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#InsideTheBox with Dr Andy Gray | Essential Medicines – Essential to Whom?

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#InsideTheBox is a column by Dr Andy Gray, a pharmaceutical sciences expert at the University of KwaZulu-Natal and Co-Director of the WHO Collaborating Centre on Pharmaceutical Policy and Evidence Based Practice. (Photo: Supplied)

By Andy Gray

In the first of a new series of monthly columns for Spotlight, Dr Andy Gray considers what we mean when we refer to medicines as “essential” – something that is routinely done by the WHO and health authorities in many countries.

That every health system needs medicines, including vaccines, to treat and prevent and at times to cure diseases is obvious. However, that immediately begs a series of questions – which medicines, where, and for whom?

For nearly 50 years, the World Health Organization (WHO) has provided guidance in the form of the Model List of Essential Medicines. For almost 20 years, WHO has also provided a Model List of Essential Medicines for Children. The most recent version, issued in 2023 and due to be revised in 2025, lists over 500 medicines, including 361 specifically for children.

Those figures draw attention to a core principle that not all medicines approved by national medicines regulatory authorities, and therefore legally marketed, are considered necessary.

The WHO defines essential medicines as “those that effectively and safely treat the priority healthcare needs of the population”. It adds that the primary drivers for selecting a limited list of medicines are efficiency and effectiveness: “The use of a limited number of carefully selected medicines can lead to improved supply, better prescribing practices and lower costs.”

The initial essential medicines definition contains a highly contested component – how does one determine the “priority healthcare needs of the population”?

One element should surely be the prevalence of the condition for which the medicine is indicated. However, that alone is insufficient. The common cold is, as the name implies, ubiquitous. Should that mean that cough mixtures are essential? If the evidence of a clinically relevant health benefit from the use of cough mixtures is lacking, that should surely rule them out. The common cold is also self-limiting, without long-term consequences.

By contrast, infection with hepatitis C virus can result in serious illness and death, but also spread to others, and in some patients become a chronic disease associated with increased risk of liver cancer or cirrhosis. In that case, treating the condition not only benefits the patient, but also prevents others from being infected with the same virus. For many years, the available treatments for hepatitis C were not very effective and associated with severe adverse effects. Once new, highly effective and safer treatments became available around a decade ago, the pressure was on to consider them as essential.

That is where another part of the WHO definition comes into play: “Essential medicines should always be available within functioning health systems, in sufficient quantities to meet patient needs. They should be available in appropriate dosage forms for the intended uses and patients, be of assured quality, and be affordable for both individuals and the health system.”

But how can affordability be measured?

One approach is to consider whether the added benefits are worth the extra cost, compared to existing medicines. That approach, based on a technique called incremental cost-effectiveness analysis, does not consider the possible impact of a new medicine on the total pharmaceutical or health budget. A stunningly effective new medicine may simply be unaffordable if needed by a large number of patients, unless additional resources can be secured for the health system. In an era of fiscal restraint and shifting donor priorities, “new money” is increasingly unlikely to be found.

An even more pressing problem is posed when a new medicine becomes available that makes a significant difference to clinical outcomes, for example changing a previously fatal condition into a manageable chronic condition. The new medicine may only be needed by a few patients, but if it is very expensive it may pose a threat to available budgets and be unaffordable to individual patients and their families. Rare diseases, and the medicines to treat them, ask uncomfortable questions about how public health priorities are decided, how affordability is assessed, and how society as a whole values access to medicines. The population level perspective runs headlong into the individual.

How it works in SA

South Africa, like more than 150 other countries, has established medicines selection structures and procedures and developed a national essential medicines list (EML). The medicines selected for the EML inform the state tender system, allowing the state to use its buying power to exert downward pressure on medicine prices. Medicines procured in that way are used almost exclusively in the public sector, in health facilities operated by provincial and local government.

However, the separation between public and private sectors is not that simple. Medical schemes use similar considerations of cost effectiveness and budget impact to determine the reimbursement rules and formularies for each of their benefit options. In some cases, there are nationally-determined algorithms for specific conditions – the Chronic Disease List – that have to be covered as prescribed minimum benefits. Those algorithms have not been updated as frequently as might be desired, and certainly not as frequently as the standard treatment guidelines and EML applied in the public sector. As a result, when challenged regarding denial of coverage, the medical schemes regulator has tended to look to the state’s position as defining a standard of care. However, the reduced prices available to the state may not be accessible to the private sector.

In other words, and even before National Health Insurance is implemented, the questions of which medicines, where, and for whom remain vexing. They have to be faced, however, if any health system is to ensure the progressive realisation of the right of access to healthcare services, responsibly and effectively using the available resources.

