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Health24.com | New study raises more health concerns over vaping: It may trigger lung damage like that seen in emphysema
The health profile of vaping just took another knock: New research suggests that e-cigarettes can cause the same lung changes that lead to emphysema in smokers.
Researchers tested lung fluid from 41 people – nonsmokers, smokers and people who vape – and found that the lungs of both smokers and vapers had elevated levels of protease enzymes, a precursor condition to emphysema in smokers.
The nicotine in vaping liquids is responsible for the increase in protease enzymes, said the team from the University of North Carolina (UNC) School of Medicine, in Chapel Hill.
The bottom line is that “vaping may not be safer than cigarette smoking”, study senior author Robert Tarran said in a UNC news release. He’s a professor of cell biology and physiology, and member of the university’s Marsico Lung Institute.
As Tarran’s team explained, chronic over-activity of protease enzymes in lung cells damages tiny sensitive air sac structures in the lungs.
In smokers, this damage is thought to be the cause of emphysema, an often fatal form of chronic obstructive pulmonary disease (COPD) that results in progressive shortness of breath. There is no cure.
The new findings gave pause to one lung care specialist.
“I have seen many patients using e-cigarettes as a mechanism to stop smoking cigarettes,” noted Dr Thomas Kilkenny, who wasn’t involved in the new research.
“Unfortunately, this study calls into question the safety of vaping as a tool to stop smoking. It also demonstrates that a whole generation of young people may be setting themselves up to develop emphysema,” he added.
That’s because the popularity of vaping is surging among American teens, even as traditional smoking rates decline. In 2018, more than 3.6 million middle and high school students were current e-cigarette users, according to the US Food and Drug Administration. That was up by 78% from just the prior year among high school kids, and by 48% among middle school students.
Not the first warning
And the new findings are not the first to warn about potential health risks of e-cigarettes. One 2018 study by another UNC team found that lung fluid from vapers and smokers contained elevated levels of emphysema-promoting proteases and other immune defense proteins.
This month, the US Centers for Disease Control and Prevention said it is investigating more than 150 recent cases of sudden, serious lung disease in otherwise healthy young people who vape.
Patricia Folan directs the Center for Tobacco Control at Northwell Health in Great Neck, New York. Reviewing the new study, she said science is chipping away at the notion that vaping is “safe”, or at
Also last year, another study from Tarran’s lab detected toxic compounds in commonly used vaping liquids.least safer than smoking.
“Studies like this one will add to the scientific research and help educate practitioners, as well as the public, about the potential health hazards associated with vaping and dispel some of the myths surrounding their safety and effectiveness for quitting other tobacco use,” Folan said.
Any health gains spurred by declines in traditional smoking might be offset by the rise in vaping, Folan added.
“The majority of emphysema cases are directly related to cigarette smoking,” she said. “Smoking rates have been decreasing but vaping rates are increasing. Because of the use of these new products, the rates of emphysema may not decrease as we had hoped.”
For their part, Tarran’s team said they now plan to conduct a larger study of lung protease enzyme levels in hundreds of participants.
The study was published August 22 in the American Journal of Respiratory and Critical Care Medicine.
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Health24.com | 3 foods and ingredients that can worsen your back pain
Backache is one of the most common types of chronic pain, and can seriously compromise your quality of life. But staying committed to a healthy, nutritional diet, among other things, can relieve the pain and make one feel a lot better.
Inflammation
There’s a good and bad side to inflammation. It plays a positive role in injuries and infections by signalling the immune system to repair injuries and fight off infections. However, an immune system that is out of balance causes inflammation to run rampant. Chronic inflammation has been linked to several diseases such as diabetes and cancer, and can also lead to backache.
A healthy digestive system can ensure a good muscular system, and anything that affects your digestion can also affect your muscles. Many foods have been shown to affect inflammation, a common cause of back pain. In short, therefore, foods and ingredients that trigger inflammation should be eliminated or limited in your diet. These include:
1. Preservatives
In order to extend the shelf life of many foods, additives and preservative are added. These can trigger an immune response which can affect the joints in your back, leading to back pain. Look out for foods that contain carboxyl, parabens, cellulose, benzoic acid and potassium sorbate – all have been found to have an inflammatory effect on the body.
