Tag Archives: disease

Study on mice: Exercising later in life can keep your muscles young

Exercising can not only make you feel younger, but it can also actually keep you younger as well. A study on mice suggests that exercising, even later in life, can do wonders for your muscles. In addition to underscoring the importance of staying active, the study could also help us uncover some of the secrets of rejuvenation.

Even though some diseases are inherited, we can still improve our overall health through lifestyle choices such as diet and exercise. Still, whatever the reason, the genes related to some of these conditions must be expressed for them to develop. So how does this happen?

A new study has brought us closer to an answer by mapping the genetic changes involved in rejuvenating the muscle cells of elderly mice put on an exercise program.

Turning genes on and off

The analysis centers on DNA, the “blueprint” for our bodies. DNA consists of four bases, called cytosine, guanine, adenine, and thymine, and the process used to help manage these massive helixes: a methyl molecule composed of one carbon and three hydrogen atoms. These atoms attach themselves to one of the four bases (cytosine) to form what’s known as a CpG site.

When this occurs, the CpG becomes methylated and the site produces proteins to regulate something in the body — whatever that something may be. In contrast, the region becomes unmethylated when you lose that methyl group, turning that gene off. In this way, a process called DNA methylation can promote or inhibit the expression of specific genes — whether it’s stopping a tumor, preventing cancer, or activating genes responsible for causing wrinkles in old age. This process is constant, occurring billions of times a second in every cell throughout the body, and we’re just starting to understand it.

DNA methylation is one of the many mechanisms of epigenetics, where inborn or acquired changes in DNA don’t touch the actual sequence – meaning a person can potentially reverse things like fat deposits through diet or exercise. More and more studies are starting to suggest that this is an unharnessed and robust process, linked to longevity and the regulation of lifespan in most organisms on earth.

The current study attempts to further this theory using lifestyle interventions such as exercise to roll back genetic aging in skeletal muscle – measuring the animal’s ‘epigenetic clock’ for accuracy. This clock is measured via methylation levels in the blood to reflect exposures and disease risks independent of chronological age, providing an early-warning system and a true representation of a period of existence.

Kevin Murach, an assistant professor at the University of Arkansas, says, “DNA methylation changes in a lifespan tend to happen in a somewhat systematic fashion. To the point, you can look at someone’s DNA from a given tissue sample and with a fair degree of accuracy predict their chronological age.”

Using exercise to turn back the clock

The study design was relatively simple: mice nearing the end of their natural lifespan, at 22 months, were given access to a weighted exercise wheel to ensure they built muscle. They required no coercion to run on the wheel, with older mice running from six to eight kilometers a day, mostly in spurts, and younger mice running up to 10-12 kilometers.

Results from the elderly mice after two months of weighted wheel running suggested they were the epigenetic age of mice eight weeks younger, compared to sedentary mice of the same maturity.

The team also used the epigenetic clock to map a multitude of genes involved in the formation and function of muscles, including those affected by exercise. Blood work indicated that the genes usually over methylated (hypermethylated) in old age resumed normal methylation in the active aged mice, unlike those mapped in their sedentary counterparts.

For instance, the rbm10 gene is usually hypermethylated in old age, disrupting the production of proteins involved in motor neuron survival, muscle weight & function, and the growth of striated muscle. Here it was shown to undergo less methylation in older mice who exercised, improving its performance. Normal methylation levels also resumed across the Timm8a1 gene, keeping mitochondrial function and oxidant defense at workable levels – even where neighboring sites exhibited dysfunctional epigenetic alterations.

More work is needed to harness DNA methylation

Murach notes that when a lifespan is measured incrementally in months, as with this mouse strain, an extra eight weeks — roughly 10 percent of that lifespan — is a noteworthy gain, further commending the importance of exercise in later life.

He adds: that although the connection between methylation and aging is clear, methylation and muscle function are less clear. Despite these sturdy results, Murach will not categorically state that the reversal of methylation with exercise is causative for improved muscle health. “That’s not what the study was set up to do,” he explained. However, he intends to pursue future studies to determine if “changes in methylation result in altered muscle function.”

And, “If so, what are the consequences of this?” he continued. “Do changes on these very specific methylation sites have an actual phenotype that emerges from that? Is it what’s causing aging or is it just associated with it? Is it just something that happens in concert with a variety of other things that are happening during the aging process? So that’s what we don’t know.”

He summarizes that once the medical community has mapped the mechanics of dynamic DNA methylation in muscle, their work could provide modifiable epigenetic markers to improve muscle health in the elderly. 

Scientists identify the specific gene that protects against severe COVID-19

Researchers from Karolinska University have discovered a gene that reduces the severity of Covid infections by 20%. In their paper the scientists state that this explains why the disease’s symptoms are so variable, hitting some harder than others.

Why do some people fall severely ill from COVID-19 while others don’t? In addition to risk factors like age or obesity and plenty of other environmental factors, it also comes down to our varying genetic makeup. Therefore, researchers across the globe have begun the mammoth task of mapping the genes involved in making people more susceptible to catching SARS-CoV-2 (COVID-19) and developing a severe infection.

These large-scale efforts have thrown up more than a dozen genomic regions along the human chromosome containing large clusters of genes associated with severe COVID-19. However, the specific causal genes in these regions are yet to be identified, hampering our ability to understand COVID-19’s often selective pathology.

Now, scientists build on these findings to pinpoint a gene that confers protection from critical illness.

Neanderthal DNA protects against severe COVID-19

The previous studies from 2020 concentrated on the genetic data of people of European ancestry recorded by multi-disciplinary teams all over the world for the 1000 Genomes Project. This monumental collaboration uncovered a specific segment of DNA known as the OAS1/2/3 cluster, which lowers the risk of developing an acute COVID-19 infection by 20%. Inherited from Neanderthals in roughly half of all people outside of Africa, this segment is responsible for encoding genes in the immune system.

The genetic array came about as a result of the migration of an archaic human species out of the African continent about 70,000 years ago who mated and mingled DNA with Neanderthals reproduced in their offspring’s haplotypes, a set of inheritable DNA variations close together along a chromosome. 

However, most human haplotypes outside Africa now include DNA from Neanderthals and Denisovans (an ancient human originating in Asia). Consequently, this ancient region of DNA is heaving with numerous genetic variants, making it challenging to distinguish the exact protective gene that could serve as a target for medical treatment against severe COVID-19 infection.

A possible solution is that people of African descent do not contain these archaic genes in their haplotypes, making them shorter and easier to decipher.

To test this theory, the researchers checked the 1000 Genomes project database for individuals carrying only parts of this DNA segment – focusing on individuals with African ancestry who lack heritage from the Neanderthals. Remarkably, the researchers found that individuals of predominantly African ancestry had the same protective gene cluster as those of European origin.

Genetic studies should be a multi-cultural affair

Once they established this, the researchers collated 2,787 COVID-19 cases with the genetic data of 130,997 individuals of African ancestry to reveal the gene variant rs10774671 G thought to convey protection against COVID-19 hospitalization. Their results correspond to a previous, more extensive study of individuals of European heritage, with analysis suggesting it is likely the only causal variant behind the protective effect.

Surprisingly, this previously ‘useless’ ancient variant was found to be widespread, present in one out of every three people of white European ancestry and eight out of ten individuals of African descent.

In evolutionary terms, the researchers write that the variant exists today in both these gene pools “as a result of their inheritance from the ancestral population common to both modern humans and Neanderthals.” Accordingly, their data adds more weight to the standard held theory that a common ancestor originated in Africa millions of years ago before sharing their DNA across the globe.

And while there’s much more to uncover regarding the newly discovered variant, the researchers can firmly suggest at this stage that the protective gene variant (rs10774671 G) works by determining the length of a protein encoded by the gene OAS1. As the longer version of the protein is more effective at breaking down the virus than the unaltered form, a life-threatening infection is less likely to occur.

Using genetic risk factors to design new COVID-19 drugs

Despite their promising results, the team cautions that the 1000 Genomes Project does not provide a complete picture of this genomic region for different ancestries. Nevertheless, it’s clear that the Neanderthal haplotype is virtually absent among individuals of primarily African ancestry, adding, “How important it is to include individuals of different ancestries” in large-scale genetic studies.

Senior researcher Brent Richards from McGill University says that it is in this way “we are beginning to understand the genetic risk factors in detail is key to developing new drugs against COVID-19.”

