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.

Scientist’s Plasma Shot That Could Prevent COVID-19 Isn’t Being Considered by The Government

That the use of plasma (shown effective in many other cases) isn’t being considered is another inefficiency by the (U.S. at least) governmental response to the coronavirus pandemic.

It might be the next best thing to a coronavirus vaccine.

Scientists have devised a way to use the antibody-rich blood plasma of COVID-19 survivors for an upper-arm injection that they say could inoculate people against the virus for months.

Using technology that’s been proven effective in preventing other diseases such as hepatitis A, the injections would be administered to high-risk healthcare workers, nursing home patients, or even at public drive-through sites — potentially protecting millions of lives, the doctors and other experts say.

The two scientists who spearheaded the proposal — an 83-year-old shingles researcher and his counterpart, an HIV gene therapy expert — have garnered widespread support from leading blood and immunology specialists, including those at the center of the nation’s COVID-19 plasma research.

But the idea exists only on paper. Federal officials have twice rejected requests to discuss the proposal, and pharmaceutical companies — even acknowledging the likely efficacy of the plan — have declined to design or manufacture the shots, according to a Times investigation. The lack of interest in launching development of immunity shots comes amid heightened scrutiny of the federal government’s sluggish pandemic response.

There is little disagreement that the idea holds promise; the dispute is over the timing. Federal health officials and industry groups say the development of plasma-based therapies should focus on treating people who are already sick, not on preventing infections in those who are still healthy.

Dr. Anthony Fauci, director of the National Institute of Allergy and Infectious Diseases at the National Institutes of Health, said an upper-arm injection that would function like a vaccine “is a very attractive concept.”

However, he said, scientists should first demonstrate that the coronavirus antibodies that are currently delivered to patients intravenously in hospital wards across the country actually work. “Once you show the efficacy, then the obvious next step is to convert it into an intramuscular” shot.

But scientists who question the delay argue that the immunity shots are easy to scale up and should enter clinical trials immediately. They say that until there’s a vaccine, the shots offer the only plausible method for preventing potentially millions of infections at a critical moment in the pandemic.

“Beyond being a lost opportunity, this is a real head-scratcher,” said Dr. Michael Joyner, a Mayo Clinic researcher who leads a program sponsored by the Food and Drug Administration to capitalize on coronavirus antibodies from COVID-19 survivors. “It seems obvious.”

The use of so-called convalescent plasma has already become widespread. More than 28,000 patients have already received the IV treatment, and preliminary data suggest that the method is safe. Researchers are also looking at whether the IV drip products would prevent new infections from taking root.

The antibodies in plasma can be concentrated and delivered to patients through a type of drug called immune globulin, or IG, which can be given through either an IV drip or a shot. IG shots have for decades been used to prevent an array of diseases; the IG shot that prevents hepatitis A was first licensed in 1944. They are available to treat patients who have recently been exposed to hepatitis B, tetanus, varicella and rabies.

[…]

The proposal for an injection approach to coronavirus prevention came from an immunization researcher who drew his inspiration from history.

Dr. Michael Oxman knew that, even during the 1918 flu pandemic, the blood of recovered patients appeared to help treat others. Since then, convalescent plasma has been used to fight measles and severe acute respiratory syndrome, or SARS, among other diseases.

Like other doctors, Oxman surmised that, for a limited time, the blood coursing through the veins of coronavirus survivors probably contains immune-rich antibodies that could prevent — or help treat — an infection.

[…]

Throughout May, researchers and doctors at Yale, Harvard, Johns Hopkins, Duke and four University of California schools sent a barrage of letters to dozens of lawmakers. They held virtual meetings with health policy directors on Capitol Hill, but say they have heard no follow-up to date.

Dr. Arturo Casadevall, the chair of the National COVID-19 Convalescent Plasma Project, said he spoke to FDA officials who told him they do not instruct companies on what to produce. Casadevall told The Times that the leaders of the national project were “very supportive of the need to develop” an IG shot rapidly and that he believed it would be “very helpful in stemming the epidemic.”

Joyner, of the Mayo Clinic, said there are probably 10 million to 20 million people in the U.S. carrying coronavirus antibodies — and the number keeps climbing. If just 2% of them were to donate a standard 800 milliliters of plasma on three separate occasions, their plasma alone could generate millions of IG shots for high-risk Americans.

“At a hot-spot meatpacking plant, or at a mobile unit in the parking lot outside a mall — trust me, you can get the plasma,” Joyner said. “This is not a biological problem nor a technology problem. It’s a back-of-the-envelope intelligence problem.”

