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Author – Dr Amit Verma, Molecular Oncologist and Cancer Geneticist.

Affiliation – Dr AV Cancer Institute of Personalized Cancer Therapy and Research, Gurgaon.

Lung cancer patients are more likely to contract COVID-19 as they already have diminished lung capacity due to the damage caused by cancer. Consequently, COVID-19 can put additional strain on their lungs, and the chances of experiencing respiratory issues are also severe in such cases. In addition, a lot of cancer patients have a higher risk of developing infections in the first place.

This may be the result of cancer or the treatment that the patient undergoes. For instance, mucus in their lungs aids in the capture of bacteria. Their body then coughs these bacteria out. A lung tumour may interfere with mucus outflow and increase infection risk. Some cancer treatments can also impair immune function, increasing the patients’ susceptibility to infections. However, in general, COVID-19-related effects that lung cancer patients may experience are comparable to those that affect the general population.

These may consist of pneumonia, a secondary bacterial or viral infection, blood clots that could be dangerous, apart from acute respiratory distress syndrome that may harm to further organs, such as the kidneys, liver, and heart. Additionally, COVID-19 may result in long-term difficulties. Damage to the lungs and other organs can also take time to heal, especially for those with cancer. 

What is COVID-19 treatment for persons with lung cancer?

The Food and Drug Administration has approved a number of medications to assist treat COVID-19 in individuals at serious risk of getting extremely unwell, in addition to supportive care and symptom management.Antivirals and monoclonal antibodies are two general groups for these therapies. Antiviral medications stop the virus’s growth inside your body. Remdesivirand molnupiravir are two examples. Your immune system is assisted in battling the infection by monoclonal antibodies. Covid 19 implications also has effects on lung cancer treatment like the long term side effect such as Interstitial Lung Disease (ILD). Patients suffering from ILD cannot be administered with immunotherapy which is a choice of treatment for many eligible lung cancer patients.

How to minimise the risk of catching COVID-19 infection?

The best approach to safeguard someone against COVID-19 in case of lung cancer is to get them immunised. Most significantly, should that person become ill, that will reduce his/her risk of developing a serious illness or passing away.Additional defence strategies include putting on a mask when in public, retaining physical distance while in public or avoid densely populated/poorly ventilated places, maintaining good hygiene and frequently cleaning hands adequately.

On World Hand Hygiene Day, WHO is highlighting the urgent need for countries in the South-East Asia Region and across the world to rigorously implement hand hygiene at the point of health care delivery, accelerating progress made throughout the COVID-19 response. The theme of this year’s event – ‘Accelerate action together’ – emphasizes the critical role that strong and engaged communities of health and care workers, policy makers and civil society organizations must play in galvanizing action to prevent infections and antimicrobial resistance (AMR) in health care.

Globally, inadequate hand hygiene at the point of care is a major contributor to health care-associated infections (HAIs). HAIs affect an estimated 15 out of every 100 patients in low- and middle-income countries, killing around 1 in every 10 of those affected. They are a major cause of AMR, which occurs when bacteria, viruses, fungi and parasites change over time and no longer respond to medicines, making infections harder to treat and increasing the risk of disease spread, severe illness and death.

Inadequate hand hygiene in health care is primarily caused by limited awareness of and access to safe water, sanitation and hygiene (WASH) in health care facilities. Globally, 1 in 8 health care facilities has no water service, one in 5 has no sanitation service, and one in 6 has no hand hygiene facilities at the points of care. At present, six countries of the Region ensure that at least 60% of health care facilities provide basic WASH services, and the same number of countries are implementing the WHO/UNICEF WASH FIT tool, which all countries should urgently adopt.

Momentum continues to build, in accordance with the Region’s Flagship Priorities on achieving universal health coverage (UHC), preventing and combating AMR, and accelerating reductions of maternal, neonatal and under-five mortality. Since 2016, all countries of the Region have implemented the Region’s Strategy for Patient Safety 2016–2025, which covers all core aspects of quality of care, patient safety and infection prevention and control (IPC). The Strategy is aligned with the Global Patient Safety Action Plan 2021–2030.