2. Sugar
Sugar is one of the biggest culprits of inflammation, but one of the hardest to cut down on. (Note that this doesn’t apply to natural sugars found in dairy and fruit.) Sugar in your diet can create inflammation both directly and indirectly. High levels of sugar can for example boost insulin levels – and chronically high insulin leads to inflammation.
If your eat foods that are high in sugar every day you’re keeping your sugar and insulin chronically high, leaving your joints subject to constant inflammation. Reducing your sugar intake may be challenging at first, but will greatly benefit you in the long-run.
3. Red meat
Red meat, burgers and popular processed meats like hot dogs, sausages and bacon are associated with high inflammation and should be avoided if you suffer from back pain. Red meat contains a sugar called Neu5GC, which promotes inflammation. It would be sensible to reduce your intake of these foods in order to reduce inflammation and subsequent pain.
Eating healthily is not that difficult. Reduce your consumption of the above meat products and rather concentrate on unprocessed foods that are high in antioxidants and healthy fats, such as:
- Fruits, especially all types of berries
- Dark green, leafy vegetables
- Nuts, grains and legumes
- Omega-3 foods, such as fish and flaxseed
Try keeping a diary of everything you eat, and track your level of back pain based on that. Once you get into the swing of healthy eating, you could start feeling a noticeable difference in your level of back pain.
Keep in mind that people with the least amount of back pain are the ones who exercise regularly, maintain a healthy body weight and follow a proper diet.
Image: iStock
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Optimists are more likely to live longer than those with a negative life view a US study has found.
Elusive key to stopping neglected tropical diseases
Researchers at the University of Alberta have found an important protein in the cells of a deadly infectious parasite, opening the door to less harmful treatment for millions of people suffering from diseases like sleeping sickness in Africa and Chagas disease in South America.
The parasite, trypanosome, is transmitted through insect bites. In a study published in Life Science Alliance, U of A cell biologist and Canada Research Chair in Cell Biology Rick Rachubinski, and research associates Hiren Banerjee and Barbara Knobloch, found that a protein called PEX3, long believed not to exist in the parasite, was in fact present and essential for their viability.
PEX3 is a critical component of the cell biology of many living things, including humans, plants and trypanosomes. It helps make and regulate parts of the cells called peroxisomes, which help break down fatty acids and amino acids in the body to create energy.
In a trypanosome, there are specialized peroxisomes that are vital for regulating the process of turning glucose in a host’s blood into energy. Disrupting the PEX3 required for making them could be an effective way to target and kill the parasite without harming the host, according to the researchers.
“Finding PEX3 in trypanosomes has been very difficult. People have been looking for years and just could not find it,” said Rachubinski, who is also a member of the U of A’s Women and Children’s Health Research Institute. “Some people said it didn’t exist, that it was a different mechanism, but we believed that the simplest answer was that we just hadn’t found it yet.”
Finding PEX3 in trypanosomes eluded Rachubinski and his team for years until, by chance, they attended a lecture given by a researcher from Cambridge University.
In the lecture, the presenter mentioned using HHpred, a computer program offered by the Max Planck Institute for Developmental Biology in Germany, to search for proteins based on how they are predicted to fold, or turn into functional proteins, rather than the traditional way of searching by amino acid chains. Inspired, Rachubinski rushed back to his lab and used the program to compare human PEX3 against trypanosomal proteins. To his surprise, the program found a previously uncharacterized trypanosomal protein that was 95 per cent similar in its folded structure to human PEX3.
“It really was a ‘Eureka!’ moment. After years of searching, we throw this into the computer and 10 minutes later we have the answer,” he said. “It was really kind of elegant.”
Banerjee, who is the first author on the study, agreed.
“It was a great moment for our lab, especially when you have all these other papers saying PEX3 is not there,” he said.
Rachubiniski and his team are now in the process of identifying a drug treatment that targets and disrupts enough of the trypanosome’s PEX3 interactions with partner proteins to prevent the parasites from creating enough energy to survive in the body.
While current treatments for trypanosomal diseases can be highly toxic to hosts, the team’s hope is that this new approach will result in drugs that are not only safe for the hosts, but also cheap to produce and distribute.
For Rachubinski, the search for cures for neglected tropical diseases like sleeping sickness (also called human African trypanosomiasis) has been a lifelong endeavour. As an undergraduate, he was inspired by Paul de Kruif’s 1926 book Microbe Hunters, a collection of biographies and true-life stories of the scientists and researchers who first began the fight against bacteria.