If these results are anything to go by, we could be on the cusp of novel treatments that can harness the immune system to fight this disease.

Immune cells from the common cold offer protection against COVID-19, researchers find

If one in 10 cold infections are from coronaviruses, then antibodies produced from these illnesses could surely give a bit more protection against COVID-19, right? A new study has just provided the answer to this question by showing that immunity induced by colds can indeed help fight off the far more dangerous novel coronavirus.

Image credits: Engin Akyurt.

A study from Imperial College London that studied people exposed to SARS-CoV-2 or COVID-19 found that only half of the participants were infected, while the others tested negative. Before this, researchers took blood samples from all volunteers within days of exposure to determine the levels of an immune cell known as a T cell – cells programmed by previous infections to attack specific invaders.

Results show that participants who didn’t test positive had significantly higher levels of these cells; in other words, those who evaded infection had higher levels of T cells that attack the Covid virus internally to provide immunity — T cells that may have come from previous coronavirus infections (not SARS-CoV-2). These findings, published in the journal Nature Communications, may pave the way for a new type of vaccine to prevent infection from emerging variants, including Omicron.

Dr. Rhia Kundu, the first author of the paper from Imperial’s National Heart & Lung Institute, says: “Being exposed to the SARS-CoV-2 virus doesn’t always result in infection, and we’ve been keen to understand why. We found that high levels of pre-existing T cells, created by the body when infected with other human coronaviruses like the common cold, can protect against COVID-19 infection.” Despite this promising data, she warns: “While this is an important discovery, it is only one form of protection, and I would stress that no one should rely on this alone. Instead, the best way to protect yourself against COVID-19 is to be fully vaccinated, including getting your booster dose.”

The common cold’s role in protecting you against Covid

The study followed 52 unvaccinated people living with someone who had a laboratory-confirmed case of COVID-19. Participants were tested seven days after being exposed to see if they had caught the disease from their housemates and to analyze their levels of pre-existing T cells. Tests indicated that the 26 people who tested negative for COVID-19 had significantly higher common cold T cells levels than the remainder of the people who tested positive. Remarkably, these cells targeted internal proteins within the SARS-CoV-2 virus, rather than the spike protein on its surface, providing ‘cross-reactive’ immunity between a cold and COVID-19.

Professor Ajit Lalvani, senior author of the study and Director of the NIHR Respiratory Infections Health Protection Research Unit at Imperial, explained:

“Our study provides the clearest evidence to date that T cells induced by common cold coronaviruses play a protective role against SARS-CoV-2 infection. These T cells provide protection by attacking proteins within the virus, rather than the spike protein on its surface.”

However, experts not involved in the study caution against presuming anyone who has previously had a cold caused by a coronavirus will not catch the novel coronavirus. They add that although the study provides valuable data regarding how the immune system fights this virus, it’s unlikely this type of illness has never infected any of the 150,000 people who’ve died of SARS-CoV-2 in the UK to date.

Other studies uncovering a similar link have also warned cross-reactive protection gained from colds only lasts a short period.

The road to longer-lasting vaccines

Current SARS-CoV-2 vaccines work by recognizing the spike protein on the virus’s outer shell: this, in turn, causes an immune reaction that stops it from attaching to cells and infecting them. However, this response wanes over time as the virus continues to mutate. Luckily, the jabs also trigger T cell immunity which lasts much longer, preventing the infection from worsening or hospitalization and death. But this immunity is also based on blocking the spike protein – therefore, it would be advantageous to have a vaccine that could attack other parts of the COVID virus.

Professor Lalvani surmises, “The spike protein is under intense immune pressure from vaccine-induced antibodies which drives the evolution of vaccine escape mutants. In contrast, the internal proteins targeted by the protective T cells we identified mutate much less. Consequently, they are highly conserved between the SARS-CoV-2 variants, including Omicron.” He ends, “New vaccines that include these conserved, internal proteins would therefore induce broadly protective T cell responses that should protect against current and future SARS-CoV-2 variants.”

New COVID variant identified in France — but experts say we shouldn’t fear it

Scientists have identified a previously unknown mutant strain in a fully vaccinated person who tested positive after returning from a short three-day trip to Cameroon.

Academics based at the IHU Mediterranee Infection in Marseille, France, discovered the new variant on December 10. So far, the variant doesn’t appear to be spreading rapidly and the World Health Organization has not yet labeled it a variant of concern. Nevertheless, researchers are still describing and keeping an eye on it.

The discovery of the B.1.640.2 mutation, dubbed IHU, was announced in the preprint server medRxiv, in a paper still awaiting peer review. Results show that IHU’s spike protein, the part of the virus responsible for invading host cells, carries the E484K mutation, which increases vaccine resistance. The genomic sequencing also revealed the N501Y mutation — first seen in the Alpha variant — that experts believe can make COVID-19 more transmissible.  

In the paper, the clinicians highlight that it’s important to keep our guard and expect more surprises from the virus: “These observations show once again the unpredictability of the emergence of new SARS-CoV-2 variants and their introduction from abroad,” they write. For comparison Omicron (B.1.1.529) carries around 50 mutations and appears to be better at infecting people who already have a level of immunity. Thankfully, a growing body of research proves it is also less likely to trigger severe symptoms.

Like many countries in Europe, France is experiencing a surge in the number of cases due to the Omicron variant.

Experts insist that IHU, which predates Omicron but has yet to cause widespread harm, should not cause concern – predicting that it may fade into the background. In an interview with the Daily Mail, Dr. Thomas Peacock, a virologist at Imperial College London, said the mutation had “a decent chance to cause trouble but never really materialized. So it is definitely not one worth worrying about too much at the moment.”

The strain was first uploaded to a variant tracking database on November 4, more than two weeks before Omicron was sequenced. For comparison, French authorities are now reporting over 300,000 new cases a day thought to be mostly Omicron, with data suggesting that the researchers have identified only 12 cases of IHU over the same period. 

On the whole, France has good surveillance for COVID-19 variants, meaning health professionals quickly pinpoint any new mutant strains. In contrast to Britain, which only checks three in ten cases for variants. The paper’s authors state that the emergence of the new variant emphasizes the importance of regular “genomic surveillance” on a countrywide scale.

Sterilised insects could help control mosquito-borne diseases

A form of tiger mosquito birth control and drones may help stem the spread of some tropical diseases. Image credit – James Gathany/CDC, public domain.

The bite of the Asian tiger mosquito may be little more than a pin-prick, but it leads to tens of thousands of deaths globally each year. 

The tiny aggressive insect, named for its striped appearance, carries a range of unpleasant viruses that cause diseases including yellow fever, dengue fever, Chikungunya, Zika and Japanese encephalitis. While these are seen largely as tropical diseases, the spread of mosquitoes that carry them has raised fears the viruses could also become more common in Europe.

The European Centres for Disease Control (ECDC) predicted ten years ago that tiger mosquitoes would spread throughout Europe and climate change is now threatening to make their spread even more likely. ‘Even the southern part of Sweden is potentially suitable climatically for this mosquito, though it has not arrived there yet,’ said Professor Jan Semenza, who leads an ECDC section which assesses infectious disease threats. 

The stripy pest, which is also known as Aedes albopictus, is originally from Southeast Asia, but arrived in Albania in the 1970s before reaching Italy in the 1990s. It initially colonised the Mediterranean coast, then steadily expanded northward, and is now found across much of France, Greece, Bosnia, parts of Spain, southern Portugal, and Germany. It has even been found in greenhouses in the Netherlands. During the summer, the mosquitoes have now become a nuisance in some places.

But with the mosquitoes can come disease. So far outbreaks have been relatively contained and in low numbers, but there have been cases of dengue in Croatia, France and Spain. In Italy, hundreds of people fell ill from Chikungunya in 2017. Two cases of locally caught Zika occurred in the south of France in 2019.

The diseases can be carried to Europe by people infected with the virus traveling from countries in South America and Asia where they are endemic. Brazil, for example, has been a hotspot this year for dengue fever. If these people are bitten by a tiger mosquito in Europe, the insect can then transmit the virus to other people it bites.

‘We have seen an increase in vector capacity due to climate change,’ warns Prof. Semenza, with warmer temperatures allowing the biting insects to survive over winter. ‘Dengue has a huge disease burden worldwide. It can morph into a life-threatening condition, so we are concerned about it moving into Europe.’

