But new studies of experimental updates to the Moderna and Pfizer vaccines mark a critical first step toward an alternative if the virus eventually outsmarts today’s shots.

“We need to be ahead of the virus,” said Dr. Nadine Rouphael of Emory University, who is helping to lead a study of Moderna’s tweaked candidate. “We know what it’s like when we’re behind.”

It’s not clear if or when protection would wane enough to require an update but, “realistically we want to turn COVID into a sniffle,” she added.

Viruses constantly evolve, and the world is in a race to vaccinate millions and tamp down the coronavirus before even more mutants emerge. More than 119 million Americans have had at least one vaccine dose, and 22% of the population is fully vaccinated, according to the Centers for Disease Control and Prevention. Much of the rest of the world is far behind that pace.

Already an easier-to-spread version found in Britain just months ago has become the most common variant now circulating in the United States, one that’s fortunately vaccine-preventable.

But globally, there’s concern that first-generation vaccines may offer less protection against a different variant that first emerged in South Africa. All the major vaccine makers are tweaking their recipes in case an update against that so-called B.1.351 virus is needed. Now experimental doses from Moderna and Pfizer are being put to the test.

In suburban Atlanta, Emory asked people who received Moderna’s original vaccine a year ago in a first-stage study to also help test the updated shot. Volunteer Cole Smith said returning wasn’t a tough decision.

“The earlier one, it was a great success and, you know, millions of people are getting vaccinated now,” Smith told The Associated Press. “If we’re helping people with the old one, why not volunteer and help people with the new one?”

The study, funded by the National Institutes of Health, isn’t just testing Moderna’s experimental variant vaccine as a third-shot immune booster. Researchers at Emory and three other medical centers also are enrolling volunteers who haven’t yet received any kind of COVID-19 vaccination.

They want to know: Could people be vaccinated just with two doses of the variant vaccine and not the original? Or one dose of each kind? Or even get the original and the variant dose combined into the same injection?

Separately, the Food and Drug Administration has given Pfizer and its German partner BioNTech permission to start similar testing of their own tweaked vaccine. The companies called it part of a proactive strategy to enable rapid deployment of updated vaccines if they’re ever needed.

The Moderna and Pfizer vaccines, like the majority of COVID-19 vaccines being used around the world, train the body to recognize the spike protein that is the outer coating of the coronavirus. Those spikes are how the virus latches onto human cells.

Mutations occur whenever any virus makes copies of itself. Usually those mistakes make no difference. But if a lot of changes pile up in the spike protein—or those changes are in especially key locations—the mutant might escape an immune system primed to watch for an intruder that looks a bit different.

The good news: It’s fairly easy to update the Moderna and Pfizer vaccines. They’re made with a piece of genetic code called messenger RNA that tells the body how to make some harmless spike copies that in turn train immune cells. The companies simply swapped out the original vaccine’s genetic code with mRNA for the mutated spike protein—this time, the one from South Africa.

Studies getting underway this month include a few hundred people, very different than the massive testing needed to prove the original shots work. Scientists must make sure the mRNA substitution doesn’t trigger different side effects.

On the protection side, they’re closely measuring if the updated vaccine prompts the immune system to produce antibodies—which fend off infection—as robustly as the original shots do. Importantly, lab tests also can show if those antibodies recognize not just the variant from South Africa but other, more common virus versions, too.

Some good news: Antibodies aren’t the only defense. NIH researchers recently looked at another arm of the immune system, T cells that fight back after infection sets in. Lab tests showed T cells in the blood of people who recovered from COVID-19 long before worrisome variants appeared nonetheless recognized mutations from the South African version. Vaccines trigger T cell production, too, and may be key to preventing the worst outcomes.

Still, no vaccine is 100% effective—even without the mutation threat, occasionally the fully vaccinated will get COVID-19. So how would authorities know an update is needed? A red flag would be a jump in hospitalizations—not just positive tests—among vaccinated people who harbor a new mutant.

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AI-powered algorithm released to detect the third wave in South Africa

AI-powered algorithm released to detect the third wave in south africa

An artificial intelligence (AI)-based algorithm that has been designed by the University of the Witwatersrand (Wits University) in partnership with iThemba LABS, the Provincial Government of Gauteng and York University in Canada, shows that there is a low risk of a third infection wave of the COVID pandemic in all provinces of South Africa.