The antibody injections, for now, do not appear to be a high priority for the government or the industry.

Grifols, on April 28 — the same day that the U.S. topped 1 million confirmed coronavirus cases — made a major product announcement that would “expand its leadership in disease treatment with immunoglobulins.”

The product was a new vial for IG shots — to treat rabies.

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).

Does Vitamin D Help Protect People from COVID-19? Some Evidence Suggests Yes

A comprehensive global study published in 2017 on respiratory infections would say yes:

A new global collaborative study has confirmed that vitamin D supplementation can help protect against acute respiratory infections. The study, a participant data meta-analysis of 25 randomized controlled trials including more than 11,000 participants, has been published online in The BMJ.

“Most people understand that vitamin D is critical for bone and muscle health,” said Carlos Camargo of the Department of Emergency Medicine at Massachusetts General Hospital (MGH), the study’s senior author. “Our analysis has also found that it helps the body fight acute respiratory infection, which is responsible for millions of deaths globally each year.”

Additionally, a professor of respiratory infection and immunity at Queen Mary University of London had this to say about vitamin D:

“Vitamin D could almost be thought of as a designer drug for helping the body to handle viral respiratory infections,” he said. “It boosts the ability of cells to kill and resist viruses and simultaneously dampens down harmful inflammation, which is one of the big problems with Covid.”

The pharmaceutical industry obviously can’t make enormous profits from vitamin D, and that’s part of why it hasn’t been explored more as a protective mechanism. With all the benefits of vitamin D and the lack of downsides to it however, it is worth getting enough vitamin D (through sufficient sunlight exposure and a good diet) to protect against respiratory infections such as the flu and COVID-19.

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.

New Blood Test Offers Detection of 50 Types of Cancer

Another helpful advance in modern medicine.

A new blood test that can detect more than 50 types of cancer has been revealed by researchers in the latest study to offer hope for early detection.

The test is based on DNA that is shed by tumours and found circulating in the blood. More specifically, it focuses on chemical changes to this DNA, known as methylation patterns.

Researchers say the test can not only tell whether someone has cancer, but can also shed light on the type of cancer they have.

Dr Geoffrey Oxnard of Boston’s Dana-Farber Cancer Institute, part of Harvard Medical School, said the test was now being explored in clinical trials. “You need to use a test like this in an independent group at risk of cancer to actually show that you can find the cancers, and figure out what to do about it when you find them,” he said.

Writing in the journal Annals of Oncology, the team reveal how the test was developed using a machine learning algorithm – a type of artificial intelligence. Such systems pick up on patterns within data and as a result learn to classify it.

The team initially fed the system with data on methylation patterns in DNA from within blood samples taken from more than 2,800 patients, before further training it with data from 3,052 participants, 1,531 of whom had cancer and 1,521 of whom did not.

Using this information, the system sorted the samples into groups based on the methylation patterns. The team then taught the system which groups reflected which type of cancer.

“In pregnant women we look in their free-floating DNA for foetal abnormalities,” said Oxnard. “We know this [approach] exists, the question is how do you fine-tune and perfect the art of looking for cancer in this free-floating DNA? And that is what the machine learning did.”

The team then tested the trained system on another set of samples from 1,264 individuals, about half of whom had cancer.

The results reveal that less than 1% of those without cancer were wrongly identified by the system as having the disease. “It is really important you don’t tell non-cancer patients they have cancer,” said Oxnard.

When it came to identifying people with cancers the team found that, across more than 50 different types of cancer, the system correctly detected that the disease was present 44% of the time – although the team stress that figure could differ if the test was used to screen a general population, rather than those known to have cancer.

Detection was better the more advanced the disease was. Overall, cancer was correctly detected in 18% of those with stage I cancer, but in 93% of those with stage IV cancer.

The team say the results are exciting as they offer the possibility of a new way to screen for cancers that are otherwise difficult to detect. For example, the system correctly identified 63% of those with stage I pancreatic cancer, rising to 100% in stage IV.

The team further found that the system could shed light on the type of cancer. For 96% of samples deemed to show cancer, the test was able to offer a prediction for in which the tissue the cancer originated, with 93% of these predictions found to be correct.

Dr David Crosby, head of early detection at Cancer Research UK, said that detecting cancers in their early stages is important as they are less aggressive and more treatable.

Although this test was still at an early stage of development, the initial results were encouraging, he said. “And if the test can be fine-tuned to be more efficient at catching cancers in their earliest stages, it could become a tool for early detection.”

But Crosby added there was work to do. “More research is needed to improve the test’s ability to catch early cancers and we still need to explore how it might work in a real cancer screening scenario,” he said.

