Study of 670,450 American Women Shows Almost Half of Them Are Receiving the Wrong UTI Treatment

Many American healthcare professionals are still prescribing incorrect antibiotics treatments for too long of a duration.

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Across the United States, in both rural and urban settings, most women with private health insurance are receiving inappropriate treatment for their urinary tract infections (UTIs), according to a new study. 

Of the 670,450 women included in this research, all of whom had been diagnosed with uncomplicated UTIs between the ages of 18 and 44, nearly half received the wrong antibiotics and over three quarters were prescribed the medicine for too long. (A UTI is declared ‘uncomplicated’ when the patient has no abnormality or disease that could predispose them to more frequent infections.)

The results are largely consistent from location to location, although patients in more rural settings were more likely to be prescribed antibiotics for longer. 

Over the course of the study, from 2011 to 2015, there was only a slight improvement in proper antibiotic prescriptions based on current clinical guidelines.

“Inappropriate antibiotic prescriptions for uncomplicated urinary tract infections are prevalent and come with serious patient- and society-level consequences,” says epidemiologist Anne Mobley Butler from the Washington University School of Medicine, St. Louis.

“Our study findings underscore the need for antimicrobial stewardship interventions to improve outpatient antibiotic prescribing, particularly in rural settings.” 

The research was funded in part by several pharmaceutical companies, including Sanofi Pasteur, Pfizer, and Merck. The results were peer-reviewed and fall largely in line with the findings of previous studies, which suggest up to 60 percent of antibiotics prescribed in intensive care units are “unnecessary, inappropriate, or suboptimal”.

Nor is this just a problem in the US. Around the world, UTIs are one of the most common infections leading to emergency room visits. In the United Kingdom, it’s the second most common reason for prescribing antibiotics. 

Not only does taking the wrong antibiotic have worse outcomes for the individual patient, longer prescriptions are not necessarily better and can cause bacteria to grow resistant, making recurrence more likely and future infections harder to treat. 

Today, it’s estimated one in three uncomplicated UTIs in women are resistant to the popular combined antibiotic drug Bactrim (sulfamethoxazole and trimethoprim), and one in five are resistant to five other common antibiotics. 

An estimate of the number of deaths related to antibiotic-resistant UTIs is hard to establish due to a lack of research and monitoring, but some studies suggest that in US hospitals alone it could be around 13,000 lives lost per year. And some people suffer recurrent, resistant infections for years on end with little to no relief.

In light of these emerging concerns, in 2010 the Infectious Diseases Society of America (IDSA) and the European Society for Microbiology and Infectious Diseases updated their clinical practice guidelines. Based on results from various studies, they now recommend several first-line antibiotic agents and durations to best treat UTIs while minimizing the risk of antibiotic resistance.

That advice, however, is clearly not getting through to physicians and healthcare professionals. Many are still prescribing non-recommended antibiotics for improper durations.

Figuring out where the most inappropriate prescriptions are happening could help us target areas where we need to improve adherence to antibiotic guidelines. In the US, rural areas experience numerous health disparities compared to more urban areas, and yet this is the first large-scale study to evaluate how that impacts UTI treatment.

The authors are not sure why longer antibiotic treatments for UTIs are especially prevalent in rural areas, but suggest it could have to do with access to care and physician awareness. In rural areas, women may be given longer prescriptions to avoid future travel if that treatment fails.

Studies also show late-career physicians are more prevalent in rural locations and are more likely to prescribe antibiotics for longer, possibly because they have not heard of updated guidelines. 

“Accumulating evidence suggests that patients have better outcomes when we change prescribing from broad-acting to narrow-spectrum antibiotics and from longer to shorter durations,” explains Butler.

“Promoting optimal antimicrobial use benefits the patient and society by preventing avoidable adverse events, microbiome disruption, and antibiotic-resistant infections.”

When up to 60 percent of women can suffer from a UTI at some point in their life, it’s clearly vital that guidelines for treatment are better enforced, especially as antibiotic resistance increases.

This particular study was only based on commercially insured individuals, which means those who are uninsured or who receive public insurance were not considered. Rural areas were also loosely defined, including small towns as well as ‘exurbs’ on the edges of urban areas, and men, who also suffer from UTIs (albeit at a lower rate), were not included. 

Future research should focus on filling these gaps, but in the meantime, the trend reinforces the idea that clinicians need to periodically review clinical practice guidelines, even for common conditions that they have been treating for years.

“In recent years, little effective progress has been achieved to reduce inappropriate antibiotic prescribing for uncomplicated UTI,” the new paper concludes

“Given the large quantity of inappropriate prescriptions annually in the United States, as well as the negative patient- and society-level consequences of unnecessary exposure to antibiotics, antimicrobial stewardship interventions are needed to improve outpatient UTI antibiotic prescribing, particularly in rural settings.”

The study was published in Infection Control & Hospital Epidemiology.

Don’t Take Ibuprofen or Acetaminophen Before Receiving a COVID-19 Vaccine

Regardless of what one thinks about the COVID-19 vaccines and the current amount of data on them, everyone reading this will probably know someone that will receive a COVID-19 vaccine. The current evidence suggests that taking drugs such as ibuprofen or acetaminophen is one of the worst things people can do before receiving one of the COVID-19 vaccines. The human body needs a proper immune response to develop immunity to the virus and the drugs will plausibly interfere with that immune response, very possibly leading to a reduced level of immunity. That reduced level of immunity may lead to a susceptibility to COVID-19 later on.

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Taking OTC pain medications ahead of your shot to try and decrease symptoms is not recommended by the CDC, because it’s not clear how that could affect the vaccine’s effectiveness.

The concern is that pre-treating with pain medications that reduce fevers and inflammation (like acetaminophen and ibuprofen) could dampen your immune system’s response to the vaccine.

That’s because your immune system responds to vaccines through a process called “controlled inflammation,” Dr. Colleen Kelley, an associate professor of medicine at Emory University School of Medicine, told USA Today in January.

Covid messenger RNA vaccines work by giving cells genetic material that tells them how to make a non-infectious piece of the virus. The immune system then creates antibodies against it — which is controlled inflammation — and can remember how to trigger an immune response if exposed to the virus in the future.