The AI-powered early detection system functions by predicting future daily confirmed cases, based on historical data from South Africa’s past infection history, that includes features such as mobility indices, stringency indices and epidemiological parameters.

“These parameters are consistent with clinical public health measures that can contain, control and mitigate against the COVID-19 pandemic,” says Dr. James Orbinski, Director of the York University Dahdaleh Institute for Global Health Research.

The AI-based algorithm works in parallel, and supports the data of an already existing algorithm that is based on more classical analytics. Both of these algorithms work independently and are updated on a daily basis. The existence of two independent algorithms adds robustness to the predictive capacity of the algorithms. The data of the AI-based analysis is published on a website that is updated on a daily basis.

“The current data shows us the risk for a third infection wave of COVID-19 is small across most of provinces in South Africa, but we still remain highly vulnerable,” says Professor Bruce Mellado, Director of the Institute for Collider Particle Physics at Wits University.

It is crucial that South Africans continue to adhere to the South African government’s COVID regulations and take all necessary precautions to prevent the spread of the pandemic.

The advent of infection waves is driven by circumstances that are difficult to predict and therefore to control. In this complex environment, early detection algorithms can provide an early warning to policy makers and the population. Early detection algorithms are able to issue an alert when the data displays a significant change that is consistent with the advent of a new wave.

While algorithm-based predictions can never be 100% accurate, Mellado is confident that the model presents a very good prediction over at least a two-week period. While predictions can be made over longer-term periods, these predictions become less accurate.

The model is trained on the interim period in between waves one and two in all of the South African provinces. The algorithm was tested with data taken during the period of past peaks to evaluate its performance.

“AI technology provides us with invaluable potential to develop early detection and alert systems that are highly needed for rapid and dynamic decision making under risk and uncertainty under the current pandemic,” says Ali Asgary, Professor of Disaster & Emergency Management and Associate director of York University’s Advanced Disaster, Emergency, and Rapid-response Simulation (www.adersim.info.yorku.ca)

AI is very effective in navigating through complex problems with a large number of parameters and dimensions, while at the same time learning from the data. Data hides within itself a wealth of information that AI can extract efficiently.

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To combat gum disease, help oral bacteria evolve

To combat gum disease, help oral bacteria evolve

Liver disease, from metabolic and bacterial causes, is a growing concern. What connects these dots? The gut, or more specifically, bacteria in the gut. Bacteria that cause inflammation in the mouth are transported through the digestive tract to the gut and liver, where they can cause liver inflammation. Lipopolysaccharides, important structural molecules in some bacteria, act as endotoxins, producing systemic effects that can manifest as non-alcoholic fatty liver disease (NAFLD). Now, a multidisciplinary team from the University of Tsukuba show that exercise could be used to improve the oral environment in people with NAFLD, potentially leading to a new treatment for the disease.

These researchers previously demonstrated that exercise benefits patients with NAFLD by reducing fat, inflammation, and scarring in the liver; improving the liver’s response to and clearance of the endotoxin; and reducing gum disease. With the latest study in their series, they add another signpost to uncharted territory:

“We know that exercise has innumerable benefits to health overall and for these specific conditions,” says corresponding author Professor Junichi Shoda. “With this study, we sought to characterize underlying mechanisms—that is, show how exercise alters physiology and how altered physiology induces changes in oral bacteria.”

The researchers carried out biochemical and genetic analyses on saliva from overweight men with NAFLD and gum disease before and after 12-week exercise or diet programs. Men in both groups were able to lose fat mass, but those following dietary restrictions also lost muscle mass, whereas those following the exercise program gained muscle mass. “More importantly, we found that reductions in lactoferrin, lipopolysaccharide, and IgA concentrations were only evident in the men who followed the exercise regimen,” Professor Shoda explains, “which suggested that the oral environment had been significantly altered by exercise.”

The samples from the exercise group also showed increased bacterial diversity and changes in the relative constituent bacterial populations. In the overall population, more bacteria expressed genes related to environmental information processing, and less bacteria expressed genes related to genetic information processing and metabolism. In fact, bacteria expressed fewer genes for producing lipopolysaccharides.

“Therefore, it seems that, in people with both non-alcoholic liver disease and gum disease, exercise causes a biochemical shift in the environment of the mouth that favors the survival of less harmful bacteria,” explains Professor Shoda.

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