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.

Experimental Drugs Reverse Arthritis in Rats Study

The science shows potential results in treating a debilitating condition.

People with osteoarthritis, or “wear and tear” arthritis, have limited treatment options: pain relievers or joint replacement surgery. Now, Salk researchers have discovered that a powerful combination of two experimental drugs reverses the cellular and molecular signs of osteoarthritis in rats as well as in isolated human cartilage cells. Their results were published in the journal Protein & Cell on January 16, 2020.

“What’s really exciting is that this is potentially a therapy that can be translated to the clinic quite easily,” says Juan Carlos Izpisua Belmonte, lead author and a professor in Salk’s Gene Expression Laboratory. “We are excited to continue refining this promising combination therapy for human use.”

Affecting 30 million adults, osteoarthritis is the most common joint disorder in the United States and its prevalence is expected to rise in coming years due to the aging population and increasing rate of obesity. The disease is caused by gradual changes to cartilage that cushions bones and joints. During aging and repetitive stress, molecules and genes in the cells of this articular cartilage change, eventually leading to the breakdown of the cartilage and the overgrowth of underlying bone, causing chronic pain and stiffness.

Previous research had pinpointed two molecules, alpha-KLOTHO and TGF beta receptor 2 (TGFβR2), as potential drugs to treat osteoarthritis. αKLOTHO acts on the mesh of molecules surrounding articular cartilage cells, keeping this extra-cellular matrix from degrading. TGFβR2 acts more directly on cartilage cells, stimulating their proliferation and preventing their breakdown.

While each drug alone had only moderately curbed osteoarthritis in animal models of the disease, Izpisua Belmonte and his colleagues wondered if the two drugs would act more effectively in concert.

“We thought that by mixing these two molecules that work in different ways, maybe we could make something better,” says Paloma Martinez-Redondo, a Salk postdoctoral fellow and co-first author of the new study.

The researchers treated young, otherwise healthy rats with osteoarthritis with viral particles containing the DNA instructions for making αKLOTHO and TGFβR2.

Six weeks after the treatment, rats that had received control particles had more severe osteoarthritis in their knees, with the disease progressing from stage 2 to stage 4. However, rats that had received particles containing αKLOTHO and TGFβR2 DNA showed recovery of their cartilage: the cartilage was thicker, fewer cells were dying, and actively proliferating cells were present. These animals’ disease improved from stage 2 to stage 1, a mild form of osteoarthritis, and no negative side effects were observed.

“From the very first time we tested this drug combination on just a few animals, we saw a huge improvement,” says Isabel Guillen-Guillen, the paper’s co-first author. “We kept checking more animals and seeing the same encouraging results.”

Further experiments revealed 136 genes that were more active and 18 genes that were less active in the cartilage cells of treated rats compared to control rats. Among those were genes involved in inflammation and immune responses, suggesting some pathways by which the combination treatment works.

To test the applicability of the drug combination to humans, the team treated isolated human articular cartilage cells with αKLOTHO and TGFβR2. Levels of molecules involved in cell proliferation, extra-cellular matrix formation and cartilage cell identity all increased.

“That’s not the same as showing how these drugs affect the knee joint in humans, but we think it’s a good sign that this could potentially work for patients,” says Martinez-Redondo.

The research team plans to develop the treatment further, including investigating whether soluble molecules of the αKLOTHO and TGFβR2 proteins can be taken directly, rather than administered through viral particles. They also will study whether the combination of drugs can prevent the development of osteoarthritis before symptoms develop.

“We think that this could be a viable treatment for osteoarthritis in humans,” says Pedro Guillen, director of the Clinica CEMTRO and co-corresponding author.

Parrots That Show Selfless Kindness

A good study has recently been done on grey parrots.

experiment

According to Charles Darwin, helping others just doesn’t make sense. Yet we’ve seemingly seen altruism time and again in the animal kingdom: in primates, in canines, in cetaceanspinnipeds, even vampire bats. Now, for the first time, it’s been demonstrated in birds.

The kind bird is one of the titans of avian intelligence, the African grey parrot (Psittacus erithacus). New experiments have shown these birds happily helping each other acquire treats, without any assumption or anticipation that their altruism will be reciprocated.

“We found that African grey parrots voluntarily and spontaneously help familiar parrots to achieve a goal, without obvious immediate benefit to themselves,” explained behavioural biologist Désirée Brucks of the Max Planck Institute for Ornithology.

But the birds take it one step further. Unlike primates, for example, the parrots display no anger or envy if one of their friends receives favourable treatment, instead seeming quite content that good things are happening to a buddy.