Throughout the COVID-19 response, key stakeholders in the Region participated in an array of WHO-supported IPC trainings, as well as a Regional consultation aimed at aligning key interventions with the Global Patient Safety Action Plan. In October 2022, WHO conducted a Regional capacity-building workshop on WASH, climate resilience and the environmental sustainability of health care facilities. Actionable guidance was provided on implementing the WASH FIT tool and the Eight Practical Steps to Achieve Universal Access to Quality of Care.

Across the Region, countries continue to intensify action to improve quality of care, patient safety and IPC at the primary health care (PHC) level, in line with the recommendations of another WHO-supported meeting in October 2022, as well as the Region’s overall focus on reorienting health systems towards quality, accessible, affordable and comprehensive PHC to build health system resilience and achieve UHC.

Today, WHO has several messages. First, to health and care workers: Perform hand hygiene at the point of care, when it is needed, according to the WHO ‘5 Moments for Hand Hygiene’ and using the appropriate technique. Second, to IPC practitioners: Lead the way for clean hands, providing actionable resources and feedback to health and care workers for immediate improvement.

Third, to policy makers: Invest in hand hygiene as a priority patient safety intervention, ensuring dignity of care and increasing health care efficiency. Fourth, to people who access health care: Observe hand hygiene in health facilities and join WHO’s global Hand Hygiene for All initiative, which highlights how everyone, everywhere can promote hand hygiene in schools, workplaces and other institutional settings. Increased society-wide uptake of adequate and regular hand hygiene – including in the home – will reduce morbidity from a range of communicable diseases, not least diarrhoea and respiratory infections.

In the shadow of the COVID-19 crisis, Region-wide improvements in hand hygiene must be sustained and accelerated. For that, communities of actors in health care and civil society must come together to identify gaps, challenges and opportunities at the point of care, with a focus on avoiding duplication and fragmentation, and maximizing resource efficiency. Operational research should support these endeavours and will also help countries develop and maintain fully costed hand hygiene roadmaps.

On World Hand Hygiene Day, WHO reiterates its commitment to ‘Accelerate action together’, in all countries of the Region, to implement hand hygiene at the point of health care delivery, for fewer HAIs, reduced AMR, and safer, more effective and efficient health care facilities for all.

MIT engineers have designed a new nanoparticle sensor that could detect early diagnosis of cancer with a simple urine test. The sensors, which can diagnose many different cancerous proteins, could also be used to distinguish the type of a tumour or how it is responding to treatment.

The nanoparticles are designed so that when they encounter a tumour, they shed short sequences of DNA that are excreted in the urine. Analyzing these DNA “barcodes” can reveal distinguishing features of a particular patient’s tumour. The researchers designed their test so that it can be performed using a strip of paper, similar to an at-home Covid test, which they hope could make it affordable and accessible to as many patients as possible.

“We are trying to innovate in a context of making technology available to low- and middle-resource settings. Putting this diagnostic on paper is part of our goal of democratizing diagnostics and creating inexpensive technologies that can give you a fast answer at the point of care,” says Sangeeta Bhatia, the John and Dorothy Wilson Professor of Health Sciences and Technology and of Electrical Engineering and Computer Science at MIT and a member of MIT’s Koch Institute for Integrative Cancer Research and Institute for Medical Engineering and Science.

In tests in mice, the researchers showed that they could use the sensors to detect the activity of five different enzymes that are expressed in tumours. They also showed that their approach could be scaled up to distinguish at least 46 different DNA barcodes in a single sample, using a microfluidic device to analyze the samples.
Bhatia is the senior author of the paper, which appears today in Nature Nanotechnology. Liangliang Hao, a former MIT research scientist who is now an assistant professor of biomedical engineering at Boston University, is the lead author of the study.

