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.

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.

Reducing the Very Overpriced Cost of Healthcare

As is known to many people, American healthcare is far more expensive than necessary.

One of most enduring, economically and socially damaging, downright frustrating facts about life in the United States is how expensive health care is here. Not only does U.S. health care cost far more than in other advanced economies, but compared with the nations that spend less, we have worse or equivalent health outcomes. In fact, U.S. life expectancy now lags behind that of all the advanced economies.

An MRI scan that cost $1,400 here went for $450 in Britain and $190 in Holland. Thirty tablets of a drug to reduce the risk of blood clots (Xarelto) cost $380 here, $70 in Britain, $80 in Switzerland and $60 in Holland. Hospital admission for angioplasty is $32,000 here, $15,000 in Australia, $12,000 in Britain, $7,000 in Switzerland, $6,000 in the Netherlands.

Add to those differences the latest outrage in health-care costs: surprise medical billing, when even well-insured patients can wake up from surgery finding that they owe thousands of dollars, because someone treating them while they were unconscious was out of their insurance network.

Princeton economists Anne Case and Angus Deaton (a Nobel winner) recently summarized the problem by labeling it an $8,000-a-year annual health-care tax paid by U.S. families. This is the difference in costs between what we pay for health care and what people in other countries pay. As Case put it: “We can brag we have the most expensive health care. We can also now brag that it delivers the worst health of any rich country.”

Why call this expense a tax? Well, for one, if you want health coverage, you can’t escape it. But even if you don’t — and good luck with that — you still can’t escape the tax, as both employer- and government-provided health care extract payments through lower paychecks and public financing.

Case and Deaton may be erring on the low side in their $8,000-per-family figure. The Organization for Economic Cooperation and Development puts per-person spending in the United States at $8,950 a year. That compares with $5,060 in Germany, $3,470 in Canada and just $3,140 in Britain. If we assume a family of three, we would get an annual health-care tax of $11,670 compared with Germany and more than $17,000 compared with the cost of health care in Britain.

How can such differences persist, especially in a service where consumption is so essential to well-being? If ice cream were that much more expensive here, we’d have a lot to squawk about, for sure. But it wouldn’t be a matter of life and death.

An obvious, and correct, answer as to why U.S. health care is so expensive is because we do so little, relative to other systems, to control costs. But it’s worse than that. We do a fair amount to make health care more expensive.

First, our system of private insurance costs far more than single-payer systems like Canada’s, and also more than countries with private but heavily regulated insurers like Germany. OECD data show that as a share of health spending, our administrative costs are three times that of Canada’s and twice that of Germany’s. Getting our administrative costs closer to those in other countries would require regulating private insurers and expanding public coverage, but it could save us at least 10 percent of our total health-care bill.

Next, we pay twice as much to our health-care providers and for prescription drugs as everyone else. The latter costs us more than $3,000 per family per year. We pay more than twice as much for medical equipment, costing us a bit less than $1,500 per family per year. Doctors and dentists cost us close to an extra $750 per family per year.

One reason for the outsize costs of these inputs to U.S. health care is that government policy protects our providers. When it comes to manufactured goods, like cars and clothes and almost everything on the shelves of Walmart, economists and policymakers push for “free trade” and more competition. But when it comes to health-care providers, these same authorities turn protectionist.

In areas like prescription drugs and medical equipment, this protection is explicit: Manufacturers are granted patent monopolies. The government will arrest anyone who sells protected items in competition with a patent holder.

In the case of doctors, we have maintained or increased barriers that make it difficult for qualified foreign physicians to practice in the United States. We also prevent other health-care professionals, such as physicians’ assistants and nurse practitioners, from doing many tasks for which they are entirely competent. There is a similar story with dentists and dental hygienists.

Other countries directly control drug prices. In France, the government determines whether a new drug is an improvement or a copycat, and, if the drug is deemed useful, the government negotiates drug prices with the manufacturers and caps their revenue. When sales exceed the cap, the manufacturer must rebate most of the difference back to the government.

Here in the United States, we give drug companies and medical equipment manufacturers’ patent monopolies and allow them to charge whatever they want. We don’t even let the government use its massive leverage to negotiate lower drug prices for Medicare beneficiaries. That’s what makes these goods expensive; they’re almost always relatively cheap to produce.