Dengue was endemic in Greece in the early 20th century but was eliminated. ‘We don’t want a recurrent of this type of disease in Europe,’ added Prof. Semenza. 

But rising numbers of mosquitoes capable of carrying disease makes it more likely that these viruses could become established in Europe once again. Another disease-carrying insect – Aedes aegypti, also known as the yellow fever mosquito – is also threatening a return to Europe after it was eradicated there in the 20th century. Originally from Africa, it is present today near the Black Sea, on the Portuguese island of Madeira and north-eastern Turkey.

But with many insecticides now prohibited in Europe due to their toxicity and the wider harm they cause to the environment, there are fewer options for controlling the mosquitoes.

Made with Flourish

Insect birth control

Dr Jérémy Bouyer, a biologist and mosquito expert at the French Agricultural Research Centre for International Development (CIRAD) in Montpellier, predicts Europe could face an uncontrolled dengue epidemic within the next five to ten years unless more is done to control mosquito populations. 

‘The Aedes tiger mosquitoes are very difficult to control,’ said Dr Bouyer. The insects tend to breed on relatively small sites, which makes targeting them difficult, he said. ‘Rather than ponds or lakes, they like human-made habitats.’ 

But we may not be entirely defenceless against these mosquito pests. Dr Bouyer is developing a new approach to combat mosquitoes as part of a research project called REVOLINC. Over the next few years, he will be releasing tens of thousands of sterile male yellow fever mosquitoes on Reunion Island, a French territory in the Indian Ocean.

When released, the males should mate with wild females and produce sterile eggs, and so suppress the numbers of mosquito larvae. However, the males will also be coated with a secret weapon – a biopesticide called pyriproxyfen, which mimics hormones in insects and restricts their growth. The males transfer this biopesticide onto the female when they try to mate with them, and she contaminates her eggs and larvae habitat. It means eggs fertilised by unsterilised males are also unable to mature from larvae into adult mosquitoes.

‘Even if the sterile males don’t succeed with the females, they still transmit the biopesticide,’ said Dr Bouyer. ‘We have shown that this might increase the impact of control by between 10 and 100 times, so we might need to release fewer male mosquitoes.’

To rear enough insects, Dr Bouyer and his colleagues have developed technologies for veritable mosquito factories at the International Atomic Energy Agency (IAEA) facility in Seibersdorf, Austria, where the larvae are reared on stacks of trays submerged in water, each supporting 18,000 of the wrigglers. The larvae are then sorted by sex when they pupate before the young males are sterilised with a finely balanced dose of radiation – enough to achieve almost complete sterility, but leaving them healthy enough to be able to mate when released. The sterile males can then be shipped in chilled boxes.

Drone attack

On Reunion Island, male mosquitoes were previously released in canisters placed on the ground. But 90% of the insects will not travel more than 100 metres from this spot.

In an attempt to improve the distribution of the sterile male insects, Dr Bouyer is also working on a project called MOSQUAREL, which will use drones to release mosquitoes from the air. He has already used a 12kg drone in Brazil to release 50,000 sterile male mosquitoes per flight and is hoping to trial a lighter 900g drone capable of releasing 30,000 mosquitoes at a time. The advantage of this smaller drone is that it would be permitted to fly over residential areas in Europe.

‘To treat a city with sterile insects, you need to drive a vehicle along roads, stop every 100 metres and release a box of mosquitoes,’ said Dr Bouyer. ‘It takes two hours for two vehicles to treat 30 hectares.’ A drone launched from the back of a truck could treat the same area in ten minutes, he said, and is quicker, cheaper and distributes the insects more evenly over an area.  

The new drone will also be tested in Valencia, Spain, with the release of sterile tiger mosquitoes in a citrus tree production area, in collaboration with the Spanish state-owned rural development company Tragsa

Dr Bouyer is also hoping to use the drone to release sterile yellow fever mosquitoes coated with biopesticide on Reunion Island, targeting three small populations of mosquitoes.

But while Reunion has a few isolated pockets of yellow fever mosquitoes, which Dr Bouyer hopes to wipe out, tiger mosquitoes are a bigger problem on the island. Reunion has experienced an increase in dengue fever cases since the beginning of 2018, and a particularly bad outbreak this year brought a number of deaths. Warmer temperatures and wet conditions have allowed tiger mosquitoes to flourish, so Dr Bouyer plans to target these insects next. But releasing sterile males coated with biopesticide alone will not work.

Both Aedes mosquito species only need minuscule amounts of water for their larvae, which often develop on rubbish items, in discarded plastic or in old tyres. So reducing such man-made larval habitat in urban areas will also be necessary to ensure the drone drops can have more of an impact.

‘If we suppress them in one site, then we can prevent dengue around there,’ said Dr Bouyer. ‘That is the best success we could hope for – to protect people.’

The research in this article was funded by the EU. If you liked this article, please consider sharing it on social media.

This post Sterilised insects could help control mosquito-borne diseases was originally published on Horizon: the EU Research & Innovation magazine | European Commission.

The way humans modify environments makes them more likely to cause outbreaks

The transformation of natural landscapes into farmland and cities is favoring animals such as bats, the possible source of the novel coronavirus, to carry more diseases. This is the main finding of a new study found which looked at how ecosystems change as people expand on them.

Credit Flickr Wagner Cassimiro (CC BY 2.0)

A group of researchers, led by the Center for Biodiversity at the University of London, looked at data from 6,801 ecological communities from six continents. They found that animals known to carry pathogens that can infect humans were more common in landscapes intensively used by people.

The evidence was obtained from a dataset of 184 studies, which incorporate almost 7,000 species, 376 of which carry human-shared pathogens. The findings show that we have to alter the way we use the land across the world so as to reduce the risk of infectious diseases in the future, the researchers argued.

Many factors are involved in a disease spillover, which is when a pathogen moves from an animal into humans, causing disease outbreaks, which can later become a pandemic. Close contact with wild animals through trade or habitat loss, for example, increases the risk of new diseases.

Bats have been mentioned as the possible origin of the novel coronavirus, with other animals also playing a role in the spillover to humans. Wild animals that face possible extinction due to human exploitation were found to carry over twice as many viruses that can lead to human disease.

“The way humans change landscapes across the world, from natural forest to farmland, for example, has consistent impacts on many wild animal species, causing some to decline while some others persist or increase,” said lead-author Rory Gibb in a press release. “Animals that remain in more human-dominated environments are those that are more likely to carry infectious diseases.”

The study found that species that host zoonotic pathogens, those which can move from animals to humans, accounted for a higher proportion of the animal species found in environments that have been altered by humans, compared with more wild habitats.

The same finding was replicated in animals that usually carry more pathogens of any kind, whether they affect humans or not. This shows, according to the researchers, that similar factors could be influencing whether a species can tolerate humans and how likely it is to carry zoonotic diseases.

“Other studies have found that outbreaks of emerging zoonotic infectious diseases appear to be increasingly common — our findings may help to explain that pattern, by clarifying the underlying ecological change processes that are interacting to drive infection risks,” said co-lead author Dr. David Redding in a press release.

The study was published in the journal Nature.

Chemical exposure, not just genetics, could induce gluten intolerance

The risk of developing celiac disease (the most extreme form of gluten intolerance) in young people seems to be associated with elevated blood levels of toxic chemicals found in pesticides, nonstick cookware, and fire retardants.

A new study from the NYU Grossman School of Medicine suggests that children and young adults with high blood levels of dichlorodiphenyldichlorethylenes (DDEs), a class of chemicals associated with pesticides, were twice as likely to be diagnosed with celiac disease compared to their peers. Celiac disease is an immune disorder that creates severe reactions in the gut to foods containing gluten.

Gender matters, too

“Our study establishes the first measureable tie-in between environmental exposure to toxic chemicals and celiac disease,” says senior study author and pediatric gastroenterologist Jeremiah Levine, MD.

“These results also raise the question of whether there are potential links between these chemicals and other autoimmune bowel diseases, which all warrant close monitoring and further study,” says Levine, a professor in the Department of Pediatrics at NYU Langone.

The team analyzed chemical levels in the blood of 30 children and young adults (aged 3 to 21), who were newly diagnosed with celiac disease at NYU Langone Hassenfeld Children’s Hospital. The results were compared to a similar analysis of 60 young people of similar age, gender, and race.

