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Letters to the Editor Issue 282

by Letters(more info)

listed in letters to the editor, originally published in issue 282 - November 2022

Study Reveals High Neurodegenerative Risk Among Former International Rugby Players

A study led by the University of Glasgow has revealed the first major insights into lifelong health outcomes in former international rugby union players.

In findings published in the Journal of Neurology, Neurosurgery and Psychiatry,[1] the researchers found that former international rugby players had an approximately two and a half times higher risk of neurodegenerative disease than expected, with risk of disease varying by subtype, but not by player position.  

Led by consultant neuropathologist Prof Willie Stewart, Honorary Professor at the University of Glasgow, the research team compared health outcomes among 412 male, Scottish, former international rugby players and over 1,200 matched individuals from the general population.

The results showed that while age at death was slightly higher among former rugby players, they were also at higher risk of a neurodegenerative disease diagnosis compared to their matched controls. This risk varied by disease subtype ranging from around a doubling of risk of a dementia diagnosis, to an over 10-fold risk of motor neuron disease diagnosis.

In their previous findings from the landmark FIELD study, which was funded by The Football Association and The Professional Footballers Association, the research team reported the first data on neurodegenerative risk among former professional footballers.  

The current study is a continuation of this ground-breaking research into brain health outcomes among former contact sports athletes, and represents the largest study to date looking in this detail at neurodegenerative disease risk among former rugby players.

Prof Willie Stewart said:

“This latest work under our FIELD program of research demonstrates that risk of neurodegenerative disease is not isolated to former footballers, but also a concern for former rugby players.

“As such, this study provides further insight into the association between contact sports and neurodegenerative disease risk. Of particular concern are the data on motor neuron disease risk among our rugby players, which is even higher than that for former professional footballers. This finding requires immediate research attention to explore the specific association between rugby and the devastating condition of motor neuron disease.”

The study also found that, although rugby union players had a higher risk of death overall from neurodegenerative disease, they were less likely to die of respiratory disease. And while deaths in former rugby players were lower than expected up to age 70, they was no difference to matched population controls over that age.

Dr Emma Russell, researcher at the University of Glasgow and first author on the study, said:

“An important aspect of this work has been the ability to look across a range of health outcomes in former professional rugby players, allowing us to build a clear picture of health in this population.

“Our data show that, in contrast to our previous findings in former professional football players, rugby players do not appear to benefit from a reduced risk of death due to cardiovascular disease or cancer, suggesting the possibility of sport-specific influences on lifelong health.”

The study used national electronic health records on death certificates, data on hospitalization and dispensed prescribing for dementia and causes of death in Scottish former international rugby union players. Players included were all aged 30 years or over at the end of 2020. The final cohort for analysis comprised 412 former international rugby players and a comparison group of 1,236 matched members of the general population.

In parallel work, also led by Professor Stewart, a specific pathology linked to brain injury exposure, known as chronic traumatic encephalopathy (CTE), has been described in a high proportion of the brains of former contact sport athletes, including former rugby players.

Professor Stewart said:

“Taking these new results in rugby, together with our pathology work and previous FIELD studies in football, the risk exposure of concern must remain repetitive head impacts and head injuries. As such, precautionary approaches should be adopted to reduce unnecessary head impacts and better manage head injuries across all contact sports.”

The paper ‘Neurodegenerative disease risk among former international rugby union players.’ is published in Journal of Neurology, Neurosurgery and Psychiatry, and also includes funding from The US National Institutes of Neurological Disorders and Stroke and NHS Research Scotland.


  1. Emma R Russell, Daniel F Mackay, Donald Lyall, Katy Stewart, John A MacLean, James Robson, Jill P Pell, William Stewart Neurodegenerative disease risk among former international rugby union players. Journal of Neurology, Neurosurgery & Psychiatry. Published Online First: 04 October 2022.

Further Information on Prof Willie Stewart’s previous FIELD studies

Further Information

For more information contact Elizabeth McMeekin or Ali Howard in the University of Glasgow Communications and Public Affairs Office on Tel: 0141 330 4831 or Tel: 0141 330 6557; or or The office can also be reached at



Researchers Develop a New Approach to Improve Future Diagnosis of Alzheimer’s Disease

Alzheimer’s Disease (AD) is one of the most common neurodegenerative diseases, affecting 50 million patients worldwide and that figure is expected to increase by 50% by 2050.