“This one, to me, has been really rewarding because it’s been a constant theme throughout my career,” Rachubinski said. “This is a worldwide problem, and I’ve always believed that affluent nations like ours should help emerging nations that don’t have the resources to deal with burdens like neglected tropical diseases.
“Knowing this discovery could help millions of people is very satisfying to me.”
Rachubinski’s research was made possible in part through funding from the Canadian Institutes of Health Research.
Wild ground-nesting bees might be exposed to lethal levels of neonics in soil
In a first-ever study investigating the risk of neonicotinoid insecticides to ground-nesting bees, University of Guelph researchers have discovered at least one species is being exposed to lethal levels of the chemicals in the soil.
Examining the presence of these commonly used pesticides in soil is important given the majority of bee species in Canada make their nests in the ground.
This study focused on hoary squash bees, which feed almost exclusively on the nectar and pollen of squash, pumpkin and gourd flowers.
Researchers found that the likelihood that squash bees are being chronically exposed to lethal doses of a key neonicotinoid, clothianidin, in soil was 36 per cent or higher in squash fields.
That means 36 per cent of the population is probably encountering lethal doses, which is well above the acceptable threshold of 5 per cent, in which 95 per cent of the bees would survive exposure.
“These findings are applicable to many other wild bee species in Canada that nest on or near farms,” said U of G School of Environmental Sciences professor, Nigel Raine, who holds the Rebanks Family Chair in Pollinator Conservation and worked on the study with PhD student and lead author Susan Chan.
“We don’t yet know what effect these pesticides are having on squash bee numbers because wild bees are not yet tracked the same way that honeybee populations are monitored. But we do know that many other wild bee species nest and forage in crop fields, which is why these findings are so concerning.”
Published in Scientific Reports, the study began with Chan collecting soil samples from 18 commercial squash fields in Ontario. Pesticide residue information from these samples and a second government dataset from field crops was used by Chan and colleagues Prof. Ryan Prosser, School of Environmental Sciences, and Dr. Jose Rodríguez-Gil to assess the risk to ground-nesting squash bees.
The research comes as Health Canada places new limits on the use of three key neonicotinoids, including clothianidin, while it decides whether to impose a full phase-out of these pesticides. Neonics have been linked to concerns about honeybee colony health, with research showing these bees can ingest dangerous amounts through nectar or pollen.
“Current risk assessments for insecticide impacts on pollinators revolve around honeybees, a species that rarely comes into contact with soil,” said Raine. “However, the majority of bee species live most of their life in soil, so risks of pesticide exposure from soil should be a major factor in these important regulatory decisions.”
“Until now, no one has examined the risk to bees from neonics in soil despite the fact these pesticides are applied directly to seeds planted into the ground, or sprayed directly onto soil at planting, and can persist for months after application,” said Chan.
“Only about 20 per cent of the neonicotinoid insecticide applied to coated seeds is actually taken up into the crop plant; the rest stays in the soil and can remain there into subsequent seasons.”
Squash bees are at particular risk because they prefer the already-tilled soil of agricultural fields for their elaborate underground homes. And as they build their nests, they move about 300 times their own body weight worth of soil.
Since the bees don’t eat soil, it’s difficult to know exactly how much pesticide residue enters the bees. But the researchers calculated that even if they are conservative and assume only 25 per cent of the clothianidin enters the bee, the risk of lethal exposure in pumpkin or squash crops is 11 per cent — still above the widely accepted threshold of 5 per cent.
The team also examined the exposure risk in field crops, since many ground-nesting bee species live near corn and soybean fields, which use neonics as well. They found that 58 per cent of ground-nesting bees would be exposed to a lethal dose of clothianidin while building their nests even if only 25 per cent of the clothianidin in the soil enters the bee.
“Pumpkin and squash farmers face a dilemma in that they want to protect pollinators, such as the squash bee, because they are vital to crop production, but at the same time need to protect their crops from pests,” said Chan.
“New approaches are needed that allow farmers to control pests and protect pollinators simultaneously. My advice to farmers is if you find an aggregation of squash bees nesting on your farm, protect these key pollinators from exposure to neonicotinoids by either not using them at all, or at least not using them near the aggregation. Creating pesticide-free places to nest will help your population of squash bees to grow over time.”