The authors report that men and women react differently to such exposure to toxins. Women make up the majority of celiac cases, they note, and the team found that they were eight times more likely to develop gluten intolerance following higher-than-normal exposure to pesticides.

Furthermore, young women with elevated blood levels of non-stick chemicals known as perflouoroalkyls (PFAs) — including Teflon — were five to nine times more likely to have celiac disease.

Young men with high blood levels of of fire-retardant chemicals polybrominated diphenyl ethers (PBDEs) were twice more likely to be diagnosed with celiac disease.

The study didn’t establish a clear cause and effect relationship between these chemicals and celiac disease, but the authors note that they are all known to disrupt animal and human hormone levels, which are key to controlling both sexual development and immune defenses against infection. The authors call for more in-depth research on the topic.

Our understanding up to now is that celiac disease, which affects around 1% of the world’s population, is largely genetically-driven. However, if other studies support the results of this study, it could radically alter our understanding of this condition, alongside other autoimmune disorders.

The paper “Persistent organic pollutant exposure and celiac disease: A pilot study” has been published in the journal Environmental Research.

Washington might already have hundreds of undetected coronavirus cases

A new analysis published by computational biologist Trevor Bedford suggests that the virus has been circulating in the state of Washington since mid-January, and the real number of cases is in the hundreds.

“I expect Seattle now to look like Wuhan around ~1 Jan, when they were reporting the first clusters of patients with unexplained viral pneumonia. We are currently estimating ~600 infections in Seattle.”

Seattle faces a big challenge. Image credits: Sabine Ojeil.

The new Wuhan

The Covid-19 outbreak is reaching a turning point: the window of containment is still open but is closing rapidly, so we’ll know pretty soon if we can escape a pandemic or not.

The good news is that this is controllable — we’re seeing this in China. The number of cases outside of Wuhan, where the outbreak emerged, has decreased significantly in recent days, giving hope that we can still escape a worldwide pandemic.

But we might not be aware of how many cases we are dealing with in the first place.

Cases in China (outside the outbreak’s epicenter) are dropping. Image credits: World Health Organization.

Trevor Bedford, the head of a computation epidemiology lab, analyzed the mutations observed in Seattle patients. According to the genetic sequences of patients in the Seattle-King County region, the virus has been around since mid-January — when the first U.S. patient (a man who returned from Wuhan) was detected. This means that there is over a month during which the virus has escaped detection, and during which it has likely spread far beyond the number of confirmed cases.

The reason why it has escaped detection is probably because most cases were mild and were confused for a simple cold or a flu. But this was further accentuated by the fact that the CDC failed to deliver mass testing in a timely manner.

Effectively, Seattle is in the position that Wuhan was on January 1, when it first understood that it had an outbreak of the virus, but did not understand the amplitude of the outbreak and the speed at which it was spreading.

This puts Seattle in a very uncomfortable spot: impose strict quarantine measures, or risk a spread like the one seen in Wuhan.

Chinese authorities moved slowly at first and tried to downplay the problem — which is similar to what some politicians in the US are doing. However, after three weeks, it imposed draconian measures, the most severe ever seen in modern history, both inside and outside the city.

It is very unlikely that such measures will be deployed in Seattle or elsewhere in the US, which makes the situation even more dangerous. China escaped a country-wide epidemic because it acted early — in Seattle, that window may be shut.

We need to act as soon as possible, Bedford says. Measures have to be taken “yesterday” if we want them to still be effective and avoid the emergence of a new coronavirus epicenter in the heart of the United States.

Your resistance to flu is shaped by previous flu’s, and their type

How hard the flu hits us has a lot to do with our first experience of the disease, a new paper reports.

Image via Pixabay.

Researchers at the University of California Los Angeles (UCLA) and the University of Arizona may finally have an explanation as to why different people seem to have such different reactions to the flu. And, to a large extent, they report, it has to do with your childhood.

Early experience

“Our immune system often struggles to recognize and defend against closely related strains of seasonal flu, even though these are essentially the genetic sisters and brothers of strains that circulated just a few years ago,” said lead author Katelyn Gostic, currently a postdoctoral fellow at the University of Chicago.

“This is perplexing because our research on bird flu shows that deep in our immune memory, we have some ability to recognize and defend against the distantly related, genetic third cousins of the strains we saw as children.

An individual’s ability to fight off the flu is related to the number of different flu strains they contracted during their lifetime and the order in which they did so. Prior exposure to a pathogen, be it in the wild or controlled (in a vaccine) is known as immunological imprinting.

For the study, the team set out to determine whether immunological imprinting could explain differences in how people respond to the flu. They used health records from the rizona Department of Health Services to track how different varieties of the virus affect people at various ages, focusing on the H3N2 and H1N1 strains. These strains were selected as both have led to seasonal outbreaks over the past few decades, so there was enough data on them to work from.

In very broad lines, H3N2 is more closely associated with severe flu cases in elderly people and causes the majority of flu-related deaths. H1N1 seems more partial to children and young adults and is far less deadly.

The data showed that people who were first exposed to H1N1 during childhood were less likely to require hospitalization if they re-encountered the strain later on in life compared to those who were first infected with H3N2. Similarly, this latter group would be more resistant to subsequent reinfections of H3N2.

The team looked at the evolutionary relationship between the two strains and report that they belong to two different branches of the influenza family. Further research revealed that while infection with any of the strains does somewhat boost resistance against any other, the best effects are seen with strains from the same family that an individual has battled before. Furthermore, your first exposure seems to grant you extra protection against related strains in the future: people who had their first run-in with flu as children in 1955 (N1H1 strain) were significantly more likely to be hospitalized with an H3N2 infection than an H1N1 infection when both strains were circulating.

However, the team also found that people whose first childhood exposure was to H2N2 did not have better protection when they later encountered H1N1 (although the two strains are closely related). They are still unsure as to why this is.

“We hope that by studying differences in immunity against bird flus — where our immune system shows a natural ability to deploy broadly effective protection — and against seasonal flus — where our immune system seems to have bigger blind spots — we can uncover clues useful to universal influenza vaccine development.”

The paper “Childhood immune imprinting to influenza A shapes birth year-specific risk during seasonal H1N1 and H3N2 epidemics” has been published in the journal PLOS Pathogens.

Cut down on dairy and sweets if you’re struggling with acne, study concludes

In addition to mental stress and unsound skin hygiene, poor dietary habits are associated with acne, a team of researchers reports. In particular, sweets and acne seem to go hand in hand.

Acne is a common skin condition which affects most people at some point in their life. It commonly manifests through spots and oily skin, but it can also cause pustules and severe pain. Although acne cannot be cured, it can be controlled with treatment, and it can be influenced by lifestyle.

Acne is estimated to affect one in 10 people globally, making it the eighth-most prevalent disease worldwide. It is particularly prevalent in teenagers and young adults, with some estimates reporting that it affects up to 40% of adult females. While it is not the most harmful of conditions, it can cause significant long-term discomfort, and its high prevalence makes it important to study.

The good news is that even without medical treatment, simple lifestyle changes can reduce acne incidence. A study presented at the 28th Congress of the European Academy of Dermatology and Venereology in Madrid analyzed the exposure of different worsening factors to see which exacerbates acne the most. The study followed over 6,700 participants in six countries from North America, South America, and Europe. According to researchers, this is the first study of its type.

The results showed that the most significant dietary association was dairy consumption: 48.2% of individuals with acne consumed dairy products on a daily basis, compared to 38.8% who didn’t. Sweets such as pastries and chocolate also had a similar prevalence (37% vs 27.8%). Soda juices (35.6% vs 31%) were also significant factors. All in all, it seems that there is a significant association between sweets and acne.

Acne risk factors. Image credits: EADV.

Researchers also report an unexpected association: 11.9% of acne sufferers consume anabolic steroids, vs just 3.2% without acne. Consumers of whey proteins also have a higher incidence of acne (11% vs 7%). Exposure to pollution and stress were also more frequently observed in participants with acne compared to control participants. Professor Brigitte Dréno, lead author and an associate of Vichy Laboratories comments:

“Acne is one of the most common reasons why people with skin issues contact a dermatologist. Its severity and response to treatment may be influenced by internal and external factors, which we call the exposome. For the first time, this study allows us to identify the most important exposome factors relating to acne from patient questioning prior to any treatment prescription.”