But OTC pain-relieving medications “reduce the production of inflammatory mediators,” Kelley said. That’s why it’s important to wait until after you’ve gotten the vaccine (and have started creating an inflammatory response already) to take pain medication.

Research on children has shown that those who take acetaminophen before getting vaccines have a lower immune response than those who didn’t. And a recent study out of Yale found that giving mice nonsteroidal anti-inflammatory drugs (aka “NSAIDS”) before being exposed to SARS-CoV-2 led to fewer protective antibodies from the virus.

The exception is for people who normally take these types of OTC pain medications as part of their routine to manage another medical condition. Those individuals should […] check with their doctor for additional guidance.

Experimental Drug Quickly Reduces Age-Related Mental Decline

The compound, known as ISRIB, holds potential for reversing numerous cognitive problems in humans. Mice are used in scientific studies due to having genes that are approximately 85 percent similar to the genes of humans.

Just a few doses of an experimental drug can reverse age-related declines in memory and mental flexibility in mice, according to a new study by UC San Francisco scientists. The drug, called ISRIB, has already been shown in laboratory studies to restore memory function months after traumatic brain injury (TBI), reverse cognitive impairments in Down Syndrome, prevent noise-related hearing loss, fight certain types of prostate cancer, and even enhance cognition in healthy animals.

In the new study, published December 1, 2020 in the open-access journal eLife, researchers showed rapid restoration of youthful cognitive abilities in aged mice, accompanied by a rejuvenation of brain and immune cells that could help explain improvements in brain function.

“ISRIB’s extremely rapid effects show for the first time that a significant component of age-related cognitive losses may be caused by a kind of reversible physiological ‘blockage’ rather than more permanent degradation,” said Susanna Rosi, PhD, Lewis and Ruth Cozen Chair II and professor in the departments of Neurological Surgery and of Physical Therapy and Rehabilitation Science.

“The data suggest that the aged brain has not permanently lost essential cognitive capacities, as was commonly assumed, but rather that these cognitive resources are still there but have been somehow blocked, trapped by a vicious cycle of cellular stress,” added Peter Walter, PhD, a professor in the UCSF Department of Biochemistry and Biophysics and a Howard Hughes Medical Institute investigator. “Our work with ISRIB demonstrates a way to break that cycle and restore cognitive abilities that had become walled off over time.”

Could Rebooting Cellular Protein Production Hold the Key to Aging and Other Diseases?

Walter has won numerous scientific awards, including the Breakthrough, Lasker and Shaw prizes, for his decades-long studies of cellular stress responses. ISRIB, discovered in 2013 in Walter’s lab, works by rebooting cells’ protein production machinery after it gets throttled by one of these stress responses — a cellular quality control mechanism called the integrated stress response (ISR; ISRIB stands for ISR InhiBitor).

The ISR normally detects problems with protein production in a cell — a potential sign of viral infection or cancer-promoting gene mutations — and responds by putting the brakes on cell’s protein-synthesis machinery. This safety mechanism is critical for weeding out misbehaving cells, but if stuck in the on position in a tissue like the brain, it can lead to serious problems, as cells lose the ability to perform their normal activities, Walter and colleagues have found.

In particular, recent animal studies by Walter and Rosi, made possible by early philanthropic support from The Rogers Family Foundation, have implicated chronic ISR activation in the persistent cognitive and behavioral deficits seen in patients after TBI, by showing that, in mice, brief ISRIB treatment can reboot the ISR and restore normal brain function almost overnight.

The cognitive deficits in TBI patients are often likened to premature aging, which led Rosi and Walter to wonder if the ISR could also underlie purely age-related cognitive decline. Aging is well known to compromise cellular protein production across the body, as life’s many insults pile up and stressors like chronic inflammation wear away at cells, potentially leading to widespread activation of the ISR.

“We’ve seen how ISRIB restores cognition in animals with traumatic brain injury, which in many ways is like a sped-up version of age-related cognitive decline,” said Rosi, who is director of neurocognitive research in the UCSF Brain and Spinal Injury Center and a member of the UCSF Weill Institute for Neurosciences. “It may seem like a crazy idea, but asking whether the drug could reverse symptoms of aging itself was just a logical next step.”

ISRIB Improves Cognition, Boosts Neuron and Immune Cell Function

In the new study, researchers led by Rosi lab postdoc Karen Krukowski, PhD, trained aged animals to escape from a watery maze by finding a hidden platform, a task that is typically hard for older animals to learn. But animals who received small daily doses of ISRIB during the three-day training process were able to accomplish the task as well as youthful mice, much better than animals of the same age who didn’t receive the drug.

The researchers then tested how long this cognitive rejuvenation lasted and whether it could generalize to other cognitive skills. Several weeks after the initial ISRIB treatment, they trained the same mice to find their way out of a maze whose exit changed daily — a test of mental flexibility for aged mice who, like humans, tend to get increasingly stuck in their ways. The mice who had received brief ISRIB treatment three weeks before still performed at youthful levels, while untreated mice continued to struggle.

To understand how ISRIB might be improving brain function, the researchers studied the activity and anatomy of cells in the hippocampus, a brain region with a key role in learning and memory, just one day after giving animals a single dose of ISRIB. They found that common signatures of neuronal aging disappeared literally overnight: neurons’ electrical activity became more sprightly and responsive to stimulation, and cells showed more robust connectivity with cells around them while also showing an ability to form stable connections with one another usually only seen in younger mice.

The researchers are continuing to study exactly how the ISR disrupts cognition in aging and other conditions and to understand how long ISRIB’s cognitive benefits may last. Among other puzzles raised by the new findings is the discovery that ISRIB also alters the function of the immune system’s T cells, which also are prone to age-related dysfunction. The findings suggest another path by which the drug could be improving cognition in aged animals, and could have implications for diseases from Alzheimer’s to diabetes that have been linked to heightened inflammation caused by an aging immune system.

“This was very exciting to me because we know that aging has a profound and persistent effect on T cells and that these changes can affect brain function in the hippocampus,” said Rosi. “At the moment, this is just an interesting observation, but it gives us a very exciting set of biological puzzles to solve.