DNA barcodes

For several years, Bhatia’s lab has been developing “synthetic biomarkers” that could be used to diagnose cancer. This work builds on the concept of detecting cancer biomarkers, such as proteins or circulating tumour cells, in a patient’s blood sample. These naturally occurring biomarkers are so rare that it’s nearly impossible to find them, especially at an early stage, but synthetic biomarkers can be used to amplify smaller-scale changes that occur within small tumours.
In previous work, Bhatia created nanoparticles that can detect the activity of enzymes called proteases, which help cancer cells to escape their original locations, or settle into new ones, by cutting through proteins of the extracellular matrix. The nanoparticles are coated with peptides that are cleaved by different proteases, and once these peptides are released into the bloodstream, they can then be concentrated and more easily detected in a urine sample.
The original peptide biomarkers were designed to be detected based on small engineered variations in their mass, using a mass spectrometer. This kind of equipment might not be available in low-resource settings, so the researchers set out to develop sensors that could be analyzed more easily and affordably, using DNA barcodes that can be read using CRISPR technology.

For this approach to work, the researchers had to use a chemical modification called phosphorothioate to protect the circulating DNA reporter barcodes from being broken down in the blood. This modification has already been used to improve the stability of modern RNA vaccines, allowing them to survive longer in the body.
Similar to the peptide reporters, each DNA barcode is attached to a nanoparticle by a linker that can be cleaved by a specific protease. If that protease is present, the DNA molecule is released and free to circulate, eventually ending up in the urine. For this study, the researchers used two different types of nanoparticles: one, a particle made from polymers that have been FDA-approved for use in humans, and the other a “nanobody” — an antibody fragment that can be designed to accumulate at a tumour site.

Once the sensors are secreted in the urine, the sample can be analyzed using a paper strip that recognizes a reporter that is activated by a CRISPR enzyme called Cas12a. When a particular DNA barcode is present in the sample, Cas12a amplifies the signal so that it can be seen as a dark strip on a paper test.
The particles can be designed to carry many different DNA barcodes, each of which detects a different type of protease activity, which allows for “multiplexed” sensing. Using a larger number of sensors provides a boost in both sensitivity and specificity, allowing the test to more easily distinguish between tumour types.

Disease signatures

In tests in mice, the researchers showed that a panel of five DNA barcodes could accurately distinguish tumours that first arose in the lungs from tumours formed by colorectal cancer cells that had metastasized to the lungs.
“Our goal here is to build up disease signatures and to see whether we can use these barcoded panels not only read out a disease but also to classify a disease or distinguish different cancer types,” Hao says.

For use in humans, the researchers expect that they may need to use more than five barcodes because there is so much variety between patients’ tumours. To help reach that goal, they worked with researchers at the Broad Institute of MIT and Harvard led by Harvard University Professor Pardis Sabeti, to create a microfluidic chip that can be used to read up to 46 different DNA barcodes from one sample.

This kind of testing could be used not only for detecting cancer, but also for measuring how well a patient’s tumor responds to treatment and whether it has recurred after treatment. The researchers are now working on further developing the particles with the goal of testing them in humans. Glympse Bio, a company co-founded by Bhatia, has performed phase 1 clinical trials of an earlier version of the urinary diagnostic particles and found them to be safe in patients.

In addition to Bhatia, Hao, and Sabeti, the study’s co-authors include Renee T. Zhao, Nicole L. Welch, Edward Kah Wei Tan, Qian Zhong, Nour Saida Harzallah, Chayanon Ngambenjawong, Henry Ko, and Heather E. Fleming.
The research was funded by the Koch Institute Support (core) Grant from the National Cancer Institute, a Core Center Grant from the National Institute of Environmental Health Sciences, the Marble Center for Cancer Nanomedicine at the Koch Institute, the Koch Institute Frontier Research Program, the Virginia and D.K. Ludwig Fund for Cancer Research, and a Pathway to Independence Award from the National Cancer Institute.

According to a recent study, having both diabetes and tooth loss correlates to lower cognitive function and quicker cognitive decline in older persons.