This is fixable. It would take regulating costs, reducing reimbursements to providers and increasing competition.

The pharmaceutical industry’s rationale for cost-exploding medical patents is that it helps incentivize research and innovation. Without them, it’s likely that pharmaceuticals and medical equipment companies would do less speculative research. But it would take a fraction of the savings from reducing such protectionism to replace patent-support research with publicly supported research (for which we already spend $40 billion a year).

In terms of boosting competition, allowing foreign doctors whose training meets our standards to more easily practice medicine here would bring U.S. physicians’ pay in line with international standards. Of course, our doctors pay much more for their education than doctors trained elsewhere, so part of this new structure would also require reducing the domestic cost of medical education and alleviating some of the educational debt burden that U.S.-trained doctors have acquired.

Increasing competition would also require using antitrust measures to push back on the pricing power engendered by the consolidation of both hospital groups and medical practices. An analysis by the New York Times of 25 metro areas found that hospital mergers “have essentially banished competition and raised prices for hospital admissions.”

Even if we succeed in raising competition and reducing protectionism, health care will still be too expensive for many low- and moderate-income families, many of whom have suffered stagnant incomes in recent decades. Like every other wealthy country, we will need to get on a path to universal coverage. But whatever form that takes, if we can significantly reduce our current health-care tax, the savings will easily be large enough to extend quality, affordable coverage to every American.

USA Memory Champion on Improving One’s Memory

The American memory champion’s results give credence to the notion that (as with other things in life) you can get good at anything you practice at — including memory.

In 2009, after Nelson Dellis’s grandmother Josephine passed away from Alzheimer’s disease (which may have a hereditary component), he was inspired to find ways to keep his own brain healthy and sharp.

“I was a good student, but my memory was average,” Dellis, 35, tells CNBC Make It.

Dellis scoured the internet looking for tips to improve his memory and joined a few forums where professional “memory athletes” (people who train their memory skills for high performance) chatted about different memory techniques. Then he listened to “Quantum Memory: Learn to Improve Your Memory with The World Memory Champion,” an audiobook by Dominic O’Brien, a seven-time world memory champion.

“After that, I went off and, through trial and error, figured out what [techniques] worked well for me,” Dellis says.

Today Dellis, author of the book “Remember It” and a four-time USA Memory Champion (an annual competition for elite mental athletes), is a full-time memory coach based in Miami, Florida. He charges $250 an hour for private lessons to the likes CEOs and billionaires, including Mark Cuban and Sara Blakely.

Here are Dellis’ top three tips on improving your memory and staying sharp.

1. Go offline

Dellis says one the easiest memory tips that he’s learned over the years is to take time to totally disconnect from technology — including your smartphone — for at least an hour a day.

That’s because presence is important for memory, says Dellis.

“Your brain is a processing unit,” he says. “If your brain isn’t present to receive [information] (i.e., you’re distracted and not paying attention), how on earth do you think it’s going to be able to remember it? You’ll be surprised how powerful your natural memory is if you just try and pay attention.”

Dellis’s advice is supported by research: According to a 2017 study from the McCombs School of Business at The University of Texas at Austin, researchers found the mere presence of a smartphone reduces cognitive capacity, affecting one’s brain to hold and process data.

2. Think in pictures

“My goal whenever I memorize something is to turn it into a mental picture in my mind,” he says, which is “any mental representation of what you’re trying to memorize, using as many of your senses as possible.” It could be an association, a sound, a feeling — anything that’s “meaningful” to you, Dellis says.

That’s because it’s much easier to remember a picture of something that you are familiar with than words relating to something new and difficult, he says. (Studies in older adults have shown that pictures can help with memory.)

Dellis uses the example of remembering the name chervil (an herb) to buy at the grocery store.

“Most people might not even know what that is. So I might break that word down into what it sounds like: ‘sure-vill.’ So maybe my meaningful image could be, me saying ‘sure!’ enthusiastically to a ’vill’ain. The more context the better. Maybe I’m agreeing with this villain, because if I don’t, he’ll take all the chervil in the world and secretly garnish all the food in the world and ruin the taste of everything,” Dellis says.