Current AD diagnosis methods like cognitive, physical and radiological assessments can be often subjective, time-consuming and invasive to the patient.

Through this research, it is hoped that patient experiences will be enhanced by receiving a more accurate and quicker diagnosis.

Dr Fei He and Dominik Klepl, researchers within the Centre for Computational Science and Mathematical Modelling at Coventry University, have developed a unique diagnosis approach that analyses the brain dynamics from electroencephalography (EEG) signals which measure brain electrical activity.[1]

This ground-breaking research uses an energy landscape concept from statistical physics to model the patients’ EEG signals and suggests that the findings could be used to improve diagnosis of Alzheimer’s Disease.

This approach performs significantly better than alternative baseline diagnosis models and offers high levels of accuracy.

The energy landscape of the brain is a method of analysis that can be used to quantify the dynamics of brain transitions between stable states. These brain states illustrate different patterns of brain activities, i.e., the activation or depression in different brain regions at a specific time.

The EEG dynamics in those suffering with Alzheimer’s is more constrained than non-sufferers, with the energy landscape of the brain showing more localised activity.

The results indicate that Alzheimer’s patients’ EEG signals are less complex, showing the increased difficulty of changing between brain states in comparison to non-sufferers.

In the future, this approach could be used for analysing other neurological disorders, including Parkinson’s disease.

Dr Fei He, Assistant Professor, Research Centre for Computational Science and Mathematical Modelling, said:

“Our research shows the importance of studying the global dynamics of the brain in characterising neurological disorders, such as Alzheimer’s Disease. The energy landscape technique together with EEG could offer promising tools to support the diagnosis and characterise the severity of Alzheimer’s Disease of a patient. This work also demonstrates the importance of multi-disciplinary research, such as integrating techniques from statistical physics, signal processing and machine learning, in tackling global challenges like neurodegenerative disease.”

This research forms part of a collaborative project, featuring: Dr Ptolemaios G. Sarrigiannis, Department of Neurophysiology, Royal Devon and Exeter NHS Foundation Trust, Dr Daniel J. Blackburn, Department of Neuroscience, University of Sheffield, Dr Min Wu, Institute for Infocomm Research, A*STAR, Singapore and Dr Matteo De Marco, Department of Life Sciences, Brunel University London.


  1. Klepl, F. He, M. Wu, M. D. Marco, D. J. Blackburn, and P. G. Sarrigiannis, Characterising Alzheimer’s Disease With EEG-Based Energy Landscape Analysis. IEEE Journal of Biomedical and Health Informatics 26, (3): 992-1000. March 2022, .

About Coventry University

Coventry University is a global, modern university with a mission of Creating Better Futures. We were founded by entrepreneurs and industrialists in 1843 as the Coventry School of Design and we continue to have strong links with the public and private sectors, providing job-ready graduates with the skills and creative thinking to improve their communities. With a proud tradition of innovative teaching and learning, Coventry University has world-class campus facilities, the UK’s first standalone 5G network, and a digital community of learning. Our students are part of a global network that has 50,000 learners studying for Coventry University degrees in more than 40 different countries and partnerships with 150 higher education providers worldwide.

We have greatly increased our research capacity and capability with a focus on impactful research, delivered for and with partners to address real-world challenges and support businesses and communities to grow. The depth and breadth of the rapidly growing research portfolio was validated by the latest UK research assessment, which saw us jump 22 places in the research power rankings. Over two centuries, we have flourished in Coventry and Coventry University Group now also delivers access to our range of high-quality services and partnerships through bases in London, Scarborough, Belgium, Poland, Egypt, Dubai, Singapore and Africa. From September 2023, we will be teaching students at a new campus in China in a joint venture with the Communication University of China. In April 2022, we were honoured with the Queen’s Award for Enterprise in the category of International Trade, the UK’s most prestigious business award. In recent years, we have won many awards and vastly improved our rankings in the league tables that matter to students – but what matters to us is delivering transformational change for our students, partners, and communities around the world as we continue to evolve into a global education group.

Further Information

For further information, please contact Ben Lugg at Coventry University on 07392096956; or



Towards Improving the Safety of Homeopathic Remediation

by Dr Peter H Kay

Recently, I gave an invited talk to the 4th World Congress on Homeopathy and Traditional Medicine. I discussed the significance of homeogenetic advances particularly with respect to the safety of anti-cancer treatments involving the administration of highly diluted potentized substances. Because of the interest that followed, I now include a brief summary of my talk.

