Monthly Archives: February 2022

Asano, T., Boisson, B., Onodi, F., Matuozzo, D., Moncada-Velez, M., Maglorius Renkilaraj, M., Zhang, P., Meertens, L., Bolze, A., Materna, M., Korniotis, S., Gervais, A., Talouarn, E., Bigio, B., Seeleuthner, Y., Bilguvar, K., Zhang, Y., Neehus, A. L., Ogishi, M., Pelham, S. J., Casanova, J. L. (2021). X-linked recessive TLR7 deficiency in ~1% of men under 60 years old with life-threatening COVID-19. Science Immunology, 6(62), eabl4348. https://doi.org/10.1126/sciimmunol.abl4348

Bastard, P., Gervais, A., Le Voyer, T., Rosain, J., Philippot, Q., Manry, J., Michailidis, E., Hoffmann, H. H., Eto, S., Garcia-Prat, M., Bizien, L., Parra-Martnez, A., Yang, R., Haljasmgi, L., Migaud, M., Srekannu, K., Maslovskaja, J., de Prost, N., Tandjaoui-Lambiotte, Y., Luyt, C. E., Casanova, J. L. (2021). Autoantibodies neutralizing type I IFNs are present in ~4% of uninfected individuals over 70 years old and account for ~20% of COVID-19 deaths. Science Immunology, 6(62), eabl4340. https://doi.org/10.1126/sciimmunol.abl4340

Bastard, P., Rosen, L. B., Zhang, Q., Michailidis, E., Hoffmann, H. H., Zhang, Y., Dorgham, K., Philippot, Q., Rosain, J., Bziat, V., Manry, J., Shaw, E., Haljasmgi, L., Peterson, P., Lorenzo, L., Bizien, L., Trouillet-Assant, S., Dobbs, K., de Jesus, A. A., Belot, A., Casanova, J. L. (2020). Autoantibodies against type I IFNs in patients with life-threatening COVID-19. Science, 370(6515), eabd4585. https://doi.org/10.1126/science.abd4585

Daniloski, Z., Jordan, T. X., Ilmain, J. K., Guo, X., Bhabha, G., tenOever, B. R., & Sanjana, N. E. (2020). The Spike D614G mutation increases SARS-CoV-2 infection of multiple human cell types. eLife, 2021;10, e65365. https://doi.org/10.7554/eLife.65365

Daniloski, Z., Jordan, T. X., Wessels, H. H., Hoagland, D. A., Kasela, S., Legut, M., Maniatis, S., Mimitou, E. P., Lu, L., Geller, E., Danziger, O., Rosenberg, B. R., Phatnani, H., Smibert, P., Lappalainen, T., tenOever, B. R., & Sanjana, N. E. (2021). Identification of required host factors for SARS-CoV-2 infection in human cells. Cell, 184(1), 92105.e16. https://doi.org/10.1016/j.cell.2020.10.030

Zhang, Q., Bastard, P., Liu, Z., Le Pen, J., Moncada-Velez, M., Chen, J., Ogishi, M., Sabli, I., Hodeib, S., Korol, C., Rosain, J., Bilguvar, K., Ye, J., Bolze, A., Bigio, B., Yang, R., Arias, A. A., Zhou, Q., Zhang, Y., Onodi, F., Casanova, J. L. (2020). Inborn errors of type I IFN immunity in patients with life-threatening COVID-19. Science, 370(6515), eabd4570. https://doi.org/10.1126/science.abd4570

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Decoding the Genetics Behind COVID-19 Infection - National Institutes of Health (NIH)

The team headed by Professor Huu Phuc Nguyen, Chair of Human Genetics at Ruhr-Universitt Bochum (RUB), and Professor Roland Schroers, Head of the Department of Haematology, Oncology, Stem Cell/Immune Therapy at the University Hospital Knappschaftskrankenhaus, published their findings in theInternational Journal of Canceron 22 January 2022.