ISRIB May Have Wide-Ranging Implications for Neurological Disease

It turns out that chronic ISR activation and resulting blockage of cellular protein production may play a role in a surprisingly wide array of neurological conditions. Below is a partial list of these conditions, based on a recent review by Walter and colleague Mauro Costa-Mattioli of Baylor College of Medicine, which could potentially be treated with an ISR-resetting agent like ISRIB:

  • Frontotemporal Dementia
  • Alzheimer’s Disease
  • Amyotrophic Lateral Sclerosis (ALS)
  • Age-related Cognitive Decline
  • Multiple Sclerosis
  • Traumatic Brain Injury
  • Parkinson’s Disease
  • Down Syndrome
  • Vanishing White Matter Disorder
  • Prion Disease

ISRIB has been licensed by Calico, a South San Francisco, Calif. company exploring the biology of aging, and the idea of targeting the ISR to treat disease has been picked up by other pharmaceutical companies, Walter says.

One might think that interfering with the ISR, a critical cellular safety mechanism, would be sure to have serious side effects, but so far in all their studies, the researchers have observed none. This is likely due to two factors, Walter says. First, it takes just a few doses of ISRIB to reset unhealthy, chronic ISR activation back to a healthier state, after which it can still respond normally to problems in individual cells. Second, ISRIB has virtually no effect when applied to cells actively employing the ISR in its most powerful form — against an aggressive viral infection, for example.

Naturally, both of these factors make the molecule much less likely to have negative side effects — and more attractive as a potential therapeutic. According to Walter: “It almost seems too good to be true, but with ISRIB we seem to have hit a sweet spot for manipulating the ISR with an ideal therapeutic window.

Researchers Claim Oral Drug Blocks COVID-19 Transmission Within 24 Hours

This drug (MK-4482) is notable because it has the distinction of “MK,” as in, it was developed in part by the Merck pharmaceutical company. I’m one to often disparage the pharmaceutical companies but Merck has done notable things in its past drug research. The Merck development of MK-677 — an experimental growth hormone secretagogue that has been shown to increase hunger, increase bone density in the frail, and improve healing in humans — has shown significant potential in medicine. A former Head of the US Biomedical Advanced Research and Development Authority has said that drugs similar to MK-4482 cause birth defects, but the study authors claim that toxicity studies on MK-4482 have already been done, with the results already approved by regulators as a sign to continue with research into the drug in people.


Treatment of SARS-CoV-2 infection with a new antiviral drug, MK-4482/EIDD-2801 or Molnupiravir, completely suppresses virus transmission within 24 hours, researchers in the Institute for Biomedical Sciences at Georgia State University have discovered.

The group led by Dr. Richard Plemper, Distinguished University Professor at Georgia State, originally discovered that the drug is potent against influenza viruses.

“This is the first demonstration of an orally available drug to rapidly block SARS-CoV-2 transmission,” said Plemper. “MK-4482/EIDD-2801 could be game-changing.”

Interrupting widespread community transmission of SARS-CoV-2 until mass vaccination is available is paramount to managing COVID-19 and mitigating the catastrophic consequences of the pandemic.

Because the drug can be taken by mouth, treatment can be started early for a potentially three-fold benefit: inhibit patients’ progress to severe disease, shorten the infectious phase to ease the emotional and socioeconomic toll of prolonged patient isolation and rapidly silence local outbreaks.

“We noted early on that MK-4482/EIDD-2801 has broad-spectrum activity against respiratory RNA viruses and that treating infected animals by mouth with the drug lowers the amount of shed viral particles by several orders of magnitude, dramatically reducing transmission,” said Plemper. “These properties made MK-4482/EIDD/2801 a powerful candidate for pharmacologic control of COVID-19.”

In the study published in Nature Microbiology, Plemper’s team repurposed MK-4482/EIDD-2801 against SARS-CoV-2 and used a ferret model to test the effect of the drug on halting virus spread.

“We believe ferrets are a relevant transmission model because they readily spread SARS-CoV-2, but mostly do not develop severe disease, which closely resembles SARS-CoV-2 spread in young adults,” said Dr. Robert Cox, a postdoctoral fellow in the Plemper group and a co-lead author of the study.

The researchers infected ferrets with SARS-CoV-2 and initiated treatment with MK-4482/EIDD-2801 when the animals started to shed virus from the nose.

“When we co-housed those infected and then treated source animals with untreated contact ferrets in the same cage, none of the contacts became infected,” said Josef Wolf, a doctoral student in the Plemper lab and co-lead author of the study. By comparison, all contacts of source ferrets that had received placebo became infected.

If these ferret-based data translate to humans, COVID-19 patients treated with the drug could become non-infectious within 24 hours after the beginning of treatment.

MK-4482/EIDD-2801 is in advanced phase II/III clinical trials against SARS-CoV-2 infection.

Hangover Cure Found by Finland Researchers

This seems to be the most legitimate research done on a compound (amino acid L-cysteine) that will remove symptoms of an alcohol-induced hangover. The consumption of alcohol weakens the immune system and therefore might be something people might not want to have during a global pandemic, but if people do choose to consume alcohol, L-cysteine is relatively cheap to buy and (unlike many other remedies) has clinical data to support its efficacy.

Hangover Cure Successfully Tested on Drunk Subjects in Finland

A dose of 1,200 milligrams of amino acid L-cysteine was found to reduce alcohol-related nausea and headache, while a dose of 600 milligrams helped alleviate stress and anxiety, according to a study published in the journal Alcohol and Alcoholism by researchers at the University of Helsinki and the University of Eastern Finland.

The randomized, double-blind study had 19 healthy male volunteers consuming alcohol doses of 1.5 grams per kilogram over three hours in a controlled setting. The subjects were then asked to swallow placebo or L-cysteine tablets containing vitamin supplements.

Researchers say that as well as reducing or even eliminating hangovers entirely, L-cysteine also helps “reduce the need of drinking the next day,” thereby cutting the risk of alcohol addiction.

Binge drinking is common in Finland, with more than half a million Finns considered at risk from excessive drinking.