Discoveries which contribute to the improvement in the safety and effectiveness of all forms of health care emerge almost on a daily basis. It is therefore important that all practitioners who take responsibility for the health of the community take these discoveries into account to optimise the efficacy and safety of the treatment regime that they offer to their clients.

Homeopathy plays an important role in health care. Many years ago, Professor Khuda-Bukhsh postulated that homeopathic remedies would have the capacity to modulate the transcriptome, that is, the way that genes are expressed. His postulate was subsequently confirmed by many others.[1]

Attention was then turned to the identification of highly diluted and potentized substances that could influence the expression of the gene TP53, particularly because of its role in cancer.[2]

Studies have shown that many homeopathic remedies and highly diluted substances have the capacity to up-regulate the expression of the gene TP53.[1]

The gene TP53 encodes the protein p53. p53 plays a critical role in protecting against development and progression of most cancers because it has many anti-cancer properties. One of its properties is to instruct a cell to kill itself if its DNA has been damaged in such a way as to cause the cell to become cancerous. This cell destruction pathway is referred to as apoptosis or programmed cell death. p53 also acts as a tumour suppressor protein to arrest tumour growth and stop the formation of blood vessels in a tumour that are needed to support tumour growth.[2]

It has long been known that inheritance of some forms of TP53 which encode mutant p53 proteins (known as germline mutations) give rise to development of many different types of cancer at an early age.[2] These mutants can be readily identified by sequencing DNA from a simple blood sample or buccal smear because the mutant gene is contained within all nucleated cells within the body.

On the other hand, half of all cancers are associated with mutated forms of TP53 that are found only in the cancerous cells. These mutations are not inherited and are referred to as somatic mutations.

Although it is relatively easy to determine the genetic type of TP53 in germline DNA, as indicated, it is more difficult to determine the genetic status of cancer cell specific somatic TP53 mutations. That is because to determine the presence of a mutated TP53 gene in neoplastic cells, DNA must be isolated specifically from the neoplastic cells themselves. This often requires an invasive procedure similar to that used to obtain a biopsy specimen.

As indicated, it is well recognized that around half of all cases of cancer are associated with a mutant form of TP53. Also, it is now clear that synthesis of a mutated p53 protein in cancerous cells causes them to become partially resistant to chemotherapy and radiotherapy.[2,3,4] In other words, chemotherapy and radiotherapy are less effective treatments for cancers associated with TP53 mutations. Therefore, since half of all cancers are associated with mutant TP53 genes, for safety reasons, it makes sense to avoid the administration of highly diluted substances that up-regulate the expression of  mutant TP53 genes to those who suffer from cancer, unless the germline or somatic genetic status of the TP53 gene in their neoplastic cells is known.

Interestingly, studies have shown that some highly diluted substances have the capacity to down-regulate the expression of some genes.[5] It would be highly advantageous to determine which highly diluted substances down-regulate the expression of the TP53 gene because administration of these remedies would be applicable in cases of cancer associated with germline or somatic TP53 mutations.

I would like to bring your attention to some other genes that warrant investigation with respect to homeogenetic considerations, those that encode various cytochrome P450 enzymes.

The cytochrome P450 system comprises a set of enzymes which play an important role in metabolism of many toxic substances including pharmacological agents.

Many pharmacological drugs such as chemotherapeutic drugs are administered in an inactive form called a prodrug. Prodrugs need to be activated by certain cytochrome P450 enzymes, usually an enzyme called CYP2D6, before they can be of any help. Over-activation of the gene that encodes CYP2D6 may result in the rapid release of too much active drug leading to a toxic overdose effect.

Some chemotherapeutic drugs (and many other drugs) are metabolized by the enzyme CYP3A4. Therefore over-activation of the gene that encodes CYP3A4 has the potential to remove chemotherapeutic and other drugs before they have the opportunity to have any beneficial effect.

In conclusion, it is clear that knowledge of genes that are targeted by different potentized highly diluted substances and whether they are up-regulated or down-regulated will have a major impact in advancing the safety of health care.




  1. 10.1080/15384101.2019.1688951 Epub Nov 14 2019.
  3. Marzotto M et al., Extreme sensitivity of gene expression in human SH-SY5Y neurocytes to ultra-low doses of Gelsemium sempervirens. BMC Complement Altern Med ;14:104. 2014.