Optical genome mapping involves the extraction of very long DNA molecules, for example routinely collected blood samples or bone marrow material from patients. These long DNA molecules are labelled with dye molecules at more than half a million different positions in the entire human genome and are then moving through ultrathin nanochannels on a special chip. As the DNA molecules move through the nanochannels, a laser is used to make them visible and they are photographed using a fluorescence microscope. The images of the entire genome are then analysed using bioinformatic analyses. The aim is to identify and interpret changes in genetic regions that are relevant for the development of cancer, explains Dr. Wanda Gerding from the Bochum Department of Human Genetics.

Optical genome mapping thus facilitates genome-wide analysis of regions that are important for the classification and therapy of leukaemias using one methodology. Furthermore, it also allows the identification of new relevant genomic regions and new genes.

In the current study, the team compared the methodology to current standard diagnostics in patients with acute myeloid leukaemia as well as myelodysplastic syndromes. The researchers showed that the results obtained by optical genome mapping methodology were concordant in 93 per cent of samples compared toa conventional methodology, the so-called cytogenetic karyogram, where whole chromosomes are visualized. In 67 per cent of the samples, it was even possible to obtain additional genetic information.

The methodology can thus not only detect structural changes in the genome more accurately, but also has the potential to become an important component of routine diagnostics for patients with leukaemia. As a further benefit, genome research can provide data and new insights for further research work in the field of tumour biology, says Wanda Gerding.

For the project, the Human Genetics Department at RUB, headed by Professor Huu Phuc Nguyen, cooperated with the Haematology, Oncology, Stem Cell and Immunotherapy Department of the Knappschaftskrankenhaus Bochum, headed by Professor. Roland Schroers, a member of the Centre for Haematooncological Diseases (ZHOE) at RUB, and Professor Peter Reimer from the Haematology, Internal Oncology and Stem Cell Transplantation Department at Evangelische Kliniken Essen-Mitte. The close scientific cooperation of both departments was ensured by Dr. Deepak Vangala, Dr. Wanda Gerding, Dr. Verena Nilius-Eliliwi (funded by the Female Clinical Scientist programme of the RUB Medical Faculty) and medical student Marco Tembrink (Human Genetics, medical doctoral scholarship holder from FoRUM, Medical Faculty of the RUB (FoRUM RUB). The project received a positive vote from the Ethics Committee of the RUB Medical Faculty (No. 20-7063).

Reference:GerdingM, Tembrink M, Nilius-Eliliwi V, et al. Optical genome mapping reveals additional prognostic information compared to conventional cytogenetics in AML/MDS patients. Int. J. Cancer Res.2022. doi: 10.1002/ijc.33942

This article has been republished from the following materials. Note: material may have been edited for length and content. For further information, please contact the cited source.

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More Precise Information on the Genetic Basis of Leukemia - Technology Networks

Very low concentrations of the popular organic insecticide Spinosad have profound effects on beneficial insect species, including vision loss and neurodegeneration, new research led by the University of Melbourne and Baylor College of Medicine has found.

The study, published in eLife, used the vinegar fly Drosophila to analyse the impact of chronic exposure to low concentrations (0.2 parts per million) of Spinosad and the resulting physiological impacts on the brain and other tissues.

Spinosad is commonly used to control insect pests, including thrips, leafminers, spider mites, mosquitoes, ants and fruit flies, in both commercial and domestic settings.

Within a matter of 20 days, tiny doses of Spinosad can have an alarming impact on the brains of adult Drosophila. Observing sections of brain tissue under microscope demonstrated there was an average of 17% of the fly brains destroyed due to exposure, said Dr. Felipe Martelli from Monash University, who completed this work as part of his Ph.D. at the University of Melbourne. Neurons that serve vital functions die, leaving large vacuoles, fluid-filled sacs, in the brain. This leads to neurodegeneration, blindness and behavioural changes in adult vinegar flies. Due to the Drosophilas genetic and biochemical similarities to other insects, the research indicates that these impacts could be translated to other beneficial insects such as bees, Martelli said.

As a natural substance made by a soil bacterium, Spinosad is often thought to be less harmful to beneficial insects and is frequently used as an alternative to synthetic insecticides, according to study co-author, Professor Philip Batterham, from the School of BioSciences and Bio21 Institute at the University of Melbourne.