The researchers received funding from Catapult Cat Oy, which sells the L-cysteine supplements.

The study ran into certain difficulties. Some participants weren’t able to consume all the alcohol required and had to be excluded, some had such high tolerance levels that they experienced no hangover symptoms; and some were sidelined because they insisted on topping up the dose by heading for the bar, researcher Markus Metsala told local media.

Study: Honeybee Venom Contains a Chemical (Melittin) That Kills Breast Cancer Cells

A very real study out of Australia’s Harry Perkins Institute of Medical Research once again confirms that there are ways animal venom is applicable for medicine. This finding about honeybee venom is obviously significant since breast cancer is the most common cancer among women.

A groundbreaking discovery in Australia is giving new meaning to the term natural remedy. Using hundreds of honeybees, a new study reveals the venom in these insects’ stingers quickly kills breast cancer cells.

Dr. Ciara Duffy says honeybee venom destroys multiple types of breast cancer, even the hard to treat triple-negative variety. Her study in the journal npj Precision Oncology finds the venom not only eradicates these cancers, it also breaks up a cancerous cell’s ability to reproduce. It also contains a compound called melittin which researchers say helps this natural remedy stop the disease with remarkable speed.

“The venom was extremely potent,” the researcher from the Harry Perkins Institute of Medical Research says in a media release. “We found that melittin can completely destroy cancer cell membranes within 60 minutes.”

In just 20 minutes, melittin breaks down the chemical messages breast cancer cells transmits to trigger both cell growth and cell division. The compound suppresses the receptors that commonly overexpress themselves in triple-negative breast cancer and HER2-enriched breast cancer.

Venom was also tested against hormone receptor positive breast cancer cells and normal breast cells. With a specifically concentrated dose of the venom, researchers are able to kill 100 percent of cancer cells. At the same time, the study finds bee venom does little harm to normal cells.

“This study demonstrates how melittin interferes with signaling pathways within breast cancer cells to reduce cell replication. It provides another wonderful example of where compounds in nature can be used to treat human diseases,” Professor Peter Klinkenhe from the University of Western Australia says.

Do all bees carry this special venom?

Although there are around 20,000 different species of bees, the study finds not every insect can fight cancer. Dr. Duffy’s tests on 312 honeybees and bumblebees from Perth, Western Australia reveal bumblebee venom does not induce cancer cell death. Honeybees from other regions however, share this special ability to rapidly stop the disease.

“I found that the European honeybee in Australia, Ireland and England produced almost identical effects in breast cancer compared to normal cells,” Duffy reports.

Researchers add Perth bees are some of the healthiest members of their species. While the study dissects live bee stingers to extract melittin, it finds this compound can be successfully reproduced in labs.

“The synthetic product mirrored the majority of the anti-cancer effects of honeybee venom,” the Australian scientist adds.

Adding honeybee venom to chemotherapy treatments

Study authors say melittin can also help current cancer treatments like chemotherapy. The report discovers melittin also forms numerous pores (tiny holes) in the breast cancer cell membrane. Duffy suspects other cancer drugs may be able to use these openings to penetrate the cells and kill the disease.

“We found that melittin can be used with small molecules or chemotherapies, such as docetaxel, to treat highly-aggressive types of breast cancer. The combination of melittin and docetaxel was extremely efficient in reducing tumor growth in mice.”

Using bee venom as a medical remedy has been studied since the 1950’s, but Duffy’s team says it’s only been considered as treatment for cancer during the last two decades. More research needs to be done to find out what kind of a dose human patients will require.

How Air Pollution Can Harm Brain Health

It has long been rather stunning to me how careless many people are about air pollution. One of the most important things that people shouldn’t do is drive with their windows down in areas with significant traffic (and thus significant amounts of air pollution from vehicles). The motive for caring is rather simple — air pollution’s negative impact on brain health means possibly reduced performance on a variety of tasks, and that can negatively correlate with achieving life goals, which in turn is detrimental to human happiness and satisfaction.

Long thought to primarily harm the lungs and cardiovascular system, air pollution is now catching the attention of neuroscientists and toxicologists.

The buzz of a leaf blower and its gaseous fumes fill the air outside a lab facility at the University of Washington in Seattle. Inside the building, neurotoxicologist Lucio Costa is investigating how polluted air—such as garden tool exhaust—could be bad for the brain.

Next to the building sits a 5,500-watt diesel generator, enclosed in a metal box. Pipes carry the diesel exhaust—the same stuff emitted by diesel engines in vehicles and heavy equipment—into the facility, across an exposed ceiling and into a room where plastic cages of mice are stacked high against the wall. Tubes filter the diesel exhaust through the cages, Costa explains, in an effort to mimic the contaminated air you might breathe while sitting in traffic or living near a busy road.

After spending most of his career studying mercury, pesticides, and flame retardants, Costa knows well that many toxins in the environment can hurt the brain. But only in the last several years has the possibility of air pollution as a culprit crossed his mind. A growing body of literature on the topic inspired him to begin research in this diesel lab. “For a long time, I thought that air pollution was affecting mostly the lungs and the cardiovascular system and not the brain,” says Costa. “So I stayed away from any issue related to air pollution.”

Now, mounting evidence seems to link a variety of neurological problems to dirty air. Troubling recent findings include hallmarks of Alzheimer’s disease found in the brains of children living in Mexico City (1) and a nearly doubled risk of dementias for older women in highly polluted parts of the United States (2). Costa’s own research has identified autism-like social and behavioral issues in mice exposed to diesel exhaust (3). Today, Costa is among a growing cadre of biologists, toxicologists, and doctors raising the alarm over this pervasive yet overlooked menace to our memory, attention, and behavior.

A Global Threat

Although the coronavirus disease 2019 (COVID-19) pandemic and associated “shelter in place” policies have reduced fossil fuel use to offer a temporary respite from extreme pollution in some places, most countries face an ongoing epidemic of dirty air as a result of growing urban congestion and an uptick in climate-driven wildfires, among other factors. Indoor air pollution further plagues many of the world’s poorest communities. Around 3 billion people cook indoors over open fires or stoves fueled by wood, biomass, kerosene, or coal. In 2018, the World Health Organization (WHO) identified air pollution as the second-largest risk factor for noncommunicable disease worldwide. And the WHO’s stats don’t include the full range of neurological effects now being discovered, notes neurotoxicologist Deborah Cory-Slechta at the University of Rochester in New York.