Further Information

Please contact Dr Peter H Kay via



Simple Blood and Urine Test can help Patients with Chronic Kidney Disease

A simple blood and urine test can identify those most at risk of severe complications of chronic kidney disease. However, despite being recommended by NICE in 2021, many patients and GPs remain unaware of the test’s life-saving potential.

New research, led by the University of Glasgow and published in the British Journal of General Practice,[1] assessed patient data from across the UK and found that not enough people with chronic kidney disease were routinely being given this recommended test. The study results have prompted renewed calls from kidney specialists to encourage more patients to be given access to this test.

Chronic kidney disease is a long-term condition, where the kidneys don't work as well as they should. It's a common condition, with 10-15% of the general population affected. However, in the early stages it rarely has symptoms, and most people are unaware they have it. While it can affect anyone, it is often associated with getting older, and it is more common in people who are black or of south Asian origin.

Only a very small number of people (1 to 4%) with chronic kidney disease will progress to kidney failure requiring treatment, either dialysis or kidney transplantation. However, by using a series of simple blood and urine tests, GPs could help identify more high-risk people and refer them to hospital before they progress to this late stage. In turn, nephrologists (kidney specialists) may be able to slow patients’ progression to kidney failure, or prepare them for dialysis or transplantation, ultimately saving lives.

In 2021 NICE (National Institute for Health and Care Excellence) guidelines on chronic kidney disease recommended the use of the Kidney Failure Risk Equation (KFRE), which includes measurement of protein in the urine (albuminuria). The KFRE allows doctors to define an individual’s risk of kidney failure, allowing those most at risk to be referred for specialist care in a timely way.

The KFRE test is currently available for anybody with chronic kidney disease stage 3 or worse. However, in this study researchers found that the KFRE test is only probably performed in a tiny minority of those eligible, largely due to lack of awareness. Despite chronic kidney disease being a common condition, many patients do not know they have it and they may not understand the importance of attending for blood tests and of providing urine samples.

Albuminuria tests are cheap and easy, available to everybody, and ideally should be performed in anybody with chronic kidney disease at least once a year. The study shows that, currently, this only happens in around 20-25% of people with chronic kidney disease. Without the albuminuria tests, patients cannot have KFRE tested and therefore may miss out on important treatments. Researchers estimate around 75-80% of people with chronic kidney disease are not routinely having their urine tested for albuminuria, and may therefore be missing out on early, preventative treatments to reduce risk of kidney failure, heart disease and death.

The research also found that KFRE test results were more likely to be elevated in non-white ethnic groups, in-keeping with the previous literature suggesting that non-white people are at the greatest risk of chronic kidney disease progression.

University of Glasgow researcher and a NHS kidney specialist, Dr Jennifer Lees, said: “Kidney disease is common amongst adults, but only a small number of people need to see kidney specialists. It is important that all people with kidney disease receive the right treatments at the right time, and these blood and urine tests are an easy way to ensure this happens. Our research shows that at present, not enough people with kidney disease have their urine tested, and therefore may be missing out on the best treatments.”

Dr Michael Sullivan, from the University of Glasgow’s School of Cardiovascular and Metabolic Health, said: “GPs need to identify which patients will benefit most from referral to hospital clinics. The KFRE is effective at helping GPs identify and refer these patients early, before kidney disease becomes more advanced. More patients with kidney disease need to have access to this new tool. Our research shows that for this to be possible, more patients need to bring urine samples to their GP.”

For this study the researchers studied more than 1.8m patients in SAIL (The Secure Anonymised Information Linkage Databank, a national data safe haven of de‑identified datasets principally about the population of Wales) and around 465,000 UK Biobank participants.

The paper ‘Potential impact of NICE guidelines on referrals from primary care to nephrology’ is published in the British Journal of General Practice.[1] The work was funded by the Medical Research Council. The full study can be found here.[1]


  1. Michael K Sullivan, Bhautesh Dinesh Jani, Elaine Rutherford, Paul Welsh, Alex McConnachie, Rupert Major, David McAllister, Dorothea Nitsch, Frances S Mair, Patrick B Mark and Jennifer S Lees. Potential Impact of NICE guidelines on referrals from primary care to nephrology. British Journal of General Practice BJGP.2022.0145. 14 September 2022. DOI:

Further Information and Contact

For more information please contact Elizabeth McMeekin or Ali Howard in the University of Glasgow Communications and Public Affairs Office on Tel: 0141 330 4831 or Tel: 0141 330 6557;  or  



Getting Rid of Unwanted Transformed Cells: Possible New Directions in Cancer Therapy

Scientists elucidate the regulatory mechanisms underlying “autophagy” mediated competitive elimination of cancer cells.