This is still a preliminary study and was not yet published in a peer-reviewed journal, and the study analyzed association without discussing causality — but the findings are still significant. Several previous studies have signaled a connection between sugar and acne. Sugar itself does not cause acne, but it can trigger hormonal fluctuations inside the body. Furthermore, sugar’s oxidative properties can provoke acne breakouts and can cause the body’s insulin levels to spike, which triggers a burst of inflammation throughout the body.


The first symptom of Alzheimer’s is excessive sleepiness

New research at UC San Francisco shows that Alzheimer’s disease directly attacks brain regions responsible for wakefulness during the day.


Image via Pixabay.

Both researchers and caregivers have noted that Alzheimer’s patients can develop excessive daytime napping long before showing the memory problems associated with the disease, the paper reads. Prior studies have considered that this is just a symptom of poor nighttime sleep caused by Alzheimer’s-related disruptions in the brain regions that govern sleep, while others have argued that the sleep problems themselves contribute to the progression of the disease.

However, the new study comes to show that this is in fact caused by Alzheimer’s itself.

Sleepy brain

“Our work shows definitive evidence that the brain areas promoting wakefulness degenerate due to accumulation of tau — not amyloid — protein from the very earliest stages of the disease,” said study senior author Lea T. Grinberg, MD, Ph.D., an associate professor of neurology and pathology at the UCSF Memory and Aging Center.

The brain regions that govern sleep  (including the part of the brain impacted by narcolepsy) are among the first to degrade at the onset of Alzheimer’s disease, the team reports. Therefore, excessive daytime napping, particularly when it occurs in the absence of significant nighttime sleep problems, could serve as an early warning sign of the disease.

The findings also add to the body of evidence suggesting that tau proteins contribute more directly to the brain degeneration that drives Alzheimer’s symptoms than the more extensively studied amyloid protein.

Led by lead author Jun Oh, a Grinberg lab research associate, the team measured Alzheimer’s pathology, tau protein levels, and neuron numbers in three brain regions involved in promoting wakefulness. The team used a sample of 13 deceased Alzheimer’s patients and seven healthy control subjects, which were obtained from the UCSF Neurodegenerative Disease Brain Bank.

The brains of Alzheimer’s patients had significant tau buildup in all three wakefulness-promoting brain centers compared to the healthy controls, the team reports. These three areas were the locus coeruleus (LC), lateral hypothalamic area (LHA), and tuberomammillary nucleus (TMN). The same regions had lost as many as 75% of their neurons, the team adds.

“It’s remarkable because it’s not just a single brain nucleus that’s degenerating, but the whole wakefulness-promoting network,” Oh said. “Crucially this means that the brain has no way to compensate because all of these functionally related cell types are being destroyed at the same time.”

Oh’s team also studied brain samples from seven patients with progressive supranuclear palsy (PSP) and corticobasal disease (CBD), two distinct forms of neurodegenerative dementia caused by tau accumulation. These brains didn’t show any loss of neurons in the same three areas despite showing significant tau protein build-ups.

“It seems that the wakefulness-promoting network is particularly vulnerable in Alzheimer’s disease,” Oh said. “Understanding why this is the case is something we need to follow up in future research.”

The work also ties in with previous research by Grinberg’s team, which showed that people who died with elevated levels of tau protein in their brainstem — i.e. in the earliest stages of Alzheimer’s disease onset — had already begun to experience changes in mood, such as anxiety and depression, as well as increased sleep disturbances.

“Our new evidence for tau-linked degeneration of the brain’s wakefulness centers provides a compelling neurobiological explanation for those findings,” Grinberg said. “It suggests we need to be much more focused on understanding the early stages of tau accumulation in these brain areas in our ongoing search for Alzheimer’s treatments.”

The paper “Profound degeneration of wake-promoting neurons in Alzheimer’s disease” has been published in the journal  Alzheimer’s and Dementia.

Mini liver.

First lab-grown mini livers will allow researchers to study the organ, its diseases, and treatments

Researchers at the University of Pittsburgh (Pitt) School of Medicine have successfully grown miniature human livers in the lab.

Mini liver.

Photograph of rat liver, stripped of rat-specific cells and re-seeded with engineered human liver cells.
Image credits UPMC.

The genetically-modified diminutive organs are meant to be a test platform for scientists to simulate human liver disease progression and test therapies on. As a proof of concept, the Pitt team created one such miniliver that mimics non-alcoholic fatty liver disease (NAFLD).

DeLivering on demand

“This is the first time we can create genetically engineered human mini livers with a disease using stem cells in the lab,” said senior author Alejandro Soto-Gutierrez, Ph.D. and associate professor of pathology at Pitt’s School of Medicine.

The team creates their tiny livers by genetically-engineering human skin cells. These cells are programmed to simulate a certain disease, are then reverted back to their stem state, and then made to mature into fully-functional liver cells.

For the current paper, the team modified the cells to express a chemically activated switch that could clamp down the on SIRT1 gene (SIRT1 proteins are commonly associated with NAFLD). After turning these cells into liver cells, the researchers seeded them into rat livers (which were previously stripped of their own cells). The implanted cells matured into functional 3-D mini livers, with the blood vessels and other structural features of a normal organ.

The organ mimics non-alcoholic fatty liver disease (NAFLD), a condition which can lead to cirrhosis or even liver failure. NAFLD is quickly becoming the leading cause of chronic liver disease in the United States due to its association with obesity.

The team says that their mini livers offer researchers a unique platform to understand not just a disease and how it progresses, but also for the testing of therapeutics. It’s common for drugs to fail in clinical trials despite promising results in mice, they explain, citing the drug Resveratrol. Resveratrol acts on SIRT1, and it was effective in mouse models for the treatment of NAFLD but failed in human clinical trials.

“Mice aren’t humans,” Soto-Gutierrez said. “We are born with certain mutations, polymorphisms, that will predispose us to certain diseases, but you can’t study polymorphisms in mice, so making a mini customized human liver is advantageous.”

What sets the mini livers apart from ‘organoid‘ cultures — bundles of cells that self-assemble into simple versions of organs — is the presence of those structural features such as blood vessels, the team explains. However, they caution that the mini livers “lack the distinct zones of metabolic function” that normal livers have.

Once they fully matured, the team flipped the genetic switch they programmed into the cells (to suppress the SIRT1 gene) and the mini livers started to mimic the metabolic dysfunction observed in tissues NAFLD patients. Just like in the clinical trials, Resveratrol wasn’t effective on these livers, either.

However, the mini livers did allow the team to figure out what went wrong. Resveratrol boosts the activity of SIRT1 proteins not SIRT1 genes. When SIRT1 gene expression is suppressed, such as is the case with the micro livers and perhaps also NAFLD patients, there isn’t any protein to act on. The drug doesn’t work because it’s targeting the wrong step.

“That’s an insight that could only come from studying functional human tissue,” Soto-Gutierrez said.

“I imagine in the future we can make human livers where you can order what kind of function you want, or even enhance function.”

However, we’re a long way away from that point. These mini livers won’t be ready for clinical applications like transplantation anytime soon, Soto-Gutierrez adds.

The paper “Generation of Human Fatty Livers Using Custom-Engineered Induced Pluripotent Stem Cells with Modifiable SIRT1 Metabolism” has been published in the journal Cell Metabolism.

The age of the designer protein is upon us — and the prospects are thrilling

In what could be a game-changer for therapies used in many diseases, scientists have created the first completely artificial protein switch. The protein can work inside living cells to modify or command the cell’s internal circuitry.

It’s the first fully artificial protein developed by humans. Credit: Wikipedia Commons


Researchers at the University of California, San Francisco used computational protein design to create self-assembling proteins that present bioactive peptides only upon the addition of specific molecular “keys.” The work was published in the journal Nature.

The research team installed the switch in yeast and showed that the genetically engineered fungus could be made to degrade a specific cellular protein at a time of the researchers’ choosing. By redesigning the switch, they also demonstrated the same effect in lab-grown human cells.

“In the same way that integrated circuits enabled the explosion of the computer chip industry, these versatile and dynamic biological switches could soon unlock precise control over the behavior of living cells and, ultimately, our health,” said Hana El-Samad, and co-senior author of the report.

The switch created by the researchers was dubbed LOCKR, short for Latching, Orthogonal Cage/Key protein. LOCKR can be ‘programmed’ to modify gene expression, redirect cellular traffic, degrade specific proteins, and control protein binding interactions – using what the paper calls ‘its arm.’