There is often an assumption that organic equates to safer, but our study finds this isnt the case, Batterham said. Spinosad is now registered for use in over 80 countries, and it poses a far greater risk to beneficial insects than previously thought. Concerningly, the low concentration levels used in this study is what would be commonly found in groundwater or in the air through incidental exposure.

Based on earlier work by our research group using similar techniques to this study, Spinosad was found to have a much greater negative impact on vinegar flies at far lower doses than imidacloprid, a synthetic insecticide that has been banned in Europe for its impacts on non-target insects including honeybees, Batterham said.

While this study does not aim to pin the blame on Spinosad, it does show that having an organic label doesnt always mean safer. All insecticides, no matter their source, need to be rigorously studied for any unintended ecological impacts, Batterham said.

Martellis research was enhanced by the opportunity to do experiments in the lab of a global leader in neuroscience, Dr. Hugo Bellen, corresponding author and distinguished service professor of molecular and human genetics at Baylor.

The striking biological features that are associated with low levels of Spinosad resemble some slow progressive neurological diseases in which lysosomes are expanded, also called Lysosomal Storage Disease. These genetic diseases have also been associated with Parkinsons Disease, and there are interesting similarities in the pathogenic mechanisms caused by mutations in these genes and Spinosad, Bellen said.

A collaboration between the University of Melbourne, Baylor College of Medicine and the University of Texas, this study adds to a growing body of evidence indicating that insecticides are contributing to the global decline in population sizes of many beneficial insect species.

Large-scale insecticide application is a primary weapon in the control of insect pests in agriculture but we know that around the world, insect populations are decreasing in size by about 1% each year; this decrease is largely in insects that are not pests, Batterham said.

When you look at insect species disappearing, it's almost like randomly pulling blocks out of a Jenga tower; its destabilizing ecosystems making them vulnerable to collapse.

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An organic insecticide is more damaging to non-target insects than synthetic counterparts - Baylor College of Medicine News

54gene, the health technology company advancing African genomics research for improved global health outcomes, has announced the awarding of $64,000 in scholarships to four PhD candidates in Nigeria, Uganda and South Africa. Through the African Centre for Translational Genetics (ACTG), a non-profit initiative launched by 54gene in February 2020, the grants awarded will be used to further develop translational genomics research capacity across Africa and will cover all expenses of the recipients during their postgraduate study.

The ACTGs mission is to invest in the continents health ecosystem by empowering the next generation of African genomics scientists through the provision and implementation of scholarships, grants, fellowships, internships and training programmes. The PhD scholarship awards were the primary focus for the ACTG in 2021. Following a three month pan-African call for applications and a rigorous selection process, four successful recipients were handpicked from a total of 46 applications and were awarded grants to advance their genomics research studies in the areas of cardiometabolic diseases, cancers, neurological diseases and sickle cell disorders. The four candidates that have now been awarded the PhD scholarships are studying at different institutions spread across Africa two are based at Makerere University, Uganda, one at the University of Pretoria, South Africa and the last awardee is based at Covenant University in Nigeria.

Gomera, Rejoice University of Pretoria, South Africa

Kintu, Christopher Makerere University, Uganda

Onyia, Abimbola Covenant University, Nigeria

Soremekun, Chisom Makerere University, Uganda

54gene, through the ACTG in 2020, launched the NCD-GHS Consortium composed of Nigerian geneticists in partnership with the Nigerian Institute of Medical Research (NIMR) and the National Biotechnology Development Agencys Center for Genomics Research and Innovation (NABDA-CGRI). Preliminary findings from the Consortiums landmark study into non-communicable and cardio-metabolic diseases were shared at the American Society of Human Genetics Conference in October 2021. The study found seven distinct clusters among the 50 under-studied ethnolinguistic groups in Nigeria with some groups showing evidence of shared genomic regions with northern African and European groups. In comparison to European populations, the study also replicated previous research showing lower levels of Neanderthal genome sharing in Nigerian groups.