Among the bird kingdom, it’s the corvids – such as crows and ravens – that are probably the most famed for their wicked smarts, and with very good reason. In fact, corvids have demonstrated skills previously only observed in primates.

However, the researchers said, corvids have failed tests of altruism. But there are other smart birds out there – like parrots. Cockatoos can make their own tools, and have even demonstrated playful creativity. And African grey parrots have proven to be smarter than a human child in some tests.

So, the research team designed a test for altruism, and gave it to two different types of parrots – eight African greys, and six blue-headed macaws (Primolius couloni).

The birds had been previously trained to exchange tokens (metal washers) for treats. This training was refreshed, and the scientists assessed their subjects’ relationships with other birds of their species. Each bird was tested with one bird with whom they had a close bond, and a second bird with a less close bond.

The birds were then placed in a clear perspex enclosure, with a dividing wall between them. The front of the box had holes through which items could be exchanged with a human; and the dividing wall between the birds also had a hole, through which the two birds could also exchange items.

All the birds quickly understood the concept of swapping the washer for a piece of walnut, and were able to do so. But, when only one of two birds was given tokens, only the African grey parrots, not the macaws, also deliberately gave tokens to their buddies.

“Remarkably, African grey parrots were intrinsically motivated to help others, even if the other individual was not their friend, so they behaved very ‘prosocially,'” said zoologist Auguste von Bayern of Oxford University.

“It surprised us that 7 out of 8 African grey parrots provided their partner with tokens spontaneously – in their very first trial – thus without having experienced the social setting of this task before and without knowing that they would be tested in the other role later on. Therefore, the parrots provided help without gaining any immediate benefits and seemingly without expecting reciprocation in return.”

In all, they voluntarily gave other African grey parrots 157 out of 320 tokens – nearly half. And, interestingly, although they passed tokens regardless of their social bond, they did give more tokens to birds with whom they shared a close bond.

The macaws, by contrast, rarely passed their tokens through to the other parrot. If they did, they dropped it through the hole; and they did it more often when the human experimenter was present. This led the scientists to believe the macaws were trying to pass the token to the human, not their buddy.

The difference could be due to social differences between the species in the wild, but there was one more interesting thing. In a separate recent study, the researchers showed that, when an African grey parrot sees a friend getting a better treat, they didn’t seem particularly bothered. This is in contrast to animals such as chimpanzees, who tend to get riled up about it.

According to von Bayern, this could be because the parrots monogamously mate for life.

“Given that parrots are so closely bonded with a single individual and thus so mutually interdependent, it does not make any difference if one of them gets a better pay-off once in a while,” she said.

“What counts is that together, they function as a unit that can achieve much more than each of them on their own (in addition to raising their joint offspring). This is probably why parrots are much more tolerant towards unequal treatment than species that are not long-term monogamous, while still being excellent cooperators.”

The research has been published in Current Biology.

Drinking Tea Regularly Linked to a Longer Life

Scientists found that there really is merit to drinking green tea.

Drinking tea at least three times a week could be linked with a longer and healthier life, scientists say.

According to new research “habitual” consumption of the hot drink is associated with lower risks of cardiovascular disease and all-cause death.

But whether the tea being consumed is green or black may make a difference.

The analysis included 100,902 participants of the China-PAR project2 with no history of heart attack, stroke, or cancer.

Participants were categorised into two groups – habitual tea drinkers, those drinking three or more times a week, and never or non-habitual tea drinkers  – those drinking less than three times a week.

They were followed-up for a median of 7.3 years, in the study published in the European Journal of Preventative Cardiology.

The research suggests a 50-year-old habitual tea drinker would develop coronary heart disease and stroke 1.41 years later, and live 1.26 years, longer than someone who never or seldom drank tea.

Compared with never or non-habitual tea drinkers, habitual tea consumers had a 20% lower risk of incident heart disease and stroke, and a 22% lower risk of fatal heart disease and stroke.

They also had a 15% decreased risk of all-cause death, the study suggests.

First author Dr Xinyan Wang, of the Chinese Academy of Medical Science in Beijing, said: “Habitual tea consumption is associated with lower risks of cardiovascular disease and all-cause death.

“The favourable health effects are the most robust for green tea and for long-term habitual tea drinkers.”

Researchers analysed the potential influence of changes in tea drinking behaviour in a subset of 14,081 participants with assessments at two time points.

The average duration between the two surveys was 8.2 years, and the median follow-up after the second survey was 5.3 years.