LOCKR has a structure similar to a barrel. When opened, it reveals a molecular arm that can be engineered to control virtually any cellular process. In the paper, the researchers highlight that the switch can be used to build new biological circuits that behave like independent sensors.

“LOCKR opens a whole new realm of possibility for programming cells,” said Andrew Ng of the UC Berkeley-UCSF Graduate Program in Bioengineering. “We are now limited more by our imagination and creativity rather than the proteins that nature has evolved.”

The new switch is not the first designer protein switch ever made, but it’s the first fully artificial one — and it has a lot of applications. Having access to biotechnology tools entirely conceived of and built by humans — as opposed to editing and modifying proteins found in nature — opens a range of exciting possibilities.

LOCKR gives scientists a new way to interact with living cells, which have to control their biochemical processes to avoid death or cancer. The switch could then facilitate a new array of therapies for diverse diseases, ranging from cancer to autoimmune disorders.


Credit: Pixabay.

Dogs quarantined after vets find dangerous disease that can be passed to humans

Credit: Pixabay.

Credit: Pixabay.

A commercial breeding facility for small dogs in Marion County, Iowa, has been quarantined by state officials. According to veterinarians, the facility in southeast Iowa is the source of several cases of canine brucellosis — a dangerous disease that causes infertility problems and is transmissible to humans.

The Iowa Department of Agriculture and Land Stewardship has notified the owners of exposed dogs and has instated a 30-day quarantine on both the animals and the breeding facilities until the animals undergo thorough testing. It’s not clear at this moment how many dogs have been infected, although AHeinz57 Pet Rescue & Transport, Inc., which is based in De Soto, Iowa, said it has quarantined about 32 dogs from a breeder in relation to the disease.

“We are in the process of notifying the individuals who have custody of the exposed dogs,” the department explained in a press release. “Both the animals and the facilities are quarantined while the dogs undergo clinical testing.”

Canine brucellosis is a highly contagious disease that affects the reproductive tract of dogs, causing infertility, stillbirths, and spontaneous abortions. Although it happens very rarely, sometimes the disease can pass to humans causing flu-like symptoms such as fever, joint pain, headaches, and sweats.

If a pregnant woman is infected with the disease, perhaps due to contact with her pet dog, it can cause a miscarriage or force the woman to give birth prematurely.

There is no cure for canine brucellosis. What’s more, infected dogs may appear to be healthy, despite carrying the disease. This is why it’s standard procedure for dogs who are tested positive to be put down.

According to the state department, citizens shouldn’t panic as most pet owners are not at risk. The people most vulnerable to the disease are dog breeders, veterinary staff, and anyone who comes in contact with tissue and fluids during a canine birth.

How air pollution affects human health

Credit: Pixabay.

Since the U.S. Congress passed the Clean Air Act in 1963, the issue of air pollution has remained embedded in American consciousness. Regardless of national and global awareness, most Americans haven’t realized how air pollution affects human health or the degree of its impact, even with seemingly marginal exposure. An estimated 92 percent of the global population live in areas with dangerously high levels of air pollution.

Environmental scientists worldwide are working toward long-term solutions to the problem of air pollution and human health effects. Countries and communities must understand the extent of the impact, where it’s most concentrated, and what must be accomplished at government and individual levels to reduce population exposure.


While most of the world’s population focuses their attention on global terrorism and economics, scientists are becoming increasingly alarmed at how air pollution affects human health. Research indicates that 5.5 million people around the globe die prematurely every year due to indoor and outdoor air pollution.

People suffer both short-term and long-term health effects from air pollution, causing diseases and complications in nearly every system of the body. Some of these include:

  • Respiratory and cardiovascular diseases
  • Neuropsychiatric complications (i.e., seizures, attention deficits, palsies, migraine headaches, and mood disorders)
  • Eye irritation
  • Skin diseases
  • Cancer
  • Infertility
  • Birth defects
  • Premature death

The EPA has narrowed air pollutants down to six major offenders found in varying degrees in cities around the world.

  1. Nitrogen Oxides: Highly reactive gas primarily affecting the respiratory system
  2. Sulfur Oxides: Reactive gas linked to industry and affecting the respiratory system
  3. Particulate Matter: Extremely small particles and liquid droplets in the air affecting the respiratory system and causing premature death
  4. Carbon Monoxide: Odorless, colorless gas produced through combustion processes, deadly at high levels
  5. Ground-Level Ozone: Gas that’s a primary component of smog, affects respiratory and cardiovascular systems, and causes premature death
  6. Lead: Highly toxic metal that impacts cognitive function, hypertension, fertility, the circulatory system, and the immune system


According to an article published in the Journal of Research in Medical Sciences, low-quality vehicle fuel, usually gasoline and oil, have been found to emit greater amounts of polluting gas. This is especially true when they are used in engines that don’t meet emissions standards. Because of this, initiatives have long been underway to replace diesel and gasoline with cleaner sources of energy, such as liquified natural gas and alcohol.

In many cities, the problem extends beyond personal transportation. Public transportation vehicles contain engines that violate environmental standards. While environmental scientists work toward replacing energy sources, cities are compelled to improve public transportation systems by building or extending their subways, trams, and electrical bus routes.

It’s not just vehicles that contribute to poor air quality, though. Air pollution rises proportionately to population and industry, and it’s also affected by weather patterns and natural disasters.

According to the American Lung Association’s 2018 State of the Air report, the top five most polluted cities by ozone air pollution are:

  1. Los Angeles-Long Beach, Calif.
  2. Bakersfield, Calif.
  3. Visalia-Porterville-Hanford, Calif.
  4. Fresno-Madera, Calif.
  5. Sacramento-Roseville, Calif.

The lists organized by year-round and short-term particle pollution include the same cities at different rankings, except for Sacramento. It is replaced by Fairbanks, Ala. as the No. 1 and No. 4 city, respectively.

Of the 5.5 million people around the world who die prematurely each year due to air pollution, more than half of them occur in China and India where rapidly growing economies outpace environmental efforts. Six of the top ten cities ranked for high levels of air pollution are in India, while China’s clean air efforts have kept their cities off the top ten list.

Other cities on the WHO’s top ten list:

  • Al Jubail, Saudi Arabia
  • Pasakha, Bhutan
  • Novi Sad, Serbia
  • Cairo, Egypt


As governments and scientists work together to find solutions, you can educate yourself about air pollution and human health in your area. According to the Journal of Thoracic Disease, these steps can be taken to reduce individual exposure to air pollutants.

  • Stay indoors: Closely monitor your local air quality index reports and stay inside with doors and windows closed during peak pollution hours.
  • Clean indoor air: Use portable or central air cleaning systems to filter the air in your home.
  • Reduce exertion levels: The human body demands a greater supply of oxygen during times of increased physical activity. Consuming larger amounts of air and oxygen also increases the intake of air pollutants. Confine periods of exertion to hours with best air quality.
  • Avoid polluted microenvironments (such as trafficked roads): Don’t walk or engage in outdoor activity near traffic, especially during rush hours. When commuting, set your vehicle’s ventilation system to the recirculate mode and turn on the air conditioner.
  • Use respirators: For many people, respirators are uncomfortable and impractical. However, if you live in an area with higher air pollution levels, you’re advised to wear a properly sealed respirator when tolerable.
  • Stay informed: Knowing the state of air pollution will help you stay safe and healthy. Researching the latest journal publications, monitoring the air quality in your area and adapting to the latest innovations in pollution reduction are all great ways to combat the issue.

If your passion for the environment extends beyond staying abreast of the latest developments, consider earning an Online Environmental Studies Degree from Virginia Wesleyan University. Our program is ideal for those who want to help make a lasting impact on the future and improve humans’ relationship with the environment. We’ll equip you with the interdisciplinary courses and real-world skills required to excel in the workplace. Earn your degree on a flexible timeline that fits your schedule, often in as little as 12 months.

This article was originally published on the website of Virginia Wesleyan University and was re-posted with permission. 

Unvaccinated French child brings measles back to Costa Rica

Costa Rica has been measles-free since 2014 — until now. A five-year-old French child who was on vacation with his family has been diagnosed with the disease, becoming the first case the country has had in almost five years.

A transmission electron micrograph (TEM) of a single virus particle, or “virion”, of measles virus. Image credits: Cynthia S. Goldsmith / CDC.