K+ channel study could help develop drugs for life-threatening conditions
In every living cell, from free-living bacterium to neurons in the human brain, highly specialized small conduits, known as potassium (K+) channels, are responsible for unparalleled selective and extremely rapid transport of K+-ions across the cell membrane. This unique transport mechanism of K+-ions defines the correct functional behavior of every living cell, and by extension, effectively controls a large variety of very complex processes like the normal electrical activity of brain neurons, the rhythmical beating of the human heart and the normal immune response of the human body against life threatening pathogens.
“Understanding at the atomic level, the process exploited by K+-channels to catalyze the highly selective and very rapid transport of K+-ions across the cell membrane has tantalized biophysicist for more than five decades and remains one of the most controversial areas of research,” Texas Tech University Health Sciences Center (TTUHSC) Associate Professor Luis Cuello, Ph.D., said.
Cuello and his team from TTUHSC’s Department of Cell Physiology and Molecular Biophysics recently completed a study in which they attempted to capture at atomic resolution a picture/snapshot of one of the two ion-bound configuration that seem to coexist within the selectivity filter of K+-channel. The results from the study, “Structure, function and ion binding properties of a K+-channel stabilized in the 2,4-ion bound configuration,” were published in the Aug. 5 edition of Proceedings of the National Academy of Sciences (PNAS). The publication is one of the world’s most frequently cited multidisciplinary scientific serials that disseminate cutting-edge research spanning the biological, physical and social sciences.
Cuello said two very different competing mechanistic models have tried to explain how K+-channels achieve such highly selective K+-ions transport rate. The first, a so-called canonical model championed in 2001 by Nobel laureate Roderick Mackinnon, M.D., proposes that water and K+-ions cross the cell membrane in a single file and alternate manner. Mackinnon’s model also proposes that the region of the channel that binds the K+-ions — four ions in total — can exist in two alternating ion-bound configurations: the 1,3 (i.e., K-W-K-W) and the 2,4 ion (i.e., W-K-W-K) configurations.
However, Cuello said Bert de Groot, Ph.D., put forth a model in 2014 known as the direct knock-on mechanism that challenges that of Mackinnon. The de Groot model proposes that four K+-ions within the channel selectivity filter establish direct contact within each other while crossing the cell membrane moving in single file without intervening waters.
“This topic of research has reemerged as a highly controversial one and requires further attention from a fresh and different vantage point,” Cuello explained. “Therefore, we have approached this problem by engineering a mutant channel that could isolate selectively one of the proposed ion-bound configurations, which placed us in a unique position to provide a solid answer to a long-standing question.”
Cuello said his laboratory has provided a solid experimental demonstration in favor of Mackinnon’s canonical model by engineering a mutant channel that selectively isolates the 2,4-ion bound configuration of the selectivity filter of a K+-channel. This provided the Cuello lab with a vantage point to develop a structural snapshot that demonstrates the existence of one of the two ion-bound configurations proposed by the canonical model.
Cuello hypothesized that if the four observed K+-ions bound to a K+-channel selectivity filter is the result of the coexistence of two equally occurring alternating ion-bound configurations (i.e., 1,3 and 2,4) then it should be possible to engineer a channel mutant that will bias the equilibrium between the two configurations and selectively isolate one of them.
“We have solved the crystal structure of two mutant potassium channels — KcsA-G77A and G77C — that precisely proved our hypothesis and allowed us to take a picture at atomic resolution, for the first time ever, of the 2,4-ion bound configuration of the K+-channel selectivity filter,” Cuello said. “We are proposing that our experimental results are proving that K+-ions move in a single file, with intervening water molecules, as it was originally proposed by Dr. Mackinnon in 2001.”
Cuello credited a small group of scientists from TTUHSC’s Center for Membrane Protein Research and his Department of Cell Physiology and Molecular Biophysics colleagues for working with him to complete the published research.
“Cholpon Tilegenova, a Ph.D. student in my laboratory, was the leading author in this research article since she generated the very high-resolution crystal structures of G77 mutant channels as part of her Ph.D. dissertation work,” Cuello said. “Additionally, this work would not be possible without the invaluable participation of Marien Cortes, Nermina Jahovic, Emily Hardy, Parameswaran Hariharan and my colleague, Dr. Lan Guan, who worked very hard in the functional and thermodynamic characterization of these mutant channels. Finally, I would like to knowledge Dr. Alain Labro, Dr. Luis Reuss and Dr. Guillermo Altenberg for their invaluable advice and critical thinking during the execution of this project.”