Habitual drinkers who maintained their habit in both surveys had a 39% lower risk of incident heart disease and stroke, 56% lower risk of fatal heart disease and stroke, and 29% decreased risk of all-cause death compared to consistent never or non-habitual tea drinkers, the study suggests.

In a sub-analysis by tea type, drinking green tea was linked with around 25% lower risks for incident heart disease and stroke, fatal heart disease and stroke, and all-cause death.

However, no significant associations were observed for black tea.

Scientists found 49% of habitual tea drinkers in the study consumed green tea most frequently, while only 8% preferred black tea.

They noted a preference for green tea in East Asia, and said the small proportion of habitual black tea drinkers might make it more difficult to observe robust associations, but that the findings hint at a differential effect between tea types.

The researchers suggest a number of reasons for this.

They indicate that green tea is a rich source of polyphenols which protect against cardiovascular disease.

While black tea is fully fermented and during this process may lose antioxidant effects.

Gunter Kuhnle, professor of nutrition and food science at the University of Reading, said: “This study is an observational study and can therefore only establish an association – not a causal relationship.”

He added that the two cups per week as cut-off point was very little when compared to the average consumption of three to four cups per day in the UK.

Prof Kuhnle said: “It is not clear from the study whether there is any benefit from higher tea intake – and therefore there is no likely benefit from increasing tea intake by the majority of the British public.”

Study: Facts Misremembered to Fit Personal Biases

Reality is sometimes very unpleasant to see, but there are clearly problems in people choosing to cloud their clear views of reality.

A recent study by Ohio State researchers found that people tend to misremember information to match commonly-held beliefs.

If you’re looking for who’s responsible for all the misinformation out there, you might want to take a peek in the mirror.

OK, OK, it’s not all your fault.

Although external sources of misinformation like “fake news” and purposeful disinformation campaigns draw a lot of attention today, recent research at Ohio State University indicates we might misremember information all on our own.

In a recent study, Ohio State researchers found that when given accurate statistics on a controversial issue, people tended to misremember numbers to match their own beliefs. Then, when researchers gave study participants accurate information and asked them to convey it to others, the information grew more and more different as it was passed from person to person.

“What our research would suggest is there’s a lot of focus on external sources of misinformation, but we also have to pay attention to these internal sources,” said Jason Coronel, an assistant professor of communication at Ohio State.

For the study, participants were given factual numerical information about four societal issues. Based on pre-tests, researchers found that the numbers for two of the societal issues matched many people’s understanding of the matter. But for the other two issues, the numbers didn’t fit with their understanding.

For the numbers that were inconsistent with how people view the issue, participants were more likely to remember the numbers incorrectly, in a way that matched their probable biases.

For example, researchers presented participants with information showing there were 12.8 million Mexican immigrants in the United States in 2007, and fewer — 11.7 million — in 2014. When participants were then given a memory test, they were more likely to remember the statistics incorrectly, in a way that agreed with many people’s understanding that the number of Mexican immigrants would be higher in 2014 than 2007.

In a second portion of the study, researchers examined how memory distortions can be spread among social circles as individuals share the misinformation they created. Mimicking a game of “telephone,” researchers presented a participant with accurate numbers about a societal issue.

For example, the participant was asked to write down the numbers of Mexican immigrants in 2007 and 2014 from memory. The numbers from the first person were then given to a second person, and the process was repeated to a third person.

Researchers found that as the retellings increased from person to person, the information transformed to be more consistent with people’s understanding of the issue rather than the factual numbers.

It’s one thing to believe information yourself without fact-checking it first, said Shannon Poulsen, a doctoral student at Ohio State who conducted the study with Coronel and fellow doctoral student Matthew Sweitzer. But the second portion of the study shows the danger of then sharing inaccurate information with others, she said.

“Now the issue is not just you … now you’re sharing information,” Poulsen said.

Then, you can become part of the bigger problem, Coronel said.

“If you don’t scrutinize on what you’re remembering and you decide to talk about it and pass it on to another person, you just turned into an external source of misinformation,” Coronel said.

It may be a bit unsettling to think you can’t trust your own brain, but researchers hope the study leads to better understanding about how we remember things and encourages healthy scrutiny and skepticism.

“It can be a little bit scary,” Poulsen said. “But if it’s enough to increase … a little bit of skepticism to a point where people can be accurate, that’s great.”

People tend to think of their memories as simply a video recording device, taking in everything and repeating it back when they need it, Coronel said. But lots of research in psychology indicates memory doesn’t work that way.

Instead, think of memory as a jigsaw puzzle, he said — sometimes you’re missing some pieces, or you’ve got pieces from multiple boxes dumped on the same table.