Globally, more than 90 percent of people breathe air that fails to meet WHO standards. That includes an estimated four in 10 people in the United States, although efforts such as the US Clean Air Act and its amendments of 1990 have helped. Between 2000 and 2016, the average concentration of particulate matter (PM) with a diameter of less than 2.5 micrometers (PM2.5), tiny particles produced by combustion, fell by around 40 percent in the United States. But the country’s overall air quality has worsened since 2016. Partly to blame is a rise in wildfire smoke, which is now responsible for an estimated 40 percent of particulate matter pollution.

Yet cleaner, healthier air remains achievable, notes Dean Schraufnagel, a pulmonologist at the University of Illinois at Chicago. “There are no death certificates that say air pollution exposure,” he says. “But we know that air pollution affects every organ in the body. If we stop the air pollution at its source, we can get strikingly important health benefits.”

Schraufnagel, also the director of the Forum of International Respiratory Societies, points to one easy target: idling diesel-powered school buses. A 2019 study out of Georgia in the United States found that districts that retrofitted school buses to reduce diesel emissions reported significant increases in students’ English test scores as well as smaller improvements in math (4).

The havoc air pollution can wreak on the brain is also a new area of interest for Schraufnagel, whose research and clinical practice has long focused on lung disease. Today, he is working with international organizations to get air pollution on the minds of not just pulmonologists but also neurologists and other medical experts. “This should be a call to action,” adds Schraufnagel.

Air pollution is a cocktail of suspended gases, solids, and liquid particles. While this mix contains numerous hazardous ingredients, such as ozone, sulfur dioxide, and carbon monoxide, the component that appears most concerning for the brain is PM.

The US Environmental Protection Agency (EPA) regulates PM10 and PM2.5, defined as particles less than 10 and 2.5 micrometers in diameter, respectively. PM2.5, also known as fine particulate matter, generally comes from smoke, dust, and vehicle exhaust. Because PM2.5 is so tiny—30 times smaller than the width of the average human hair—it can remain airborne for long periods of time, infiltrate buildings, and penetrate the body. Ultrafine particles, which measure less than 0.1 micrometer across, may be even worse offenders. Yet the miniscule mass of these particles makes them difficult to monitor. They remain unregulated by the EPA.

Fine and ultrafine particulate matter tends to circumvent the mechanisms that the human body has evolved to deflect, detain, and destroy unwelcome visitors. “The health effects of air pollution are all about particle size,” says Cory-Slechta. Studies suggest that these tiny particles can even go up the nose and be carried straight to the brain via the olfactory nerve (5)—hence bypassing the blood–brain barrier. And they don’t travel alone. On their surfaces these particles carry contaminants, from dioxins and other chemical compounds to metals such as iron and lead. “PM is simply acting as a vector,” says Masashi Kitazawa, a molecular neuropathologist at the University of California, Irvine. “It might be a number of chemicals that get into the brain and act in different ways to cause damage.”

Because of their large surface area relative to their volume, the smallest particles are the biggest offenders. Cory-Slechta’s research has largely focused on lead and mercury, neurotoxic metals that are abundant in air pollution. “Ultrafine particles are like little Trojan horses,” she says. “Pretty much every metal known to humans is on these.”

Metal-toting particles that reach the brain can directly damage neurons. Both the particles themselves and their toxic hitchhikers can also cause widespread harm by dysregulating the activation of microglia, the immune cells in the brain. Microglia may mistake the intruders for pathogens, releasing chemicals to try to kill them. Those chemicals can accumulate and trigger inflammation. And chronic inflammation in the brain has been implicated in neurodegeneration (6).

Particles may also afflict the brain via the bloodstream. Research shows that small particles can slip through the plasma membrane of alveoli—the tiny air sacs in the lungs—and get picked up by capillaries. The particles are then distributed around the body in the blood. Although some of these particles may eventually breach the blood–brain barrier, a pollutant need not enter the brain to cause trouble there. The immune system can react to particles in the lung or bloodstream, too, triggering widespread inflammation that affects the brain.

Even an ingested particle could have indirect neurological effects, via the gut. Researchers now recognize strong connections between the gut microbiome and the brain (7), and studies show that delivering fine particles to the gut can cause systemic inflammation (8).

In January 2010, Cory-Slechta received a surprising request from some University of Rochester environmental medicine colleagues. Typically, the group researched the effects of air pollution on the lungs and hearts of adult animals. But they had just exposed a group of newborn mice and asked Cory-Slechta’s team to look at the brains.

At first she didn’t think much of the request. Cory-Slechta was much more concerned about deadly lead exposure in children, her research focus at the time. “I didn’t think of air pollution as a big problem for the brain,” she says. Then she examined the animals’ tissue. “It was eye-opening. I couldn’t find a brain region that didn’t have some kind of inflammation.”

Her team followed up with their own studies. In addition to inflammation, they saw classic behavioral and biochemical features of autism, attention-deficit disorder, and schizophrenia in mice exposed to pollutants during the first days after birth. The mouse brains had noticeably less white matter, particularly in the corpus callosum connecting the right and left cerebral hemispheres. In work published last November, Cory-Slechta’s group further linked short-term exposures to air pollution with impaired learning and memory in aged mice, based on measures of spontaneous movement, navigation of a maze, short-term object recognition, and the ability to discriminate odors (9). The concentrations of particulate matter used, she notes, “easily include sitting in traffic in major cities.”

[…]

Research in Ontario, Canada, found that living farther away from a major road lowered the risk of developing dementia (13). A study of nearly 3,000 Barcelona schoolchildren found that those attending schools with more traffic pollution had slower cognitive development (14). And in the United States, a study found that living in locations where ambient particulate matter exceeded EPA recommendations nearly doubled women’s risk of developing dementia. When those researchers looked specifically at older women with two copies of the APOE4 gene variant, a strong genetic factor for Alzheimer’s disease, the dementia risk associated with living in those locations jumped almost threefold (2).