The “more over-the-top and bizarre you make the image, the better.”

To practice, Dellis suggests that when you meet someone for the first time, turn their name into mental images, as he did with chervil.

“You’ll have a higher chance of remembering the person’s name, and you’ll be training your brain to get better/quicker at thinking in pictures,” he says.

3. Explore your ‘memory palace’

When you’re thinking in pictures, you need a place to store those images. So most memory athletes use a technique called the “memory palace,” according to Dellis. The technique (which dates back to the ancient Greeks) has to do with remembering things based on location

According to Dellis, a memory palace works like this: Think of a familiar place (like your house, apartment, office, etc.) and imagine a mental pathway through it. To store your images, simply imagine or “stick” each image on a location along the path in your mind. The idea is that later on when you want to retrieve the information, all you have to do is think of your memory palace, walk back through it in your mind and pick up the images you left there.

It sounds a bit crazy, but it works, according to Dellis and it allows top memory athletes to memorize thousands of pieces of information, he says.

“It’s an effective way of stringing together sets of memories because it uses more and various parts of the brain than simply short term recall (visual, emotional, language, imagination and short term memory),” neuroscientist Tara Swart tells CNBC Make It.

To practice, Dellis suggests choosing three familiar places and selecting 10 locations along your mental path through each. Start by storing daily to-do lists and grocery lists there as practice.

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.”

AI Becomes Very Good at Diagnosing Breast Cancer

Artificial intelligence is becoming more of a hot topic, and people should remember more that AI can be used both to hurt humans and (as in this case) help humans.

A computer programme can identify breast cancer from routine scans with greater accuracy than human experts, researchers said in what they hoped could prove a breakthrough in the fight against the global killer.

Breast cancer is one of the most common cancers in women, with more than 2 million new diagnoses last year alone.

Regular screening is vital in detecting the earliest signs of the disease in patients who show no obvious symptoms.

In Britain, women over 50 are advised to get a mammogram every three years, the results of which are analysed by two independent experts.

But interpreting the scans leaves room for error, and a small percentage of all mammograms either return a false positive – misdiagnosing a healthy patient as having cancer – or false negative – missing the disease as it spreads.

Now researchers at Google Health have trained an artificial intelligence model to detect cancer in breast scans from thousands of women in Britain and the United States.

The images had already been reviewed by doctors in real life but unlike in a clinical setting, the machine had no patient history to inform its diagnoses.

The team found that their AI model could predict breast cancer from the scans with a similar accuracy level to expert radiographers.

Further, the AI showed a reduction in the proportion of cases where cancer was incorrectly identified – 5.7 percent in the US and 1.2 percent in Britain, respectively.

It also reduced the percentage of missed diagnoses by 9.4 percent among US patients and by 2.7 percent in Britain.

“The earlier you identify a breast cancer the better it is for the patient,” Dominic King, UK lead at Google Health, told AFP.

“We think about this technology in a way that supports and enables an expert, or a patient ultimately, to get the best outcome from whatever diagnostics they’ve had.”

Computer ‘second opinion’

In Britain all mammograms are reviewed by two radiologists, a necessary but labour-intensive process.

The team at Google Health also conducted experiments comparing the computer’s decision with that of the first human scan reader.​

If the two diagnoses agreed, the case was marked as resolved. Only with discordant outcomes was the machine then asked to compare with the second reader’s decision.

The study by King and his team, published in Nature, showed that using AI to verify the first human expert reviewer’s diagnosis could save up to 88 percent of the workload for the second clinician.

“Find me a country where you can find a nurse or doctor that isn’t busy,” said King.

“There’s the opportunity for this technology to support the existing excellent service of the (human) reviewers.”

Ken Young, a doctor who manages mammogram collection for Cancer Research UK, contributed to the study.

He said it was unique for its use of real-life diagnosis scenarios from nearly 30,000 scans.

“We have a sample that is representative of all the women that might come through breast screening,” he said.

“It includes easy cases, difficult cases and everything in between.”

The team said further research was needed but they hoped that the technology could one day act as a “second opinion” for cancer diagnoses.