Speaking on the scholarships, Dr. Abasi Ene-Obong, CEO of 54gene, said, Developing the next generation of genomic scientists is critical in ensuring that the knowledge, resources and insights derived from homegrown research benefits not only Africans but the global population. Access to funding as well as to our international team of genetic and biomedical specialists is a unique opportunity for these talented African researchers who, like us, want to unlock the boundless potential offered by the human genomic diversity of African populations. The funding and available resources will put them at par with their counterparts in developed countries and make them more confident in leading future research studies.

With over $45 million in investment raised by the company since its launch, the PhD candidates will receive up to $4,000 annually for four years, to cover tuition fees and living expenses. Recipients will have the opportunity to work alongside leading researchers at 54gene and its partner institutions (NIMR and CGRI), who are experts in genomic data science, bioinformatics and molecular genetics. Recipients will also be given access to state-of-the-art genomic technologies and the opportunity to co-publish novel findings in collaboration with these leading scientists. PhD candidates will also be given the opportunity to work with 54genes partner institutions post-graduation.

Aminu Yakubu, VP Research Governance and Ethics at 54gene and ACTG representative said, There is incredible African talent in the genomics space, but opportunities to undertake research and conduct desired tests is limited due to inadequate infrastructure. Supporting and powering pan-African genomics research, especially for non-communicable diseases, has been a key impact marker for 54gene since the company launched in 2019. This is why we are thrilled to offer these outstanding researchers the opportunity to carry out ground-breaking research that will contribute to future health outcomes and benefit the field of genomics research on the continent and also globally.

Prof. Babatunde Salako, Chairman NCD-GHS Steering Committee and Director-General, Nigerian Institute of Medical Research (NIMR), said, Despite the global health crisis of the past two years, genomic science has not ceased to be important, nor have our scientists allowed their thirst for ground-breaking research to become extinguished. It has been a great pleasure to serve the committee by reviewing the 46 applicants, who are some of the brightest minds on the continent. This initiative is also a massive win for Africa as we deepen our efforts to become leaders in genomic research.

As 54gene expands its operations and partnerships in the coming years, the ACTG looks forward to equally expanding the coverage of its empowerment activities to reach more student scientists, junior and senior research scientists alike in academia and research institutes. Through these efforts, the ACTG is building on the giant precedent work undertaken by organizations like the Human Hereditary and Health in Africa (H3Africa) Consortium, and the African Academy of Sciences among others.

About 54gene

54gene is a health technology company centred on advancing the field of African genomics to unlock scientific discoveries as well as improve diagnostic and treatment outcomes within Africa and the global community. Founded in 2019, the company generates genetic insights from research cohorts in the worlds most diverse populations to improve the development, availability and efficacy of therapeutics and diagnostics that will prove beneficial to all populations.

About the ACTG

The ACTG is the African Centre for Translational Genetics. It is an entity designed by 54gene to facilitate precision medicine on the African continent, provide funding for translational genetics research by African scientists and re-invest in the health ecosystem by empowering the next generation of African genomic scientists through the provision and implementation of grants, internships and training for medical researchers and students.

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54gene's African Centre for Translational Genetics awards $64,000 scholarship to further genomics research - Ventures Africa

It's one of the most common medical conditions on the planet so why are the causes ofanxiety still such a mystery? Scientists are working tounravel them.

Ithappened in a split second, like a bone snapping under pressure.

One minute I was cooking dinner, monitoring babies, bath time, work emails, phone calls, deadlines and life admin. The next, the room was spinning.

I turned, and suddenly the floor began undulating beneath my feet. Negotiating the kitchen was like walking across the Turkey Trot at Coney Island. The walls fell in towards me.

I grabbed the bench to steady myself, but my fingers were tingling and there was a high-pitched ringing in my ears. Yet, I felt like I was trapped inside a glass box: sounds outside were muffled, my vision blurred, my heart racing.

There were no broken bones, but something else cracked that day, something inside my head.

I visited my doctor in a panic but despite the drama of my symptoms, the diagnosis was remarkably straightforward: "What you are describing is commonly felt by people experiencing anxiety," the doc told me gently.

Research suggests more than 25 per cent of us encounter a clinically significant episode of anxiety at some point in life.