Widely Available Drug Dexamethasone Shown to Cut Deaths by a Third in Severely Ill COVID-19 Patients

The coronavirus pandemic remains severe, but dexamethasone (a steroid) is a cheap and relatively common drug that has apparently been shown in a rigorous trial to significantly reduce mortality rates in the most severely ill COVID-19 patients. This drug is not a cure and it wasn’t shown to help patients with moderate COVID-19 symptoms, but the drug has been shown to save lives, and that’s important since presumably more people will eventually be able to recover instead of dying to the coronavirus.

An inexpensive and commonly used steroid can save the lives of people seriously ill with COVID-19, a randomized, controlled clinical trial in the United Kingdom has found. The drug, called dexamethasone, is the first shown to reduce deaths from the coronavirus that has killed more than 430,000 people globally. In the trial, it cut deaths by about one-third in patients who were on ventilators because of coronavirus infection.

“It’s a startling result,” says Kenneth Baillie, an intensive-care physician at the University of Edinburgh, UK, who serves on the steering committee of the trial, called RECOVERY. “It will clearly have a massive global impact.” The RECOVERY study announced the findings in a press release on 16 June, but its researchers say that they are aiming to publish their results quickly and that they are sharing their findings with regulators in the United Kingdom and internationally.

The RECOVERY trial, launched in March, is one of the world’s biggest randomized, controlled trials for coronavirus treatments; it is testing a range of potential therapies. The study enrolled 2,100 participants who received dexamethasone at a low or moderate dose of six milligrams per day for ten days, and compared how they fared against about 4,300 people who received standard care for coronavirus infection.

The effect of dexamethasone was most striking among critically ill patients on ventilators. Those who were receiving oxygen therapy but were not on ventilators also saw improvement: their risk of dying was reduced by 20%. The steroid had no effect on people with mild cases of COVID-19 — those not receiving oxygen or ventilation.

Shortly after the results were released, the UK government announced that it had immediately authorized use of dexamethasone for patients hospitalized with COVID-19 who required oxygen, including those on ventilators.

Rigorous study

“It is a major breakthrough,” says Peter Horby, an infectious-disease specialist at the University of Oxford, UK, and a chief investigator on the trial. Use of steroids to treat viral respiratory infections such as COVID-19 has been controversial, Horby notes. Data from steroid trials during outbreaks of SARS (severe acute respiratory syndrome) and Middle East respiratory syndrome caused by related coronaviruses were inconclusive, he says. Nevertheless, given dexamethasone’s widespread availability, and some promising results from steroid studies in previous outbreaks, Horby says RECOVERY investigators felt it important to test the treatment in a rigorous clinical trial.

Treatment guidelines from the World Health Organization and many countries have cautioned against treating people with coronavirus with steroids, and some investigators were concerned about anecdotal reports of widespread steroid treatment. The drugs suppress the immune system, which could provide some relief from patients whose lungs are ravaged by an over-active immune response that sometimes manifests in severe cases of COVID-19. But such patients may still need a fully functioning immune system to fend off the virus itself.

The RECOVERY trial suggests that at the doses tested, the benefits of steroid treatment may outweigh the potential harm. The study found no outstanding adverse events from the treatment, investigators said. “This treatment can be given to pretty much anyone,” says Horby.

And the pattern of response — with a greater impact on severe COVID-19 and no effect on mild infections — matches the notion that a hyperactive immune response is more likely to be harmful in long-term, serious infections, says Anthony Fauci, head of the US National Institute of Allergy and Infectious Disease. “When you’re so far advanced that you’re on a ventilator, it’s usually that you have an aberrant or hyperactive inflammatory response that contributes as much to the morbidity and mortality as any direct viral effect.”

“Finding effective treatments like this will transform the impact of the COVID-19 pandemic on lives and economies across the world,” said Nick Cammack, head of the COVID-19 Therapeutics Accelerator at Wellcome, a UK biomedical research charity in London, in a statement. “While this study suggests dexamethasone only benefits severe cases, countless lives will be saved globally.”

Easy to administer

So far, the only drug shown to benefit COVID-19 patients in a large, randomized, controlled clinical trial is the antiviral drug remdesivir. Although remdesivir1 was shown to shorten the amount of time that patients may need to spend in the hospital, it did not have a statistically significant effect on deaths.

Remdesivir is also in short supply. Although the drug’s maker — Gilead Sciences of Foster City, California — has taken steps to ramp up production of remdesivir, it is currently available only to a limited number of hospitals around the world. And remdesivir is complex to administer: it must be given by injection over the course of several days.

Dexamethasone, by contrast, is a medical staple found on pharmaceutical shelves worldwide and is available as a pill — a particular benefit as coronavirus infections continue to rise in countries with limited access to healthcare. “For less than £50, you can treat 8 patients and save one life,” said Martin Landray, an epidemiologist at the University of Oxford, and another chief investigator on the RECOVERY trial.

The findings could also have implications for other severe respiratory illnesses, Baillie adds. For example, steroid treatments for a condition called acute respiratory distress syndrome are also controversial. “This really gives us a very good reason to look closely at that, because the mortality benefit is so extraordinarily large,” Baillie says. “I think this will affect patients well beyond COVID-19.”

Low Vitamin D Levels Associated With Higher Coronavirus Mortality Rates

Patients with severe vitamin D deficiencies have been found in research to experience more coronavirus-related complications. Exposure to 20 or 30 minutes of sunlight a day and a healthy diet are good ways to keep high vitamin D levels.

After studying global data from the novel coronavirus (COVID-19) pandemic, researchers have discovered a strong correlation between severe vitamin D deficiency and mortality rates.

Led by Northwestern University, the research team conducted a statistical analysis of data from hospitals and clinics across China, France, Germany, Italy, Iran, South Korea, Spain, Switzerland, the United Kingdom (UK) and the United States.

The researchers noted that patients from countries with high COVID-19 mortality rates, such as Italy, Spain and the UK, had lower levels of vitamin D compared to patients in countries that were not as severely affected.