The findings of the study published in a special edition of the Journal of Dental Research focused on ageing and oral health. “Our findings underscore the importance of dental care and diabetes management for older adults in reducing the devastating personal and societal costs of Alzheimer’s disease and other related dementias,” said Bei Wu, vice dean for research at NYU Rory Meyers College of Nursing and co-director of the NYU Aging Incubator, as well as the study’s lead author.

Diabetes is a known risk factor for cognitive decline and dementia. Several of the hallmarks of diabetes–high blood sugar, insulin resistance, inflammation, and related heart disease–are thought to contribute to changes in the brain.
A growing body of research has revealed a similar connection among poor oral health, particularly gum disease and tooth loss, and cognitive impairment and dementia. Like diabetes, inflammation plays a key role gum disease, and these inflammatory processes may contribute to cognitive decline. In addition, painful gums and missing teeth can make it difficult to chew, leading to changes in diet that can result in nutritional deficiency. Nutritional deficiency, which can also be worsened by impaired glucose tolerance and insulin sensitivity in diabetes, is another risk factor for cognitive impairment and dementia.

“Poor oral health, diabetes, and cognitive decline are all connected, and we’re beginning to understand how they may influence and exacerbate one another,” said Wu.

While both diabetes and missing teeth are risk factors for dementia, little research has focused on the effects of having both conditions in the course of cognitive decline. To address this gap, Wu and her colleagues turned to the University of Michigan’s Health and Retirement Study, analyzing 12 years of data (2006-2018) from the longitudinal study in order to observe cognitive changes over time.

The researchers included 9,948 older adults who were grouped by age (65 to 74, 75 to 84, and 85 and older) in their analysis. The Health and Retirement Study included measures of memory and cognitive function, assessed every two years, along with questions about tooth loss, diabetes, and other health and demographic factors. In this analysis, the researchers were particularly interested in older adults who had lost all of their teeth.

They found that older adults aged 65 to 84 with both diabetes and complete tooth loss had worse cognitive function than their counterparts without either condition. Over time, older adults aged 65 to 74 with diabetes alone experienced accelerated cognitive decline, and those aged 65 to 84 without any teeth also experienced accelerated cognitive decline, but older adults aged 65 to 74 with both diabetes and complete tooth loss had the fastest rate of cognitive decline.

The relationship among diabetes, tooth loss, and cognitive decline was inconclusive for adults 85 and older, which may be explained by this group having overall greater cognitive impairment, potentially being healthier (as unhealthy individuals may be less likely to survive into their late 80s), or perhaps having more experience managing their diabetes.
For older adults with both poor oral health and diabetes, the researchers stress the importance of regular dental visits, adherence to diabetes treatment and self-care to control blood sugar levels, and cognitive screenings in primary care settings.

“Access to dental care for older adults–especially those with diabetes–is critical, and health care providers should educate their patients about the connection between oral health and cognition,” said Wu.

Several distinct groupings of neurons connected inside and across critical parts of the brain assist learning, remembering, and retrieving memories. A recent study led by the universities of Bristol and Heidelberg discovered that if these neuronal assemblies fail to sync up at the correct time, memories are lost.

How do you keep track of what to do next? What happens in the brain when your mind goes blank? Short-term memory relies on two key brain regions: the hippocampus and the prefrontal cortex. The researchers set out to establish how these brain regions interact with one another as memories are formed, maintained and recalled at the level of specific groups of neurons. The study, published in Currently Biology, also wanted to understand why memory sometimes fails. “Neural assemblies” — groups of neurons that join forces to process information — were first proposed over 70 years ago, but have proved difficult to pinpoint.

Using brain recordings in rats, the research team has shown that memory encoding, storage and recall are supported by dynamic interactions incorporating multiple neural assemblies formed within and between the hippocampus and prefrontal cortex. When the coordination of these assemblies fails, the animals made mistakes.

Dr Michal Kucewicz, Assistant Professor of Neurology at the Gdansk University of Technology, formerly a PhD student at the University of Bristol, and lead author, said: “Our results make potential therapeutic interventions for memory restoration more challenging to target in space and time. On the other hand, our findings have identified critical processes that determine success or failure in remembering. These present viable targets for therapeutic interventions on the level of neural assembly interactions.”