Abortion Reversal — The Dangerous Practice You’ve Probably Never Heard Of

In the United States, many more laws have been implemented that restrict or ban a woman’s ability to have an abortion. Abortion reversal is a new technique that hasn’t undergone much medical testing since the one test on it showed significant harm to the women.

Several states now require women who seek medication abortions to be provided with dubious information that the procedure could be stopped, allowing a pregnancy to continue.

But when researchers attempted to carry out a legitimate study of whether these “abortion reversal” treatments were effective and safe, they had to stop almost immediately – because some of the women who participated in the study experienced dangerous hemorrhaging that sent them to the hospital.

By passing these abortion reversal laws, “states are encouraging women to participate in an unmonitored experiment,” Creinin said.

Creinin and his colleagues detailed their concerns in a commentary in the journal Contraception, and they will publish their study in January’s edition of Obstetrics and Gynecology.

Medication abortions, which are used up to 10 weeks into a pregnancy, consist of taking two pills in sequence. The first pill in the regimen, mifepristone, loosens the pregnancy’s attachment to the uterus. The second pill, misoprostol, forces the uterus to contract to push out the pregnancy. The pills must be taken consecutively to complete the abortion, and there’s a chance the pregnancy will continue if the second pill is not taken.

A total of 862,320 abortions were provided in clinical settings in 2017, according to the Guttmacher Institute, about 39 percent of which were medication abortions. Research has shown that using these drugs is a safe way to end a pregnancy.

Some antiabortion activists and legislators claim that not taking the second pill, or giving a woman high doses of the hormone progesterone after taking mifepristone, can help stop, or “reverse,” a medical abortion.

The American College of Obstetricians and Gynecologists firmly states that “claims regarding abortion ‘reversal’ treatment are not based on science and do not meet clinical standards” and say the purported studies that underpin these antiabortion arguments lack scientific rigor and ethics.

Despite this, the claims made in these discredited studies have worked their way to antiabortion lawmakers, who in turn have put them into abortion reversal legislation that was signed by governors in North Dakota, Idaho, Utah, South Dakota, Kentucky, NebraskaOklahoma and Arkansas. The laws are currently blocked or enjoined in Oklahoma and North Dakota.

Because reliable research on these treatments is nonexistent, earlier this year, Creinin and his colleagues designed a legitimate double-blind, placebo-controlled, randomized trial that aimed to observe 40 volunteers who had already elected to have a surgical abortion.

Their goal was to see if giving progesterone to women who took the first pill in the prescribed regimen would effectively and safely halt an abortion.

After the women took the first pill in the abortion protocol, mifepristone, rather than take the second pill, misoprostol, they were either given a placebo or a dose of progesterone.

Researchers only enrolled 12 women before they had to stop the study.

Bleeding is normal during a medication abortion. But three of the women who enrolled in the UC-Davis study experienced far more serious bleeding than anyone could have anticipated when the second pill was not administered.

One woman “was so scared she called an ambulance,” while another woman startled by the amount of blood “called 911 and crawled into her bathtub”, Creinin said. A third woman who went to the emergency room needed a transfusion. One of the women had received a placebo, while two others had taken the progesterone.

Creinin and his colleagues halted the study as soon as it became clear that they could not proceed safely.

“I feel really horrible that I couldn’t finish the study. I feel really horrible that the women … had to go through all this,” Creinin said. Because the study ended prematurely, the researchers could not establish any evidence that progesterone was an effective way to stop a medication abortion.

“What the results do show, though, is that there’s a very significant safety signal” when it comes to disrupting the approved medication abortion protocol, Creinin said.

In their upcoming paper in Obstetrics and Gynecology, the researchers warn that “patients in early pregnancy who use only mifepristone may be at high risk of significant hemorrhage.”

Medical experts are so concerned about abortion reversal laws that the American Medical Association joined a lawsuit against North Dakota’s abortion reversal law, which was blocked by a federal judge in September.

The North Dakota abortion reversal law, signed by Gov. Doug Burgum (R) in March, instructed health-care providers to tell a woman “that it may be possible to reverse the effects of an abortion-inducing drug if she changes her mind, but time is of the essence” and to provide a woman with literature on how to do this. The law fails to specify what that literature would include, or what such a treatment might entail.