For some, it is a fleeting experience like mine and manyanxiety sufferersrespond well to existing treatments including cognitive behaviour therapy or medication. Yet for others, anxiety can be a crippling and chronic disability impacting all areas of life without relief.

The COVID pandemic has supercharged the numbers, with GPs and psychologists reporting a spike in patients seeking help for anxious feelings.

And while researchers emphasise the complexity of the anxiety jigsaw puzzle which can lead to diagnoses including generalised anxiety disorderor obsessive compulsive disorder there are three key areas where cutting edge research is ushering in a new way forward.

No longer is anxiety viewed as arandom condition, as sudden and uncontrollable as the symptoms it can cause.

Instead, genetics, diet and knowledge ofhowtraumatic life events can affect brain structure and development are forging promising new approaches to understanding what causes anxiety, and how to treat it.

Lets break it down.

At the QIMR Berghofer Medical Research Institute in Queensland, PhD candidate Jackson Thorp an expert in psychiatric genetics has spent years hunting for a needle in a haystack.

At the Institute's Translational Neurogenomics Lab, Thorp is using a global database of 400,000 people to identify gene variants more common in anxiety sufferers.

Using statistical analysis software to cross-check the 20,000-25,000 genes in the human genome, Thorps work aims to identify gene changes more common in people with anxiety disorders.

And just last yearThorp and his colleagues hit the jackpot.

"We found 611 genes that were linked to anxiety and many of these are also linked to depression," he says.

"This tells us genetic risk for anxiety does not come from one or two genes but hundreds. Probably even thousands of genes are responsible for increasing the risk of developing anxiety."

Research like this is so new, so pioneering, that a full picture is yet to emerge about which genes are most significant and precisely how they influence anxietys development.

The next step is to understand their role in predisposing someone to anxiety or whether specific genetic mutations could even predict it.

One of the most interesting is a gene known as DRD2, responsible for coding a dopamine receptor in the brain. This neurotransmitter is released when we associate particular activities with pleasure and is related to mental health outcomes.

Yet with Thorps research showing so many genes associated with anxiety, the reality is most of us probably have at least some genetic risk factors.

What makes one person develop an anxiety condition and not another?

"While there is a very large genetic component that does not mean you will definitely develop anxiety, it just means youre more likely to," Thorp explains.

And research reveals exactly how much more likely.

Anxiety disorders are about 30 per cent heritable, Thorp says, noting many people can see anxiety symptoms emerge repeatedly across generations of their own families.

But if genes are behind 30 per cent of our susceptibility to anxiety disorders, what influences the other 70 per cent?

A great many cases of anxiety are triggered by unknown causes, often environmental, Thorp says. "You may have a high genetic risk but if you don't have that environmental trigger then perhaps you wont develop anxiety at all," he says.

The ability for genes to turn themselves on or off in response to environmental triggers is known as epigenetics. It is common across all diseases. A genetic predisposition to diabetes, for example, does not mean you will become ill it increases your risk but how that risk interacts with lifestyle or environment can determine what happens next.

In the case of anxiety, an environmental trigger could be a one-off traumatic experience, sustained disadvantage or common lifestyle stressors.

It could even be living through COVID-19.

A spike in the numbers of people seeking help for anxiety during the pandemic shows in real time the likely role of the environment in triggering genetic susceptibility.

"If we have two people with the same environmental trigger such as the pandemic, why does one develop anxiety but not the other?" asks Thorp. "It's reasonable to ask whether one person has a higher genetic risk."

And it's possible that if it wasnt for COVID-19 that susceptibility may never have been provoked.

The way anxiety changes the structure of the brain and the neurotransmitters it releases consumes Jess Nithianantharajah, a neuroscientist from Melbournes Florey Institute of Neuroscience and Mental Health.

Nithianantharajahs goal is to understand the biological basis of anxiety and "what is really going on in the brain that changes peoples behaviour".

Unlike brain disorders like dementia which are driven by loss of brain capacity, the brain of an anxious person shows "changes in connectivity", Nithianantharajah says. "Certain circuits in the brain become over-connected or under-connected and it's interesting how connectivity changes can lead to impaired behaviours."