Since the introduction of vaccines, the number of measles cases worldwide has been dramatically reduced. But in recent years, measles has made a small but worrying resurgence in the developed world, riding the waves of non-scientific antivaxxing trends. Just a few weeks ago, the World Health Organization (WHO) warned about the dangers of preventable diseases making a comeback, calling “vaccine hesitancy” among the 10 most serious threats to human health.

“Some countries that were close to eliminating measles have seen a resurgence,” the WHO warned.

As if to illustrate that point, Costa Rican authorities have now reported that a family of French tourists, the parents 30 and 35 years of age and their 5-year-old child, have been placed in isolation at the Puntarenas Hospital, close to where the family was on vacation. The boy presented a measles-like rash, and blood tests have confirmed that he does have measles (Costa Rican doctors also found that other children at the boy’s kindergarten also had measles).

This didn’t necessarily come as a surprise to Costa Rican authorities, who were on alert for measles being reintroduced from other countries. Costa Rica didn’t have any native measles cases since 2006, but imported cases have been reported up until 2014.

“An increase in cases of measles was first reported last year in Europe and some areas of the United States, but recently, several countries in Latin America have also raised the alarm; for this reason, health authorities in Costa Rica are on alert and have began promoting a vaccination campaign that will take place in August,” a recent local news report stated.

Measles is a highly contagious disease caused by a virus. It has very unpleasant symptoms and can lead to dangerous and potentially fatal complications. Vaccination is 97% effective against the measles virus, which has been instrumental in reducing measles cases around the world. In the developing world, access to vaccination is still a problem, the WHO says.

“Measles vaccination resulted in a 80% drop in measles deaths between 2000 and 2017 worldwide. Even though a safe and cost-effective vaccine is available, in 2017, there were 110 000 measles deaths globally, mostly among children under the age of five,” the WHO reports. Before the introduction of measles vaccine, major epidemics occurred approximately every 2–3 years and measles caused an estimated 2.6 million deaths each year.

Measles cases reported in the US, 1944-2007. Other countries where vaccines were widely implemented display similar trends. Credits: CDC.

Worryingly, even in countries which had all but eradicated measles, the disease is making a comeback as a result of reduced vaccination. Antivaxxing trends and complacency are stopping some parents from getting their children vaccinated. People opting not to have their kids vaccinated are posing great threats not only to themselves, but also to others.

In France, vaccinations against measles and 11 other diseases compulsory for children, as the current health ministry has made vaccination one of its top priorities. It’s not currently clear why the boy has not yet been vaccinated.

Thankfully, the boy is now in safe hands, and there are good odds that the quarantine will be successful. The family will be held for at least a week at the hospital, and authorities are trying to figure out who the boy was in contact with.

Costa Rica provides universal health care to all its citizens and is constantly ranked as the country with the best health care in Latin America, and one of the best in the world. A recent WHO report ranked Costa Rica just ahead of the US in terms of healthcare efficiency.

The CDC advises all travelers to take their vaccines before traveling to Costa Rica: “Make sure you are up-to-date on routine vaccines before every trip. These vaccines include measles-mumps-rubella (MMR) vaccine, diphtheria-tetanus-pertussis vaccine, varicella (chickenpox) vaccine, polio vaccine, and your yearly flu shot,” the CDC page reads.

Photo showing the remains of a 20-year old woman from around 4,900 years ago, who was killed by the first plague pandemic. Credit: Karl-Göran Sjögren.

Scientists find oldest evidence of black plague in 5,000-year-old human remains

Photo showing the remains of a 20-year old woman from around 4,900 years ago, who was killed by the first plague pandemic. Credit: Karl-Göran Sjögren.

Photo showing the remains of a 20-year old woman from around 4,900 years ago, who was killed by the first known plague pandemic. Credit: Karl-Göran Sjögren.

The black plague is a deadly infectious disease that killed off more than a third of Europe’s population during the Middle Ages. However, Yersinia pestis — the bacteria responsible for the disease — has been infecting humans long before there was any historical record of it. Inside a Stone Age limestone tomb in Sweden, scientists found a previously unknown strain of the plague which is nearly 5,000 years old. It’s the earliest known infection of the plague, suggesting that the disease was one of the first major pandemics to wreak havoc among human populations.

“Plague is maybe one of the deadliest bacteria that has ever existed for humans. And if you think of the word ‘plague,’ it can mean this infection by Y. pestis, but because of the trauma plague has caused in our history, it’s also come to refer more generally to any epidemic. The kind of analyses we do here let us go back through time and look at how this pathogen that’s had such a huge effect on us evolved,” says senior author Simon Rasmussen, a metagenomics researcher at the Technical University of Denmark and the University of Copenhagen.

The site at Frälsegården, Sweden, features 78 buried individuals, all of whom died within a 200-year period. The fact that so many people died in a relatively short period hinted that an outbreak may have been responsible for their ultimate downfall.

Nicolás Rascovan, a biologist at Aix-Marseille University in Marseille, France, thinks that the likely culprit is the black plague. Rascovan and colleagues discovered an ancient strain of Yersinia pestis in the remains of a 20-year-old woman, who died 4,900 years ago. Subsequent genome sequencing revealed that the strain carries a mutation that can trigger pneumonic plague, the deadliest form of the plague. Most historical cases of the disease are due to bubonic plague, which occurs when plague bacteria spread to the lymph nodes and cause inflammation.

Previously, the oldest plague bacterium was found in individuals in a double burial in the Samara region of Russia, who both had the same strain of the bacterium at the time of death, 3,800 years ago.

Around the period the women found at the Swedish site died, Neolithic cultures throughout Europe were experiencing a steep decline. One of the leading theories explaining the spread of the black plague suggests that the disease was brought to Europe during the many multi-wave migrations of humans from the Eurasian steps, which started about 5,000 years ago. The diseases which these migratory people brought with them caused massive havoc among European Neolithic farmers, who were replaced by the newcomers — or so the theory goes.

However, genome sequencing shows that the newly found strain diverged from other strains about 5,700 years ago. The woman’s genome isn’t related to that of ancient steppe people either. This means that the strain likely evolved before the Eurasian migration, there in Europe. Between 6,500 and 5,500 years ago, some southeastern European populations started living in so-called ‘mega-settlements’, which could number up to 20,000 people — a huge population for that time. These settlements had people and animals living very close to each other, as well as food stores that attracted all sorts of pests. This is the perfect breeding grounds for deadly pathogens to evolve, the authors note, a fact that seems to be supported by evidence of settlement abandonment after 5,500 years ago.

“We think our data fit. If plague evolved in the mega-settlements, then when people started dying from it, the settlements would have been abandoned and destroyed. This is exactly what was observed in these settlements after 5,500 years ago. Plague would also have started migrating along all the trade routes made possible by wheeled transport, which had rapidly expanded throughout Europe in this period,” Rasmussen says.

What’s remarkable is that the plague seems to have made its way into relatively small and isolated settlements, as far north as Sweden. Indirectly, this seems to suggest that even at that time, there must have been intricate and well-developed trade networks which, along with other wares, also carried pestilent diseases.

There are some problems with the researchers’ plague-origin theory, however. The most obvious is that no plague strains have been found yet at any of the mega-settlements where the bacterium is supposed to have evolved. More excavations might eventually uncover black plague at such sites but even so, the findings could help unravel the complicated picture of how deadly pathogens evolved and spread among these ancient human settlements.

 “We often think that these superpathogens have always been around, but that’s not the case,” he says. “Plague evolved from an organism that was relatively harmless. More recently, the same thing happened with smallpox, malaria, Ebola, and Zika. This process is very dynamic–and it keeps happening. I think it’s really interesting to try to understand how we go from something harmless to something extremely virulent.”

The findings were reported in the journal Cell.

Homeopathy is ineffective against children’s cold and flu

Add another one to the pile: a new review of randomized controlled trials on the common cold, influenza, and pneumonia found no evidence that homeopathy is effective in any way.

Homeopathy doesn’t work, and according to everything we know about science — it can’t work.

If it’s your first time on ZME Science — first of all, welcome — there’s one thing you should know about us: we love science — and like everyone who loves something, we hate it when something else masquerades as that something we love. In this case, we’re talking about pseudoscience.