Elimination of transformed cells that can initiate cancer is necessary to maintain tissue integrity. In a new study,[1] scientists from Tokyo University of Science show how this mechanism is regulated by the cellular process “autophagy.” They found that intact autophagic vacuoles are indispensable in mediating competitive elimination of cancer cells. Conversely, perturbation of autophagy prevents cell elimination, thereby encouraging cancer cell propagation. These findings pave the way for development of novel anti-cancer therapies.

The maintenance of a healthy cell population is a dynamic process, whereby unhealthy cells are eliminated by a defence mechanism called “cell competition”. This process is crucial as unhealthy cells or cells that have accumulated detrimental “genetic mutations” (defects in genes) over time, can initiate the formation of cancer. Cell competition is achieved by healthy normal cells that surround mutant cancer cells through various mechanisms that trigger cell removal. In addition, epithelial cells (a type of cell that constitutes external and internal body surfaces such as skin and internal organs) adopt a cell-death-independent mechanism known as “apical extrusion” to recognize and eliminate transformed cells. While the role of apical extrusion in cell competition has been well elucidated, the regulatory mechanisms underlying this complex dynamic process remain elusive.

“Autophagy” is a process by which cells degrade and recycle cellular components. Dysregulation of autophagy has been implicated in various diseases, including several cancers. While autophagy is known to facilitate the growth and survival of cancer cells at advanced stages, previous studies have indicated that autophagy may have a preventive role in early stages of cancer. Does autophagy regulate the early destruction of cancer cells through cell competition?

Building on this hypothesis, Dr Shunsuke Kon, a junior associate professor at Tokyo University of Science along with Eilma Akter and a team of researchers, has now explored the potential regulatory role of autophagy in cell competition, in a new study recently published in Cell Reports.[1]

Probing deeper into the possible interplay between autophagy and cell competition, the researchers used cell lines, in which cell competition is triggered by RasV12 (a cancer-causing protein).

Dr Kon explains, “We have previously shown that when a small number of mutant cells are produced in the normal epithelial layer by activating the cancer-causing gene Ras, the mutant cells are eliminated into the lumen as loser cells. This happens as a result of cell competition between the normal epithelial cells and the Ras mutant cells.”

Using the RasV12-induced mosaic (healthy + mutant cancer cells) cell competition model and fluorescent-protein labelling, the team uncovered a fascinating set of results. They showed that the RasV12-transformed cells had an increased number of autophagosomes (structures containing degradable cytoplasmic contents). Further, they noted impairment of lysosomes, the structures that fuse with autophagosomes and mediate the breakdown of their contents; which likely, caused the increase in autophagosomes. This in turn, perturbed the “autophagic flux” (a measure of autophagic degradation) in RasV12-transformed cells.

Next, they showed that the accumulated autophagosomes and the impaired lysosomes facilitated apical elimination of the transformed (cancer) cells via cell competition. These results suggest that the intact or “non-degradable” autophagosomes are important for the elimination process. Interestingly, when the researchers ablated the autophagy gene, ATG-5 in RasV12-induced cells, they noted impairment in autophagy mediated cell competition and elimination of the transformed cells. Similarly, autophagy impaired cells exhibited resistance to elimination in a mouse model, and eventually led to chronic pancreatitis or inflammation of ducts in the pancreas, thus, corroborating their earlier findings.

Together, these findings highlight the role of autophagy in competitive elimination of mutant cancer cells and tissue homeostasis (balance). The study sheds light on the role of autophagy in cancer prevention during early stages and opens avenues for the development of novel anti-cancer therapeutics.

In this context, Dr Kon remarks, “The development of anti-cancer drugs targeting autophagy is being intensely pursued worldwide. Since the role of autophagy has been found to differ depending on the stage of cancer progression, anti-cancer strategies that take into account the stage of cancer progression can enhance treatment efficacy.”

Autophagy is surely emerging as the unsung hero that aids the removal of cancer-causing rogue cells!