In straightforward terms, our human brains are wired to respond to environmental triggers, particularly those that may suggest threat.

When we feel under siege the ancient parts of our brains that developed long before we became the sophisticated humans we are today go into "fight or flight mode".

This process floods our bodies with hormones like adrenaline or cortisol from our endocrine system, as well as neurotransmitters like noradrenaline from the brain, to either fight off the threat or flee from it.

This adaptive reflex has helped humans evolve to identify and respond to danger.

Yet there can be too much of a good thing.

In an anxious brain this response is never properly turned off. Every situation begins to feel like a threat and our bodies react as if they are under fire. Those neural pathways that are meant for emergencies are used repeatedly until they become the go-to response in almost every situation.

Nithianantharajah explains the brains threat "watchman", a tiny nut-shaped structure called the amygdala that sits alongside the hippocampus and encodes danger, becomes hyper-activated.

Neurotransmitters like glutamate that fire up the brain, get out of whack with those like Gammaaminobutyric acid (GABA), designed to calm things down.

The amygdala's crucial connections with the brains pre-frontal cortex which develops until adolescence and acts like the sensible control centre of the brain are broken down, undermining rational thought processes that might tell the amygdala "hey, no worries, you can ease off because this is all good".

"Sometimes it's hard to understand what's the chicken and what's the egg," says Nithianantharajah, adding that within the next few years a toolkit of new treatments may become available to provide more targeted mental health care. "Not everyone who presents with anxiety has the same symptoms and they dont all respond to the same drug," she says.

But what sparks mixed-up connections in the first place?

Sarah Whittle, head of the University of Melbournes Social and Affective NeuroDevelopment Lab, is researching how early life experiences shape brain development and increase the risk of anxiety.

Her fascinating research shows a threatening environment, whether it comes from within the family or from the community, can cause a childs brain to develop faster than normal.

"In essence kids have to grow up quickly to look after themselves," she says. "The circuits in the brain responsible for responding to threat, and regulating emotions, are impacted. Those same circuits are specifically involved in anxiety."

It's suspected that links between the brains ancient "limbic system", including the amygdala, and the controlling prefrontal cortex, are disrupted.

On MRI brain scans Whittle can actually see the impact of this disruption.

Kids that have experienced threat tend to have stronger connectivity between these two brain regions as they develop, she says.

Like so much research into anxiety, the work Whittle does is brand new. Conclusions cannot yet be drawn. The next step is large longitudinal studies in children from diverse backgrounds. One such study involves10,000 US children representing a cross-section of the population.

Researchers will return to these children several times over the next decade, checking their brain structure, function and connectivity and comparing findings with psychological and cognitive development.

"It is crucial when looking at children or adolescents to see how the brain develops over time or we're not getting the whole picture," Whittle says. "Waves of this US study will be coming up over the next five or six years and we'll be able to look in more detail at how trajectories of brain development got off track following exposure to stress and at what age children are most vulnerable."

We have relatively little influence over the way our genes, or the early environments we encounter as children, influence our anxiety risk. But diet is another matter.

Felice Jacka is pioneeringa growing body of research that shows how diet, something over which we all have substantial control, can influence mood.

The link between the gut and the brain is well-known: we have all experienced "butterflies" when we are nervous. Jackas research in "nutritional psychiatry" at Deakin Universitys Mood and Food Centre has made a ground-breaking connection: diet can directly influence mental health.

When Jacka announced the topic would be the focus of her 2010 PhD "many people thought I was quite bananas", she says.

But she persisted. And when her research became the first to demonstrate a correlation between diet quality and the likelihood of having a clinically significant depressive or anxiety disorder Jacka became a sensation. Her work was published on the cover of the prestigious American Journal of Psychiatry and featured in Time magazine.

Further studies continue to strengthen the link, showing those who eat diets high in vegetables and fruits, wholegrains, legumes, nuts and seeds are up to 30 per cent less likely to become depressed.

And Jacka argues that none of this should come as a surprise. The impact of diet is well-established in physical health. Why should mental health be any different?