*Gray is a Senior Lecturer at the University of KwaZulu-Natal and Co-Director of the WHO Collaborating Centre on Pharmaceutical Policy and Evidence Based Practice. This is the first of a new series of #InsideTheBox columns he is writing for Spotlight.

Note: Spotlight aims to deepen public understanding of important health issues by publishing a variety of views on its opinion pages. The views expressed in this article are not necessarily shared by the Spotlight editors.

Republished from Spotlight under a Creative Commons licence.

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Causes of Fevers of Unknown Origin in sub-Saharan Africa

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Ebola on a cell. Credit: NIH/NIAID

A new retrospective, laboratory-based observational study provides detailed insights into the causes of fevers of unknown origin in sub-Saharan Africa. Researchers examined 550 patients from Guinea who developed a persistent fever at the time of the major Ebola outbreak in 2014, but tested negative for the Ebola virus on site. The goal was to use modern diagnostic methods to better understand the underlying infectious diseases. The study is published in The Journal of Infectious Diseases.

Fever is a common symptom of many diseases, including infections, cancer, and autoimmune diseases. When the cause of a persistent fever remains unclear despite extensive investigation, it is referred to as fever of unknown origin (FUO). Approximately half of all FUO cases worldwide remain undiagnosed. In sub-Saharan Africa, malaria is often suspected and treated without laboratory confirmation or further investigation. However, 90 million pediatric hospitalisations per year in sub-Saharan Africa are due to fevers not caused by malaria but by other infections, often due to various bacteria and viruses.

A research team from the German Center for Infection Research (DZIF) and Charité – Universitätsmedizin Berlin, in collaboration with scientists from Guinea and Slovakia, conducted a retrospective observational study to thoroughly investigate the pathogen diversity of patients from Guinea with fever of unknown cause during a major Ebola outbreak in 2014. They combined epidemiological, phylogenetic, molecular, serological and clinical data.

Using serologic tests, PCR and high-throughput sequencing, at least one pathogen was detected in 275 of 550 patients. In addition to the expected malaria parasite Plasmodium, pathogenic bacteria such as Salmonella and Klebsiella strains were detected in almost one fifth of the patients. The frequent detection of resistance to so-called first-line antibiotics in the samples examined and the high rate of co-infections were also worrying: One in five infected patients had multiple infections at the same time. Pathogens causing malaria and bacterial sepsis were particularly common, occurring together in 12% of adults and 12.5% of children.

Infections with highly pathogenic viruses were also common: Yellow fever, Lassa and Ebola viruses were detected by RT-PCR in about six percent of patients. Of particular note was the detection of infection with Orungo virus, a little-known pathogen for which there are no robust assays. Using immunofluorescence assays, the researchers also identified IgM antibodies against several viruses, including Dengue, West Nile and Crimean-Congo hemorrhagic fever viruses, in patients who were PCR-negative.

“In Africa, febrile illnesses of unknown cause are often recognized and treated as malaria without further diagnosis. In our study, we were able to detect a pathogen in about half of all patients with FUO, including bacterial pathogens that cause sepsis, haemorrhagic fever viruses including Ebola, and, as expected, various strains of the malaria parasite Plasmodium,” explains the study’s last author Prof. Jan Felix Drexler.

The findings underscore the urgent need to further strengthen laboratory capacity in sub-Saharan Africa. Early detection of the infectious causes of FUO is critical for patient care, effective response to outbreaks, and development of regionally appropriate diagnostics.

“Our results show that regionally adapted treatment regimens should be discussed, that quality control in the context of outbreaks needs to be strengthened, and that knowledge of the pathogen spectrum can guide targeted strengthening of regional laboratories and translational research in the sense of point-of-care tests,” Drexler summarises the results of the study.

Source: German Center for Infection Research

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Nerves Electrify Stomach Cancer, Sparking Growth and Spread

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Image from Pixabay.

Researchers have discovered that stomach cancers in mice make electrical connections with nearby sensory nerves and use these malignant circuits to stimulate the cancer’s growth and spread.

Reported in Nature, this is the first time that electrical contacts between nerves and a cancer outside the brain have been found, raising the possibility that many other cancers progress by making similar connections.

“We know that many cancers exploit nearby neurons to fuel their growth, but outside of cancers in the brain, these interactions have been attributed to the secretion of growth factors broadly or through indirect effects,” says Timothy Wang, the Silberberg Professor of Medicine at Columbia University Vagelos College of Physicians and Surgeons, who led the study and is one of the leaders in the growing field of cancer neuroscience.

