Burning candles and fumes from cooking is harmful for people with mild asthma

A cosy set table, a nice steak in the pan, and romantic candlelight may sound like the start of a lovely evening. However, a new study from the Department of Public Health at Aarhus University suggests that you should be cautious about inhaling too much of the cosy atmosphere. Karin Rosenkilde Laursen, a postdoc at the department and co-author of the study, says:

"Our study shows that indoor air pollution caused by fumes from cooking and burning candles can lead to adverse health effects such as irritation and inflammation in young individuals with mild asthma. Among other things, we've found indications of DNA damage and signs of inflammation in the blood."

When we turn on the oven, place a pan on the hob, or light candles, ultrafine particles and gases are produced, which we then inhale. Previous studies have shown that these particles and gases can be detrimental to health. What sets this study apart is that the researchers have focused on the effects on young individuals with mild asthma, aged between 18 and 25, says Karin Rosenkilde Laursen:

"In the study, we observed that even very young individuals with mild asthma can experience discomfort and adverse effects if the room is not adequately ventilated during cooking or when burning candles. Young people are generally fitter and more resilient than older and middle-aged individuals. Therefore, it is concerning that we observed a significant impact from the particles on this particularly young age group."

But not only people diagnosed with asthma need to keep an eye on the indoor climate, she says.

"Even though the study focused on young asthmatics, its findings are interesting and relevant for all of us. Winter is approaching, a time when we tend to light many candles and perhaps are less likely to open doors and windows while cooking. By prioritising a healthier indoor climate, even when we're cosying up indoors, we may be able to help reduce the incidence of serious lung and cardiovascular diseases, as well as cancer."

Karin Rosenkilde Laursen plans to follow up this study with another examining how emissions from cooking and candles affect healthy adults.

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Common food dye can trigger inflammatory bowel diseases, animal study suggests

Long-term consumption of Allura Red food dye can be a potential trigger of inflammatory bowel diseases (IBDs), Crohn's disease and ulcerative colitis, says McMaster University's Waliul Khan. Researchers using experimental animal models of IBD found that continual exposure to Allura Red AC harms gut health and promotes inflammation.

The dye directly disrupts gut barrier function and increases the production of serotonin, a hormone/neurotransmitter found in the gut, which subsequently alters gut microbiota composition leading to increased susceptibility to colitis.

Khan said Allura Red (also called FD&C Red 40 and Food Red 17), is a common ingredient in candies, soft drinks, dairy products and some cereals. The dye is used to add colour and texture to foodstuffs, often to attract children.

The use of synthetic food dyes such as Allura Red has increased significantly over the last several decades, but there has been little earlier study of these dyes' effects on gut health. Khan and his team published their findings in Nature Communications. Yun Han (Eric) Kwon, who recently completed PhD in Khan's laboratory, is first author.

"This study demonstrates significant harmful effects of Allura Red on gut health and identifies gut serotonin as a critical factor mediating these effects. These findings have important implication in the prevention and management of gut inflammation," said Khan, the study's senior author, a professor of the Department of Pathology and Molecular Medicine and a principal investigator of Farncombe Family Digestive Health Research Institute.

"What we have found is striking and alarming, as this common synthetic food dye is a possible dietary trigger for IBDs. This research is a significant advance in alerting the public on the potential harms of food dyes that we consume daily," he said.

"The literature suggests that the consumption of Allura Red also affects certain allergies, immune disorders and behavioural problems in children, such as attention deficit hyperactivity disorder."

Khan said that IBDs are serious chronic inflammatory conditions of the human bowel that affect millions of people worldwide. While their exact causes are still not fully understood, studies have shown that dysregulated immune responses, genetic factors, gut microbiota imbalances, and environmental factors can trigger these conditions.

In recent years there has been significant progress in identifying susceptibility genes and understanding the role of the immune system and host microbiota in the pathogenesis of IBDs. However, similar advances in defining environmental risk factors have lagged, he said.

Khan said that environmental triggers for IBDs include the typical Western diet, which includes processed fats, red and processed meats, sugar and a lack of fibre. He added that the Western diet and processed food also includes large amounts of various additives and dyes.

He added that the study suggests a link between a commonly used food dye and IBDs and warrants further exploration between food dyes and IBDs at experimental, epidemiological and clinical levels.