Yet she is at pains to ensure people do not see their anxiety as a failure of their eating habits: "You did not cause your anxiety," she says.Instead, Jacka wants us to feel empowered: unlike many other risk factors for mental disorders diet is easily manipulated. "Identifying factors we can modify in order to improve mental health outcomes is very, very important," she says.

The scope of Jackas findings are fascinating.

A study of 23,000 Norwegian mothers shows their diet when pregnant is linked to the emotional health of their children, independent of other risk factors.

Another significant association shows diet quality is related to the size of a brain region called the hippocampus, a structure of densely-packed neurons that is unique in its ability to add neural connections throughout life. It is influential in learning and memory as well as mental health.

Jacka saysthe hippocampus can grow or shrink in response to environmental impacts and its size has been linked to anxiety.

"People with mental disorders often have a smaller hippocampus and as they recover the hippocampus grows again," Jacka says. "As people age the hippocampus also tends to get smaller but around 60 per cent of this age-related shrinkage maybe influenced by diet quality."

Jacka conducted a three-month study comparing the impact of diet and social support on moderate-to-severe clinical depression.

"What we saw at the end of that three months was actually quite astounding,"she says. "About a third of (the dietary support cohort) went on to have full clinical remission compared with about 8 per cent in the other condition."

But why does it work?

It is suspected pathways between the gut and brain influence the release of neurotransmitters like serotonin and gamma aminobutyric acid (GABA), two of the bodys most important "feel good" chemicals.

Diet may offer a way to "hack" these chemicals, ensuring our bodies are working optimally, with plenty of happy chemicals available to support and even boost our mood.

In addition, diet influences the function of our immune systems. "And we know that low-grade immune activation, causing inflammation, is an important factor in mental and brain health," Jacka says.

While we wait for the relationship between anxiety, genes, diet and brain structure to deliver new treatments, the ongoing role of psychotherapy in managing symptoms and changing thought patterns to restructure neural pathways cannot be overstated.

Psychologist Peter McEvoy, an anxiety specialist, has devoted many hours of clinical practice to helping people confront and overcome anxiety conditions.

"What causes anxiety is a big question and it's a complex one," says McEvoy, Professor of Psychology at Curtin University, and associate editor of the academic Journal of Anxiety Disorders.

While some individuals may experience anxiety because of "a high genetic load", McEvoy says others are more vulnerable to the "environmental load" including experiences of trauma or pandemic stressors for example.

Notwithstanding these risk factors "we don't really know why one particular individual is going to develop an anxiety disorder and another isn't," he says.

But his years of experience have highlighted one key constant in anxious patients: the need for certainty.

Intolerance of uncertainty, he says, is "ripe for breeding anxiety", noting the "but what if" cycle is a feature of many anxious thoughts. Psychotherapy is excellent at helping patients question these thought cycles.

McEvoy's research into the certainty/uncertainty principle suggests that humans are hard-wired to want to predict the future, a survival instinct that allows us to plan and prevent bad things from happening.

This urge has been quite literally built into the structure of the brain, he says.

Like Nithianantharajah and Whittle, he notes the importance of the pre-frontal cortex in "planning for things and predicting things so we can modify our risk in some way".

Uncertain situations like COVID can set up a battle inside the brain between our innate need to seek certainty, and plan contingencies to keep us safe, while facing a situation that is genuinely uncertain and even out of control.

Some people, McEvoy says, become stuck in a circular pattern of worry, trying to sort out a plan, trying to prevent a bad outcome from a perceived threat, but in reality "if we pursue that goal of achieving certainty, it is likely to lead us down the pathway of excessive worry, and anxiety".

The answer, according to McEvoy, is at once practical and yet, for someone trapped in a cycle of worry, tortuously difficult to achieve: "The goal is to learn to tolerate and accept uncertainty," he says. "To focus more on the here and now and simply ask yourself 'what is controllable today?'.'

How will you know youve reached that place of comfort? For McEvoy the answer is simple: If were still going, then were coping, were resilient. And if were feeling a little exhausted by it then thats ok too.

Words and production: Catherine Taylor

Video:Zalika Rizmal andAndrew McKenzie

Illustrations : Emma Machan

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What causes anxiety? Why is it so common? And how can it be treated? - ABC News