This does not mean that everyone — especially those without a known deficiency — needs to start hoarding supplements, the researchers caution.

“While I think it is important for people to know that vitamin D deficiency might play a role in mortality, we don’t need to push vitamin D on everybody,” said Northwestern’s Vadim Backman, who led the research. “This needs further study, and I hope our work will stimulate interest in this area. The data also may illuminate the mechanism of mortality, which, if proven, could lead to new therapeutic targets.”

The research is available on medRxiv, a preprint server for health sciences.

Backman is the Walter Dill Scott Professor of Biomedical Engineering at Northwestern’s McCormick School of Engineering. Ali Daneshkhah, a postdoctoral research associate in Backman’s laboratory, is the paper’s first author.

Backman and his team were inspired to examine vitamin D levels after noticing unexplained differences in COVID-19 mortality rates from country to country. Some people hypothesized that differences in healthcare quality, age distributions in population, testing rates or different strains of the coronavirus might be responsible. But Backman remained skeptical.

“None of these factors appears to play a significant role,” Backman said. “The healthcare system in northern Italy is one of the best in the world. Differences in mortality exist even if one looks across the same age group. And, while the restrictions on testing do indeed vary, the disparities in mortality still exist even when we looked at countries or populations for which similar testing rates apply.

“Instead, we saw a significant correlation with vitamin D deficiency,” he said.

By analyzing publicly available patient data from around the globe, Backman and his team discovered a strong correlation between vitamin D levels and cytokine storm — a hyperinflammatory condition caused by an overactive immune system — as well as a correlation between vitamin D deficiency and mortality.

“Cytokine storm can severely damage lungs and lead to acute respiratory distress syndrome and death in patients,” Daneshkhah said. “This is what seems to kill a majority of COVID-19 patients, not the destruction of the lungs by the virus itself. It is the complications from the misdirected fire from the immune system.”

This is exactly where Backman believes vitamin D plays a major role. Not only does vitamin D enhance our innate immune systems, it also prevents our immune systems from becoming dangerously overactive. This means that having healthy levels of vitamin D could protect patients against severe complications, including death, from COVID-19.

“Our analysis shows that it might be as high as cutting the mortality rate in half,” Backman said. “It will not prevent a patient from contracting the virus, but it may reduce complications and prevent death in those who are infected.”

Backman said this correlation might help explain the many mysteries surrounding COVID-19, such as why children are less likely to die. Children do not yet have a fully developed acquired immune system, which is the immune system’s second line of defense and more likely to overreact.

“Children primarily rely on their innate immune system,” Backman said. “This may explain why their mortality rate is lower.”

Backman is careful to note that people should not take excessive doses of vitamin D, which might come with negative side effects. He said the subject needs much more research to know how vitamin D could be used most effectively to protect against COVID-19 complications.

“It is hard to say which dose is most beneficial for COVID-19,” Backman said. “However, it is clear that vitamin D deficiency is harmful, and it can be easily addressed with appropriate supplementation. This might be another key to helping protect vulnerable populations, such as African-American and elderly patients, who have a prevalence of vitamin D deficiency.”

Backman is the director of Northwestern’s Center for Physical Genomics and Engineering and the associate director for Research Technology and Infrastructure at the Robert H. Lurie Comprehensive Cancer Center at Northwestern University.

The Science Behind Friendship and Its Largely Overlooked Importance

Yes, there’s scientific research on that too.

For many of us, the top of our life priority list might look something like this: family, work—maybe exercise. Time with friends can sometimes end up near the bottom.

That’s a mistake, says Lydia Denworth, a science journalist and the author of the new book “Friendship,” which was published last month by W.W. Norton & Co. Ms. Denworth interviews animal biologists studying baboons and rhesus macaque monkeys, anthropologists and neuroscientists to uncover just how important friendship is not only for happiness and emotional health, but, she argues, physical health, too. In fact, friends are key to our very survival, Ms. Denworth asserts.

Here are edited excerpts from an interview.

What does studying how animals relate to each other tell us about human friendships?

At its simplest, it’s just how critical quality social bonds and friendships are. In animals, the big measures that evolutionary biologists study are reproductive success, which they count as either how many babies you have or how long those babies live, and longevity, or how long you survive. Nonhuman primates have very structured hierarchies that they exist in, and everyone assumed that that must have more importance for how long you live and how many babies you have and how healthy they are. And it wasn’t. The most important thing was the strength of the social bonds, how positively and well and regularly an individual animal interacted with other animals. Scientists really couldn’t believe it.

How does friendship affect physical health?

Friendship literally improves your body’s cardiovascular functioning, how your immune system works, how you sleep. You can imagine the food you put in your body makes you healthy or not. But sitting in a coffee shop with someone and just chatting about what’s going on with your life, we always thought emotionally that made you feel good. But actually it really is doing much more.

A big study at Harvard of men across their lives from 20 to 80 found that the single best predictor of your health and happiness at 80 was not your wealth or your professional success. It was your relationships at 50.

What makes a good friendship?

The simple definition that biologists use is a friendship is positive, it makes you feel good, it is long-lasting and stable and it has reciprocity and cooperation in it. So there’s a little give and take. Friendship is about setting up your life so you have people you can rely on when you need them. Literally, it was for when the lions came hunting for your friends. Baboons and monkeys do better when they are together. It’s why humans were never really alone.

There’s not one way to do friendship. Some people are introverts and that’s fine. The difference between not having any close friends and having one is enormous in terms of your emotional health and physical health. Quality matters so much more than quantity. Most people only have an average of four really close friends.

Why do we become friends with one person and not another?

There’s this interesting chemistry to friendship. Just like in romance, you are more drawn to some people than you are others. Some of it is very straightforward: You are interested in the same things, you spend time in the same place. That’s one reason why we are close to relatives, because you have a head start, you spend more time with them than you do anyone else. We do tend to be better friends with people who are more like us.