Sure, you can argue that most (if not all) people believe in something illogical. Most of the time, that doesn’t do any harm — after all, what difference does it make if you read the daily horoscope or not? But some beliefs are more dangerous than others, especially when it comes to medical science. Obviously, medicine isn’t perfect and there’s still a lot of room for improvement but thanks to medical science, we live longer and healthier than all the generations before us. So why, then, would you doubt and reject it?

Homeopathy goes against everything we know about chemistry, biology, and medicine. It’s completely implausible from a theoretical standpoint, and study after study has shown that the practical effects just aren’t there. It might seem like it works (and here’s why), but the data suggests otherwise.

In a new study published in the prestigious Cochrane Database of Systematic Reviews, a team of researchers looked at how good homeopathy is in dealing with the cold, the flu, and pneumonia.

Common homeopathic ‘treatments’ for these conditions include Arsenicum album (arsenic trioxide), Euphrasia (eyebright plant), and natrum muriaticum (or as most people call it, table salt). A particular flu remedy called Oscillococcinum is derived from duck liver and heart. If that’s not enough to dissuade you, then the preparation mechanism likely will.

Homeopathic substances are heavily diluted in water, often times by a factor of a trillion or even more. Sometimes, they’re diluted so much that not a single molecule of the original substance remains — by everything we know about chemistry, there’s nothing but water left in these substances. Supposedly, this dilution makes substances stronger — which again, goes again everything we know about physics.

The researchers scoured the literature to find any studies comparing oral homeopathy medicinal products with identical placebo or self‐selected conventional treatments. They found eight such studies, and this is where it gets interesting.

Researchers did find eight suitable studies. A few of these studies did suggest some benefits, and at a quick glance, you’d say that it’s good enough — it’s published in a journal, it passed the test of peer-review, so why not? But when researchers looked closer, they found all sorts of problems, ranging from major inconsistencies to a blatant conflict of interest — three of the studies were directly funded by homeopathy manufacturers. In these studies, even the reviewers were dubious of their claims.

“One study showed a reduction in disease severity for the homeopathy group at some time points. The other study showed a reduction in number of respiratory infections over the following year in the treatment groups, although more than a quarter of participants were not accounted for in the results,” the reviewers wrote.

Meanwhile, the more rigorous studies consistently find no benefits to homeopathy. The authors give a stern conclusion:

“There is no convincing evidence homeopathic medicinal products are effective in treating ARTIs in children.”

Intriguingly, advocates of homeopathy often claim that it’s a “true” healing practice, unlike modern medicine, which is “all about the money.” However, these people conveniently disregard the fact that in the US alone, homeopathic and herbal remedies are a multi-billion dollar industry.

When you draw the line, homeopathy doesn’t work, it even can’t work (based on pretty much everything we know about science), and still it makes a lot of money. So why is it still a thing? It’s hard to say, but as always, we encourage you to leave your opinion in the comment section.

London air.

Air pollution may increase the risk of developing dementia

Air pollution seems to increase the risk of developing neurodegenerative diseases, a new study reveals.

London air.

High air pollution in London.
Image credits David Holt / Flickr.

Nobody likes dirty air — though most of us are breathing exactly that. Air pollution has been established as a risk factor for heart disease, stroke, and respiratory disease. Whether or not it has a part to play in neurodegenerative diseases such as dementia, however, remained unclear until now.

It does

For the study, the team produced estimates of air and noise pollution levels across the Greater London area, which they used to assess potential links with new dementia diagnoses.

Data on the latter was obtained from anonymized patient health records of the Clinical Practice Research Datalink (CPRD), which has been collecting data from participating general practices across the UK since 1987. The team worked with the records of under 131,000 patients: those aged 50 to 79 (in 2004), who had not been diagnosed with dementia, and were registered at either one of 75 general practices located within the London orbital M25 motorway.

Based on each patient’s postcode, the team then estimated their annual exposure to air pollutants, especially nitrogen dioxide (NO2), fine particulate matter (PM2.5), and ozone (O3). The team also estimated each patient’s proximity to heavy traffic and exposure to road noise using modeling methods and on-site measurements.

The team tracked each patient’s health until they received a diagnosis of dementia, de-registered from their practice, or died — whichever came first. Over the study period, 2181 patients (1.7%) were diagnosed with dementia, including Alzheimer’s disease.

Those patients living in the top 20% areas by NO2 levels had a massive 40% higher risk of being diagnosed with dementia compared to those living in the bottom 20%. A similar increase in risk was observed for high levels of PM2.5. These links were consistent and couldn’t be explained by any other factors the team had access to, such as smoking or diabetes. However, when restricted to specific types of dementia, the association only held for patients diagnosed with Alzheimer’s disease.

Caution to the wise, however: this is an observational study and, as such, the findings cannot be used to establish a cause-effect relationship; the findings may also only be applicable to the London area. Many factors may be involved in the development of dementia, the exact cause of which is still not known, the researchers point out.

“Traffic related air pollution has been linked to poorer cognitive development in young children, and continued significant exposure may produce neuroinflammation and altered brain innate immune responses in early adulthood,” the authors conclude.

Still, even if air pollution had a relatively modest contribution to the development of neurodegenerative diseases, overall public health gains would be significant if we made an effort to limit both it and exposure to it.

The paper “Are noise and air pollution related to the incidence of dementia? A cohort study in London, England” has been published in the journal BMJ.

Common cold.

New research shows why some people get the common cold more easily

New research shows how different human cells respond to rhinovirus, the vector of the common cold. The results could help explain why some people are more susceptible to the disease than others.

Common cold.

Image credits Myriam / Pixabay.

Common colds, asthma attacks, and a host of other diseases associated with the respiratory tract share a common cause — rhinoviruses. However, not all people are made the same: some are more resistant to the pathogen, while others collapse into bed at the merest whiff of it.

In a bid to understand why, one team from the Yale University studied how key human cells respond to the pathogen.

Where’s the chicken soup?

To get to the bottom of things, the team worked with epithelial cells harvested from the nasal passages or lungs of healthy human donors. The team exposed both types of epithelial cells — kept in cultures under the same environmental conditions — to the virus.

Epithelial cells are a specialized type of cell that creates membranes and linings throughout the body. They’re usually the first bits to come into contact with pathogens, and, as such, possess traits that help them fight off bacteria and viruses. Rhinoviruses also have to contend with these cells when trying to infiltrate the body. Upon exposure to the bugs, epithelial cells lining our airways react to the threat, usually clearing it out of our systems before it gets a foothold and triggers symptoms. In some cases, however, this mechanism doesn’t seem to work: exposed to rhinoviruses, they fall mildly, or even seriously, ill.

The team reports that under business-as-usual scenarios, nasal cells have the more robust antiviral reaction among the two samples of cells. Further lab tests involved activation of the RIG-I pathway — a pattern-recognition network that the body uses to identify pathogens — in both types of sample cells so the team could see how each operated under emergency scenarios.

Upon activation of the RIG-I network, both cell types produced antiviral responses and beefed up their defenses against oxidative stress. Viral activity usually puts oxidative stress, a kind of chemical damage, on the cells they attack — so such a reaction should help them weather the invasion. Nasal cells showed the strongest antiviral response, while bronchial (deeper respiratory system) cells exhibited the strongest oxidative resistance of the lot.


Image credits Pearson Scott Foresman.

Excellence comes at a cost, however: the team also found that cells can act against oxidative stress or viruses, but not both at the same time. This was particularly interesting as inhaled irritants — for example cigarette smoke or tree pollen — also generate oxidative stress on cells, the team explains.

Nasal cells exposed first to cigarette smoke and then to rhinoviruses were more vulnerable to the virus’ effects, the team reports.

“Your airway lining protects against viruses but also other harmful substances that enter airways. The airway does pretty well if it encounters one stressor at a time. But when there are two different stressors, there’s a tradeoff,” says lead researcher Ellen Foxman.

“What we found is that when your airway is trying to deal with another stress type, it can adapt but the cost is susceptibility to rhinovirus infection. [The cells] survive the cigarette smoke but can’t fight the virus as well. And the virus grows better.”

Foxman says their study underscores a mechanistic link between environmental exposure and our body’s ability to resist the common cold. The findings also help explain why smokers tend to be more susceptible to rhinovirus infections.

The team hopes their efforts will lead to the discovery of new strategies to combat respiratory viruses, which cause an estimated 500 million colds and 2 million hospitalizations in the United States per year.

The paper has been published in the journal Cell Reports.