Health24.com | There’s something in the air – as pollution gets worse, the prevalence of mental health conditions may rise
As air quality declines, the prevalence of mental health conditions may rise, a large, new study suggests.
Looking at data on millions of people in the United States and Denmark, researchers found correlations between air pollution exposure and rates of certain psychiatric disorders. In both countries, poorer air quality was linked to a slightly heightened risk of bipolar disorder.
No conclusive answers
And in Denmark – where childhood data was available – people who were exposed to polluted air in the first 10 years of life had increased risks of depression, schizophrenia and personality disorders.
The big caveat: None of that proves air pollution is to blame.
“These are only correlations,” said Dr John Ioannidis, a professor of medicine at Stanford University in California. “Inherently, data like these will never give you conclusive answers.”
Ioannidis wrote an editorial published with the study in the journal PLOS Biology.
At this point, he said, the findings are an “interesting observation” that can spur more research.
“If there really is a link, that would be very important,” Ioannidis said.
Brain inflammation
Andrey Rzhetsky, senior researcher on the study, agreed that the findings point to an association – and are not proof of cause and effect.
But animal research has offered clues about how polluted air might affect mental health, according to Rzhetsky, a professor in the departments of medicine and human genetics at the University of Chicago.
It’s been shown, for example, that fine particles in air pollution can travel to the rodent brain via the nose. And lab animals exposed to air pollutants have shown signs of brain inflammation, along with impaired learning and memory, as well as depression-like behaviour.
Ioannidis, however, cautioned against making too much of the animal research.
“You can find biology to explain whatever you want,” he said. But that doesn’t prove it’s actually happening in humans.
For the current study, Rzhetsky’s team mined data on two large populations to look for links between pollution and psychiatric conditions.
Stronger associations in Denmark
For the US portion, the investigators looked at health insurance claims for more than 151 million Americans – noting mental health diagnoses made between 2003 and 2013. They had no way to gauge people’s personal exposure to air pollution. But they did have information on air quality in each person’s county of residence – for the years 2000 to 2005.
The researchers broke those counties into seven groups (or septiles) based on air pollution. Overall, the prevalence of bipolar disorder was about 29% higher in the most-polluted group of counties, compared to the group with the cleanest air.
The Denmark data, meanwhile, showed stronger associations. There, Rzhetsky’s team had enough information to estimate childhood air-pollution exposure for nearly 1.5 million people born between 1979 and 2002.
The investigators found that people exposed to air pollution during their first 10 years of life had increased risks of developing bipolar disorder, major depression, schizophrenia or a personality disorder by age 37.
Again, the biggest difference was between the septile living in the most polluted areas, versus those breathing the cleanest air: Their rates of schizophrenia and personality disorders were more than doubled, while their rate of depression was 50% higher and bipolar disorder 29% higher.
Overall, the Danish data provided a “stronger signal”, Rzhetsky said. But does that mean that childhood exposure to air pollution during early brain development is more important than adulthood exposure?
At this point, it’s unclear, Rzhetsky said.
Many other exposures
The findings leave many unanswered questions, according to Ioannidis.
“Is it childhood exposure to air pollution that matters?” Ioannidis said. “Is it bad, no matter when you’re exposed? Or does it make no difference at all?”
That final question touches on the broader issue. Psychiatric disorders are complex, Ioannidis pointed out: They involve a mix of genetic vulnerability and a range of environmental influences.
And people living in the most polluted areas may have many other exposures that set them apart from people who breathe the cleanest air, Ioannidis said.
It’s not possible, of course, to conduct a trial where people are assigned to live in polluted areas. But, Rzhetsky said, there are other ways to approach the cause-and-effect question: For example, studies might look at whether the prevalence of mental health diagnoses goes down after air quality improves.
It will be important to figure out whether air pollution is, in fact, a contributor, Rzhetsky said, because air quality is something we can change.
Ioannidis made another point: There are already plenty of reasons to want cleaner air, since poor air quality is strongly linked to heart and lung disease, and to higher mortality.
“Air pollution is not good for us,” Ioannidis said. “We know that.”
Image credit: iStock