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Can we save more lives if we let resistant bacteria live?

Antibiotic resistance is a ticking bomb under public health. WHO predicts that in 2050 more people will die from infections than from cancer -- and we are talking about infections that we today consider harmless; infections that occur in a cut or wound -- or perhaps cystitis.

The reason is that bacteria are masters at adapting. When their existence is threatened, they mutate into a new and improved version of themselves that can no longer be threatened by eg antibiotics. Consequently, many disease-causing bacteria today are resistant to antibiotics.

"That's bacteria for you. They always find a way! Of course, resistance will occur; that's how evolution works," says professor and head of research, Birgitte Kallipolitis, who studies disease-causing bacteria at the Department of Biochemistry and Molecular Biology at University of Southern Denmark.

The talents of fatty acids

And that's exactly why, like other researchers around the world, she thinks it's time to find new ways to fight or neutralize the perpetually mutating bacteria.

For some years now, she and her research group have studied a particular type of fatty acid, which has proven itself interesting in this context. The researchers use listeria as a bacterial model to test the effect of these fatty acids. Elsewhere in the world, colleagues are using salmonella and cholera bacteria for similar tests.

The particular fatty acids are interesting not only because they can kill the listeria bacteria in Kallipolitis' laboratory, but they can also turn off their ability to infect and spread infection.

The researchers' experiments have shown that the fatty acids have an antimicrobial effect, ie that they can kill listeria bacteria. At first, this sounds good, but then there is the mutation thing; trying to kill the bacteria only makes it mutate into a new and resistant version of itself.

Enter the special talent of the fatty acids: They can make the resistant bacteria harmless, so that no infection occurs at all.

"Thus, the resistant bacterium is no longer a bacterium that we must try to kill -- instead, we prevent it from spreading and making us sick," Birgitte Kallipolitis explains.

No more spreading

The concept of making a disease-carrying bacterium unable to spread or make us sick is called turning off its virulence.

When you turn off the virulence of a bacterium, you prevent it from producing proteins like adhesins and invasins, which the bacterium needs to attach to a cell so that it can enter the cell.

"If a listeria bacterium cannot enter a cell, it cannot spread, and then no infection will occur," Birgitte Kallipolitis explains.

Extra help for the elderly and weak

The Listeria bacteria in Kallipolitis' experiments are only harmless as long as their virulence is switched off. When they are no longer exposed to the fatty acids that turn off their virulence, they regain the ability to spread

"But this may be the extra help that allows a patient to cope with an infection. Antivirulent medication or supplements could be good for the prevention of infections, especially in the elderly and weak," says Birgitte Kallipolitis.

The fatty acids that she and her colleagues work with, are so-called medium and long free fatty acids.

In nuts, plants and seeds

"We have especially focused on the free fatty acids, palmitoleic acid and lauric acid, which are found in nuts, seeds, plants and milk, etc. In our experiments, they show an antivirulent effect," she says.

Kallipolitis points out that you cannot eat your way to an antivirulent effect by, for example, eating nuts and seeds containing palmitoleic acid and lauric acid.

"The fatty acids must be in the free form, and that does not generally occur in food. You can buy free fatty acids as supplements but be aware that most fatty acids in supplements are locked and not in the free form.

"We do not yet know if you can achieve the effect by consuming free fatty acids. Maybe the fatty acids are metabolized before they reach the battle ground in the intestinal system, where the fight against many resistant bacteria takes place. Maybe we need pharmacists or chemists to find a way to transport the fatty acids to the scene of the battle," she explains.

Hence, a special dietary supplement or tablet is not just around the corner, she emphasizes. Before we get there, a number of tests are needed.

"The next step will be to test the antivirulence effect in a laboratory system reminiscent of the human intestinal system; here we will add listeria bacteria and see if the fatty acids will make them avirulent. If this works, it goes on to mouse experiments, and eventually it can hopefully be used prophylactically in humans," says Birgitte Kallipolitis.

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Small group of genetic variants found in extremely ill patients with COVID may help explain big differences in how sick people get

The search to better understand the tremendous range of responses to infection with the COVID-19 virus -- from symptom free to critically ill -- has uncovered in some of the sickest patients a handful of rare structural gene variants involved in body processes, like inflammation, which the virus needs to be successful.