Matt Jones, Professor of Neuroscience in the School of Physiology, Pharmacology and Neuroscience and Bristol Neuroscience and senior author of the paper, added: “Our findings add to evidence that the neural substrates of memory are more distributed in anatomical space and dynamic across time than previously thought based on the neuropsychological models.”

The next steps for the research would be to modulate neural assembly interactions, either using drugs or via brain stimulation, which Dr Kucewicz is currently doing in human patients, to test whether disrupting or augmenting them would impair or enhance remembering. The research team presumes the same mechanisms would work in human patients to restore memory functions impaired in a particular brain disorder.

According to a daily bulletin released on Saturday by the Ministry of Health and Family Welfare, India recorded 7,171 new Covid-19 cases in the last 24 hours, approximately 362 fewer than the count reported yesterday. In the last two days, the number of Covid-19 positive cases has decreased. According to official records, approximately 9,355 cases of Covid-19 were reported on Thursday, with the country recording 7,533 cases on Friday.

According to Health Ministry data, the total number of active cases in the country has dropped to 51,314 from 53,852 previously. The daily positivity rate is 3.69%, while the weekly positivity rate is 4.72 percent. According to the Health Ministry, 92.64 crore Covid-19 tests have been performed so far, with 1,94,134 tests performed in the last 24 hours.
According to the Ministry, 3,875 doses of vaccine have been administered in the last 24 hours, with a recovery rate of 98.70%.

According to the Union Ministry of Health and Welfare, the Nationwide Vaccination Drive has resulted in the administration of 220.66 crore total vaccine doses, including 95.21 crores of Second Doses and 22.87 crores of Precaution Doses.
Meanwhile, medical experts have warned that the new XBB1.16 variant has the potential to bypass people’s immune systems, and the next four weeks are critical.

Dr. Randeep Guleria, former director of AIIMS in Delhi, stated that while the country is experiencing a new surge in Covid-19 infections, the situation is not alarming. “Covid-19 cases have been on the rise across the country. But the majority of the infections are mild. The rate of hospitalisation hasn’t gone up either. It’s not a panic-like situation yet,” Guleria told ANI.

India reported 7,533 new Covid-19 cases and 11,047 recoveries in the last 24 hours with the active cases now standing at 53,852 on Friday, according to the Ministry of Health and Family Welfare.

Active cases stand at 0.12 per cent of the total cases reported in the country. Having 11,047 recoveries in the last 24 hours, India’s total recovery increased to 4,43,47,024 with the recovery stand at 98.68 per cent. Taking the daily positivity rate to 3.62 per cent.

Under the nationwide Vaccination Drive, India has so far administered 220.66 crore Covid vaccine doses (95.21 cr second dose and 22.87 cr precaution dose), of which 4,775 doses were administered in the last 24 hours.

A total of 92.63 crore tests conducted so far with 2,08,112 tests conducted in the last 24 hours, the ministry said.

A recent study from Cedars-Sinai’s Smidt Heart Institute suggests that prolonged COVID-19 may be caused by immune system dysfunction. The study, published in BMC Infectious Diseases, discovered that people with long COVID-19 produced antibodies against the virus that causes COVID-19 for months longer than expected after receiving the COVID-19 vaccine.

When a person is infected, the immune system usually responds by producing antibodies that prevent germs from entering cells. Vaccines mimic an infection so that the body’s immune system knows when it encounters a virus to release specific antibodies. When the suspected infection is gone, the immune system eventually stops producing antibodies in both cases.

“There’s general consensus that some level of aberrant immune response happens in long COVID-19, and this study adds to the evidence to suggest this is true,” said Catherine Le, MD, co-director of the Cedars-Sinai COVID-19 Recovery Program and a senior author of the study.

Long COVID-19 is a condition in which people experience COVID-19-related symptoms three months or more after being infected with the virus that causes COVID-19. It is estimated that 65 million people worldwide suffer from Long COVID-19. Fatigue, shortness of breath, and cognitive dysfunction such as confusion and forgetfulness are common symptoms. Some symptoms can be incapacitating.