“Now that we know the communication between the two is more direct and electrical, it raises the possibility of repurposing drugs designed for neurological conditions to treat cancer.”

The wiring of neurons to cancer cells also suggests that cancer can commandeer a particularly rapid mechanism to stimulate growth.

“There are many different cells surrounding cancers, and this microenvironment can sometimes provide a rich soil for their growth,” Wang says. Researchers have been focusing on the role of the microenvironment’s immune cells, connective tissue, and blood vessels in cancer growth but have only started to examine the role of nerves in the last two decades.

“What’s emerged recently is how advantageous the nervous system can be to cancer,” Wang adds. “The nervous system works faster than any of these other cells in the tumour microenvironment, which allows tumours to more quickly communicate and remodel their surroundings to promote their growth and survival.”

Cancer-neuron connections resemble synapses

As a gastroenterologist, Wang’s research has focused on stomach and other GI cancers. About 10 years ago, he discovered that cutting the vagus nerve in mice with stomach cancer significantly slowed tumour growth and increased survival rate.

Many different types of neurons are contained in the vagus nerve, but the researchers focused here on sensory neurons, which reacted most strongly to the presence of stomach cancer in mice. Some of these sensory neurons extended themselves deep into stomach tumours in response to a protein released by cancer cells called Nerve Growth Factor (NGF), drawing the cancer cells close to the neurons. After establishing this connection, tumours signalled the sensory nerves to release the peptide Calcitonin Gene Related Peptide (CGRP), inducing electrical signals in the tumour.  

Though the cancer cells and neurons may not form classical synapses where they meet – the team’s electron micrographs are still a bit fuzzy – “there’s no doubt that the neurons create an electric circuit with the cancer cells,” Wang says. “It’s a slower response than a typical nerve-muscle synapse, but it’s still an electrical response.”

The researchers could see this electrical activity with calcium imaging, a technique that uses fluorescent tracers that light up when calcium ions surge into a cell as an electrical impulse travels through.  

“There’s a circuit that starts from the tumour, goes up toward the brain, and then turns back down toward the tumour again,” Wang says. It’s like a feed-forward loop that keeps stimulating the cancer and promoting its growth and spread.”

Migraine drugs as a potential cancer treatment

For stomach cancer, CGRP inhibitors that are currently used to treat migraines could potentially short-circuit the electrical connection between tumours and sensory neurons.

In Wang’s study, CGRP inhibitors administered to mice with stomach cancer reduced the size of the tumors, prolonged survival, and prevented the tumors from spreading.

“Based on our analysis of stomach cancer data from patients, we believe that the circuits we’ve found in mice also exist in humans and targeting them could be an additional useful therapy,” Wang says.

Sensory neurons may also use CGRP to stimulate cancer through more indirect pathways. Unpublished findings from Wang’s lab suggest that the neurons promote stomach cancer growth via contact with connective tissue cells in the tumour microenvironment. And other researchers have found that sensory nerves may, possibly through CGRP, cause T cell exhaustion and turn off immune responses directed at other types of cancers.

“But we think it all starts with the cancer cell setting up a neural circuit,” Wang says.

“Nerves are an underappreciated master regulator of normal growth and regeneration in animals. We know that when organs form during development, the nerves lead the way. From that point of view, it was not unexpected that nerves would be driving tumour growth as well.”

Source: Columbia University Irving Medical Center

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These Newly Discovered Brain Cells Enable us to Remember Objects

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Discovery of ‘ovoid cells’ reshapes our understanding of how memory works, and could open the door to new treatments for Alzheimer’s disease, epilepsy and more.

Ovoid cells. Photo credit: Dr. Mark Cembrowski

Take a look around your home and you’ll find yourself surrounded by familiar comforts – photos of family and friends on the wall, well-worn sneakers by the door, a shelf adorned with travel mementos.

Objects like these are etched into our memory, shaping who we are and helping us navigate environments and daily life with ease. But how do these memories form? And what if we could stop them from slipping away under a devastating condition like Alzheimer’s disease?

Scientists at UBC’s faculty of medicine have just uncovered a crucial piece of the puzzle. In a study published today in Nature Communications, the researchers have discovered a new type of brain cell that plays a central role in our ability to remember and recognise objects. 

Called ‘ovoid cells,’ these highly-specialised neurons activate each time we encounter something new, triggering a process that stores those objects in memory and allowing us to recognise them months, even years, later.

“Object recognition memory is central to our identity and how we interact with the world,” said Dr Mark Cembrowski, the study’s senior author, and an associate professor of cellular and physiological sciences at UBC and investigator at the Djavad Mowafaghian Centre for Brain Health. “Knowing if an object is familiar or new can determine everything from survival to day-to-day functioning, and has huge implications for memory-related diseases and disorders.”