"The virus has to attach to our cells, it has to get inside our cells and it has to multiply inside our cells. It also has to attract inflammation," says Dr. Ravindra Kolhe, director of the Georgia Esoteric and Molecular Laboratory at the Medical College of Georgia at Augusta University. "We have identified genes with structural changes in very sick individuals that are part of all four of these essential processes."

In apparently the first study of its kind, investigators used optical genome mapping, to get a thorough, three-dimensional assessment of the genome of 52 severally ill patients with COVID-19.

In nine of the sickest patients, they identified seven rare structural variants affecting a total of 31 genes involved in key pathways mediating the response between a person, or host, and a virus. These include innate immunity, our frontline immune defense against invaders like viruses; the inflammatory response, a key response to an infection that, gone awry, can also destroy the lungs of some of the sickest patients; and the ability of a virus to replicate and spread. As an example, one variant they identified can lead to overexpression of keratin genes. Keratins are proteins that are the structural components of things like our hair and nails, but that also have been identified as key to the transmission of both flu viruses and the COVID-19 virus between cells and are known to be upregulated in the respiratory tract during an infection.

"It's a hyperactivation of the normal systems," says Kolhe, corresponding author of the study, published by the international collaborative COVID-19 Host Genome Research consortium in the journal iScience.

"Millions of people get infected, and fortunately only a very small percentage become symptomatic, and a very small percentage of the symptomatic individuals require oxygen and a small percentage of those individuals are hospitalized and die," Kolhe says. "But even a small percentage amounts to millions of people and that is too many."

"Our data show that large (structural variants) identified using optical genome mapping might further explain the inter-individual clinical variability in response to COVID-19," the investigators write.

Large structural variants account for much of the genetic diversity among us, including changes that are just unique to the individual and those that can increase their risk of problems like cancer. Optical genome mapping is an emerging technology that can detect these larger variants with multiple changes, like deletion or insertion of genetic material and/or when a section of chromosome is reversed.

The investigators say that while more work needs to be done, their findings about the potential role of structural variants in the host-virus interaction point toward the need to look for genetic variations, ideally with a simple- to-use blood assay. Once identified, the goal would be to initiate proactive moves for these individuals like ensuring vaccination and boosting and potentially more aggressive treatment early on, like monoclonal antibody therapy, to help these individuals better combat COVID, Kolhe says.

Clinical studies have identified factors like older age, being male, hypertension, diabetes and other chronic conditions as risk factors associated with the degree of illness from COVID-19. The nine sickest patients in this study shared common comorbid conditions, 32 of the patients required mechanical ventilation to support their breathing and a total of 13 of the 52 patients died while in intensive care.

But in their studies, which also included individuals who were negative for the COVID-19 virus and those who were positive but asymptomatic, there were again outliers, including individuals with comorbid conditions who remained asymptomatic when infected with SARS-CoV-2 and those who were perfectly healthy but became extremely ill when infected, another indicator of a role for genetics in determining the degree of response, Kolhe says.

Kolhe notes that the large structural variants they found in the sickest patients were not caused by the virus rather used by the virus and may not increase susceptibility to other, even similar, conditions.

Overall, the individuals in this study had about 40 rare structural variants, which other studies have indicated is about average.

The COVID-19 Host Genome Research consortium currently has a membership of 34 institutions, including Duke and Columbia universities, the National Cancer Institute and the New York Genome Center, exploring different aspects of how structural variants impact the divergent individual responses to infection with the COVID-19 virus.

The group began to emerge after more commonplace gene sequencing studies, which essentially lay out the DNA in a straight line to look for problematic and smaller variations in the usual order of its four base pairs -- adenine, thymine, guanine and cytosine -- on thousands of patients have yielded little information to help explain -- and ideally predict -- the wide variations in how sick people will get. Better than 30% of the known disease-causing variants are larger than the single base pair changes sequencing can identify, according to the Human Gene Mutation Database.

Even the amount of virus in an individual does not directly correlate with how sick the individual gets, Kolhe says. "We had individuals with very high viral loads who did not even know they were positive," he says. "It is something in the host genome that is different."

Some studies have found that blood type might be a factor in predicting risk, specifically type A, and there have been some specific gene findings as well that predispose to immune deficiencies that may make people more susceptible.

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