Researchers analysed blood samples from 245 people diagnosed with long COVID-19 and 86 people who had COVID-19 and recovered to study the immune response of people with long COVID-19. All participants in the study had either one or two doses of a COVID-19 vaccine regimen.

“We examined one part of the immune system response, the production of antibodies, which is mediated by immune cells called B-cells,” Le explained.

The researchers focused on two types of antibodies that attack the virus that causes COVID-19. One of these is the spike protein antibody, which targets a protein on the virus’s surface. The nucleocapsid antibody, on the other hand, attacks the part of the virus that allows it to replicate.

The researchers discovered that people with long COVID-19 had higher levels of spike protein and nucleocapsid antibodies than people without long COVID-19. Antibody levels in people without long COVID-19 began to decline eight weeks after receiving a dose of the COVID-19 vaccine, as expected. People with long COVID-19, on the other hand, had elevated antibody levels, particularly nucleocapsid antibodies.

“What you would expect after getting a COVID-19 vaccination is a jump in your spike protein antibody levels, but you wouldn’t expect a significant increase in nucleocapsid antibody levels,” said Susan Cheng, MD, MPH, the Erika J. Glazer Chair in Women’s Cardiovascular Health and Population Science, director of the Institute for Research on Healthy Aging in the Department of Cardiology at the Smidt Heart Institute, and a senior author of the study. “You would also expect these levels to eventually decrease and not persist for so long after vaccination.”

According to the study’s authors, while this study shows that long COVID-19 affects the immune system, it is too early to draw firm conclusions from these findings.

“Theoretically, the production of these antibodies could mean that people are more protected from infection,” Le said. “We also need to investigate if the elevated immune response corresponds with severity or number of long COVID-19 symptoms.”

Blood samples from people with long COVID-19 are still being studied by researchers. They hope to find a measurable molecule that can be used to diagnose long COVID-19 and learn more about the biological processes that cause it.

Insulin is a critical treatment for type 1 diabetes and, in many cases, type 2 diabetes as well. According to the American Diabetes Association, approximately 8.4 million Americans use insulin. A team of scientists from the University of California San Diego School of Medicine, along with colleagues from other institutions, describe a key player in the defence mechanism that protects us from excessive insulin in the body in a new study published in the online edition of Cell Metabolism on April 20, 2023.

“Although insulin is one of the most essential hormones, whose insufficiency can result in death, too much insulin can also be deadly,” said senior study author Michael Karin, PhD, Distinguished Professor of Pharmacology and Pathology at UC San Diego School of Medicine. A century of research has greatly advanced medical and biochemical understanding of how insulin works and what happens when it is deficient, but how potentially fatal insulin hyperresponsiveness is prevented has remained a persistent mystery.

“While our body finely tunes insulin production, patients who are treated with insulin or drugs that stimulate insulin secretion often experience hypoglycemia, a condition that if gone unrecognized and untreated can result in seizures, coma and even death, which collectively define a condition called insulin shock.”

Hypoglycemia (low blood sugar) is a leading cause of death among diabetics. Karin, Li Gu, PhD, a postdoctoral scholar in Karin’s lab, and colleagues describe “the body’s natural defence or safety valve” that reduces the risk of insulin shock in the new study. That valve is a metabolic enzyme known as fructose-1,6-bisphosphate phosphatase, or FBP1, which regulates gluconeogenesis, a process in which the liver synthesises and secretes glucose (the primary source of energy used by cells and tissues) during sleep to maintain a steady supply of glucose in the bloodstream.

Some diabetes medications, such as metformin, inhibit gluconeogenesis without apparent adverse effects. Children born with a rare genetic disorder that causes them to produce insufficient FBP1 can also be healthy and live a long life. When the body is starved for glucose or carbohydrates, an FBP1 deficiency can cause severe hypoglycemia. Convulsions, coma, and possibly death can occur in the absence of a glucose infusion. FPB1 deficiency, when combined with glucose deprivation, causes adverse effects unrelated to gluconeogenesis, such as an enlarged, fatty liver, mild liver damage, and elevated blood lipids or fats.