Having a shared world-view turns out to be important. Scientists looked at all these people in a social network, showed them the same sets of videos and looked at how their brains responded to these videos. They could predict just by looking at the brain processing who was friends with whom. Literally, you hear and see the world more like the people you are friends with. The big question is: Is it cause or effect? Are you drawn to people who already see and process the world more similarly from the start or do you become more similar? Of course, as with so many things, the answer is probably both.

What impact is digital communication and social media having on friendships?

With relationships, it usually is net positive. One reason is just because people who are active on social media tend to have wider, bigger, more diverse social networks. What the research is showing is we tend to use social media as just an extra way to communicate with your good friends. And older adults, relationally, they absolutely benefit from social media because they have a harder time getting out or getting around or they’re further from their families. It really has opened up a new channel for people.

That doesn’t mean if you only operate online, you get all those benefits. You don’t. You need a lot of face-to-face time to get the health benefits. But it’s just not true that being online is automatically this big negative. The people for whom social media has a clearer negative effect seem to be people who are already suffering from depression maybe or loneliness.

Extreme Weather Will Continue to Worsen as the Climate Crisis Becomes More Severe

The changing climate is already having dire consequences on global societies, and the effects will become much worse in the future unless political leaders suitably address the environmental crisis of rising temperatures.

The past decade has been the hottest on record, the UN said Wednesday, warning that the higher temperatures were expected to fuel numerous extreme weather events in 2020 and beyond.​

The World Meteorological Organization, which based its findings on analysis of leading international datasets, said increases in global temperatures had already had dire consequences, pointing to “retreating ice, record sea levels, increasing ocean heat and acidification, and extreme weather”.

WMO said its research also confirmed data released by the European Union’s climate monitor last week showing that 2019 was the second hottest year on record, after 2016.

“The year 2020 has started out where 2019 left off – with high-impact weather and climate-related events,” WMO chief Petteri Taalas said in a statement, pointing in particular to the devastating bushfires that have been raging in Australia for months.

The bushfires, unprecedented in their duration and intensity, have claimed 28 lives and highlighted the type of disasters that scientists say the world will increasingly face due to global warming.

The fires have already destroyed more than 2,000 homes and burnt 10 million hectares (100,000 square kilometres) of land – an area larger than South Korea or Portugal.

“Unfortunately, we expect to see much extreme weather throughout 2020 and the coming decades, fuelled by record levels of heat-trapping greenhouse gases in the atmosphere,” Taalas said.

The UN agency said that average global temperatures during both the past five-year (2015-2019) and 10-year (2010-2019) periods were the highest ever recorded.

“Since the 1980s each decade has been warmer than the previous one,” the UN agency said in a statement, warning that “this trend is expected to continue”.

The United Nations said last year that human-made greenhouse gas emissions needed to tumble 7.6 percent each year to 2030 in order to limit temperature rises to 1.5 Celsius – the more ambitious cap nations signed up to in the landmark Paris climate deal.

Current pledges to cut emissions put Earth on a path of several degrees warming by the end of the century.

Not a fluke

Taalas said that since modern records began in 1850, the average global temperature had risen by around 1.1 degrees Celsius, and warned of significant warming in the future.

“On the current path of carbon dioxide emissions, we are heading towards a temperature increase of 3 to 5 degrees Celsius by the end of the century,” he warned.

Gavin Schmidt, director of NASA’s Goddard Institute for Space Studies, which provided one of the datasets, added that the trend line was unmistakable and could not be attributed to normal climate variability – a position taken by US President Donald Trump.

“What’s happening is persistent, not a fluke due to some weather phenomenon: we know that the long-term trends are being driven by the increasing levels of greenhouse gases in the atmosphere,” he said.

Data from the US National Oceanic and Atmospheric Administration meanwhile revealed that polar sea ice coverage continued its downward trend in 2019.

Both the Arctic and Antarctic oceans recorded their second-smallest average annual sea-ice coverage during the 1979–2019 period of record, the agency said.

Broken record

WMO also highlighted a new study published this week in Advances in Atmospheric Sciences with data showing that ocean heat content was at a record high in 2019.

The past five years were also the warmest on record in terms of ocean heat content, that study showed.

Since more than 90 percent of excess heat is stored in the world’s oceans, their heat content is a good way to quantify the rate of global warming, WMO said.

Conservationists said the UN agency’s findings were to be expected.

“It is no surprise that 2019 was the second hottest year on record – nature has been persistently reminding us that we have to pick up the pace,” said Manuel Pulgar-Vidal, leader of WWF’s global climate and energy practice, calling for dramatic measures to halt the warming trend.

“This is not so much a record as a broken record,” added Chris Rapley, a professor of climate science at University College London.

“The message repeats with grim regularity. Yet the pace and scale of action to address climate change remains muted and far from the need.”

In 2019, 27% of Denmark’s Power Was from Wind

A model of clean energy that other countries should take note of.

COPENHAGEN, Jan 2 (Reuters) – Denmark sourced almost half its electricity consumption from wind power last year, a new record boosted by steep cost reductions and improved offshore technology.

Wind accounted for 47% of Denmark’s power usage in 2019, the country’s grid operator Energinet said on Thursday citing preliminary data, up from 41% in 2018 and topping the previous record of 43% in 2017.

European countries are global leaders in utilising wind power but Denmark is far in front of nearest rival Ireland, which sourced 28% of its power from wind in 2018 according to data from industry group WindEurope.

Across the European Union, wind accounted for 14% of consumption last year, the group says.

The higher proportion of wind energy in Denmark last year was partly due to Vattenfall starting operations at the Horns Rev 3 offshore wind farm in the North Sea in August.

The share of power from wind turbines at sea increased to 18% last year from 14% in 2018, Energinet said. Onshore wind accounted for 29% last year.

The International Energy Agency (IEA) said in October that while power generated from wind turbines at sea only accounts for 0.3% of today’s global electricity generation, capacity is set to increase 15-fold over the next two decades.

Denmark aims to reduce greenhouse gas emissions by 70% by 2030, with a new climate law passed late last year targeting an increase in the share of electricity sourced from renewable power to 100%.

Denmark, home to wind turbine giant Vestas and the world’s largest developer of offshore wind Orsted, has favourable wind conditions and began investing heavily in wind power in the 1970s.