  1. Eilma Akter 6, Yukihiro Tasaki 6, Yusuke Mori, Shotaro Yamano, Yasuyuki Fujita, Shunsuke Kon 7. Non-degradable autophagic vacuoles are indispensable for cell competition. Cell Reports 40(9):111292. 30 August 2022. DOI:

About The Tokyo University of Science

Tokyo University of Science (TUS) is a well-known and respected university, and the largest science-specialized private research university in Japan, with four campuses in central Tokyo and its suburbs and in Hokkaido. Established in 1881, the university has continually contributed to Japan's development in science through inculcating the love for science in researchers, technicians, and educators. With a mission of “Creating science and technology for the harmonious development of nature, human beings, and society", TUS has undertaken a wide range of research from basic to applied science. TUS has embraced a multidisciplinary approach to research and undertaken intensive study in some of today's most vital fields. TUS is a meritocracy where the best in science is recognized and nurtured. It is the only private university in Japan that has produced a Nobel Prize winner and the only private university in Asia to produce Nobel Prize winners within the natural sciences field.

About Dr Shunsuke Kon from Tokyo University of Science

Dr Shunsuke Kon is a Junior Assoc. Prof. in the Cancer Biology Department of the Research Institute for Biomedical Sciences. He obtained his PhD from the Tohoku University Graduate School of Life Sciences in 2008.  His primary research interest is tumour biology with more than 20 publications to his credit. He has received the Best Articles of the Year award.

Funding Information

This study was supported by the Japan Society for the Promotion of Science (JSPS) Grant-in-Aid for Scientific Research on (B) 20H03166, JSPS Grant-in-Aid for Scientific Research on Innovative Areas 20H05347, the Princess Takamatsu Cancer Research Fund, the MSD Life Science Foundation, the Inamori Foundation and the Uehara Memorial Foundation (to S.K.), and by JST SPRING, Grant Number JPMJSP2151 (to E.A.).

Further Information and Contact

Indrani Das

Media Relations team, Tokyo University of Science, Japan   

YouTube link to the video summary of the research study:

Here is the link to the news story:



Breathing Power and Lung Volume Significantly Improved by Simple Resistance Breathing Exercises and Warm Steam

Four weeks and 15 minutes a day of training significantly strengthened the lung function of asthma patients. Asthma is the most common lung disease in Finland. It affects half a million people. The symptoms and lung function of patients suffering from mild asthma often improve quickly even with current asthma medications. In any case, the strength of the respiratory muscles cannot be increased with drug treatment, and in more severe cases, the drugs are not enough to eliminate all the symptoms and do not improve lung function sufficiently. A combination of counter-pressure resistance breathing training and warm steam has not been clinically studied in the treatment of asthma before. A new study shows that this combination method provides a significant improvement in respiratory muscle strength and lung function.

The results of a clinical study conducted in Finland[1]  were presented at the beginning of September during the ERS 2022 Congress of the European Pulmonary Society in Barcelona. The results show that light daily training, where resistance breathing training is combined with warm steam, strengthened respiratory muscles by 12-20 percent in just four weeks. In addition, this combination training significantly improved the functional volume of the lungs.

45 people with mild or moderate asthma participated in the study. Throughout the study, they regularly used their own asthma medication which was considered optimal. The patients were randomly divided into an experimental group and a control group. Participants in the experimental group used a WellO2 breathing training device, which uses a combination of counter-pressure resistance and warm steam. The control group continued their lives as before.

Conclusions: Light counter-pressure breathing combined with steam breathing for four weeks increases respiratory muscle strength and vital capacity (VC) in patients whose asthma and its medication are under control.


  1. Effects of counterpressure breathing with steam inhalation on lung function in stable asthma

Katri Lindberg, Ilpo Kuronen, Jukka Heinijoki, Anssi Sovijärvi 

WellO 2 Oy Tampere ( 2 University of Eastern Finland Kuopio ( 3 Medical Centre, Johanneksen Klinikka Tampere ( 4 University of Helsinki Helsinki)

Further information:

WellO2 Oy

Katri Lindberg, Specialist in Lung Diseases
Tel: +358407373712

About Ilpo Kuronen

One of the authors of the research report, Ilpo Kuronen is a minority shareholder of WellO2, which develops breathing exercise equipment. Katri Lindberg works at WellO2 Oy as an expert in lung diseases. The other authors have no ties to Wello Oy.

About Wello2

Wello2 is a versatile, lung-strengthening and cleansing breathing exercise device. It is an internationally patented Finnish innovation with over 100,000 users. The device is available in pharmacies, large retail stores, well-stocked sporting goods stores and physical therapy companies, as well as in the WellO2 online store.   

Media Contact:

Simo Kekalainen



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