To better understand FBP1’s roles, researchers created a mouse model with liver-specific FBP1 deficiency that closely resembled the human condition. The mice, like FBP1-deficient children, appeared normal and healthy until fasted, when they developed the severe hypoglycemia, liver abnormalities, and hyperlipidemia described above. Gu and her colleagues discovered that FBP1 performed multiple functions. FBP1 not only played a role in the conversion of fructose to glucose, but it also inhibited the protein kinase AKT, which is the primary conduit of insulin activity.

“FBP1 basically keeps AKT in check and protects against insulin hyper-responsiveness, hypoglycemic shock, and acute fatty liver disease,” explained first author Gu.

Gu developed a peptide (a string of amino acids) derived from FBP1 that disrupted the association of FBP1 with AKT and another protein that inactivates AKT in collaboration with Yahui Zhu, a visiting scientist from Chongqing University in China and the study’s second author.

“This peptide works like an insulin mimetic, activating AKT,” said Karin. “When injected into mice that have been rendered insulin resistant, a highly common pre-diabetic condition, due to prolonged consumption of high-fat diet, the peptide (nicknamed E7) can reverse insulin resistance and restore normal glycemic control.”

Karin said the researchers would like to further develop E7 as a clinically useful alternative to insulin “because we have every reason to believe that it is unlikely to cause insulin shock.”

At least half of all autistic children exhibit aggressive behaviour, such as punching, kicking, or name-calling, while their parents are responsible for assisting them in coping and social integration. The prevalence and definition of aggressive behaviours in autistic children, on the other hand, are unknown. To fill this knowledge gap, researchers at the University of Arkansas’ Family and Community Intervention Lab compared autistic children to non-autistic children on various types of aggressive behaviours over three critical developmental periods and discovered that parents of autistic children reported more frequent aggression at higher intensities than non-autistic children.

“Aggression represents a pervasive and serious problem faced by autistic youths and their families,” said Lauren Quetsch, assistant professor of psychology and lead author of “Understanding aggression in autism across childhood: Comparisons with a non-autistic sample.”

“While our knowledge about the unique needs of autistic children has grown exponentially over the last several decades, we still have a long way to go,” she said. “And understanding the role aggression plays in autistic youths’ lives can help us to better address our gaps in care.”

Quetsch and her colleagues collected quantitative and qualitative data on 450 autistic and 432 non-autistic children between December 2020 and March 2021. The data was divided into three age groups: those under the age of six, those aged six to twelve, and those aged thirteen to seventeen. Across these critical developmental periods, the children were compared on multiple caregiver-reported measures of aggressive and disruptive behaviour.

The data analysis by the researchers revealed that autistic children had higher levels of verbal aggression and disruptive behavioural intensity across all three stages of development. Autistic children under the age of six were more aggressive than their non-autistic peers. However, as the children grew older, their levels matched those of their non-autistic peers.

According to the qualitative study, non-autistic children more frequently expressed anger in a controlled manner, whereas autistic children were more likely to lose their temper quickly.

“We surmise that this can be attributed to several factors,” Quetsch said. “Frustration from regularly being misunderstood, challenges with recognizing emotions in others or expressing their own emotions to others, sensory overstimulation, and even co-occurring health challenges, such as physical discomfort from gastrointestinal issues and exhaustion due to irregular sleeping patterns, all likely contribute to aggression.”

Cynthia Brown, assistant professor of psychology at Pacific University, Harlee Onovbiona and Rebecca Bradley, doctoral students in clinical psychology in Quetsch’s lab at the University of Alberta, Lindsey Aloia, associate professor of communication at the University of Alberta, and Stephen Kanne, clinical paediatric neuropsychologist at Weill Cornell Medicine, were co-authors on the study with Quetsch. Autism Research, the official journal of the International Society for Autism Research, published the researchers’ findings.