Hiding in plain sight

Named for the distinct egg-like shape of their cell body, ovoid cells are present in relatively small numbers within the hippocampus of humans, mice and other animals.

Adrienne Kinman, a PhD student in Dr Cembrowski’s lab and the study’s lead author, discovered the cells’ unique properties while analysing a mouse brain sample, when she noticed a small cluster of neurons with highly distinctive gene expression.

“They were hiding right there in plain sight,” said Kinman. “And with further analysis, we saw that they are quite distinct from other neurons at a cellular and functional level, and in terms of their neural circuitry.”

To understand the role ovoid cells play, Kinman manipulated the cells in mice so they would glow when active inside the brain. The team then used a miniature single-photon microscope to observe the cells as the mice interacted with their environment.

The ovoid cells lit up when the mice encountered an unfamiliar object, but as they grew used to it, the cells stopped responding. In other words, the cells had done their jobs: the mice now remembered the objects.

“What’s remarkable is how vividly these cells react when exposed to something new. It’s rare to witness such a clear link between cell activity and behaviour,” said Kinman. “And in mice, the cells can remember a single encounter with an object for months, which is an extraordinary level of sustained memory for these animals.”

New insights for Alzheimer’s disease, epilepsy

The researchers are now investigating the role that ovoid cells play in a range of brain disorders. The team’s hypothesis is that when the cells become dysregulated, either too active or not active enough, they could be driving the symptoms of conditions like Alzheimer’s disease and epilepsy.

“Recognition memory is one of the hallmarks of Alzheimer’s disease – you forget what keys are, or that photo of a person you love. What if we could manipulate these cells to prevent or reverse that?” said Kinman. “And with epilepsy, we’re seeing that ovoid cells are hyperexcitable and could be playing a role in seizure initiation and propagation, making them a promising target for novel treatments.”

For Dr Cembrowski, discovering the highly specialised neuron upends decades of conventional thinking that the hippocampus contained only a single type of cell that controlled multiple aspects of memory.

“From a fundamental neuroscience perspective, it really transforms our understanding of how memory works,” he said. “It opens the door to the idea that there may be other undiscovered neuron types within the brain, each with specialised roles in learning, memory and cognition. That creates a world of possibilities that would completely reshape how we approach and treat brain health and disease.”

Source: University of British Columbia

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Intermittent Fasting could be Unsafe for Teenagers

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Photo by jamie he

A recent study reveals that age plays a significant role in the outcomes of intermittent fasting. Researchers from Technical University of Munich (TUM), LMU Hospital Munich, and Helmholtz Munich discovered that chronic intermittent fasting disrupted the development of insulin-producing beta cells in young mice. The findings, published in Cell Reports, raise concerns about potential risks for humans, especially teenagers.

“Intermittent fasting is known to have benefits, including boosting metabolism and helping with weight loss and heart disease. But until now, its potential side effects weren’t well understood,” says Alexander Bartelt, the Else Kröner Fresenius Professor and Chair of Translational Nutritional Medicine at TUM. In a recently published study, the team shows that intermittent fasting during adolescence could have long-term negative effects on metabolism.

Fasting improves metabolism in older mice, but not in the young

The researchers studied three groups of mice: adolescent, adult, and older animals. The mice remained without food for one day and were fed normally on two days. After ten weeks, insulin sensitivity improved in both the adult and older mice, meaning that their metabolism responded better to insulin produced by the pancreas. This is key to regulating blood sugar levels and preventing conditions like type 2 diabetes.

However, the adolescent mice showed a troubling decline in their beta cell function, the insulin-producing cells of the pancreas. Insufficient insulin production is linked to diabetes and disrupted metabolism. “Intermittent fasting is usually thought to benefit beta cells, so we were surprised to find that young mice produced less insulin after the extended fasting,” explains Leonardo Matta from Helmholtz Munich, one of the study’s lead authors.

Defective beta cells resemble those of type 1 diabetes patients

The researchers used the latest single-cell sequencing to uncover the cause of the beta cell impairment. By examining the blueprint of the pancreas, the team found that the beta cells in the younger mice failed to mature properly. “At some point, the cells in the adolescent mice stopped developing and produced less insulin,” says Peter Weber from Helmholtz Munich, also a lead author. Older mice, whose beta cells were already mature before the fasting began, remained unaffected.

This shows an accumulation of beta cells from the pancreas of an older mouse.
Beta cells from an older mouse.

The team compared their mouse findings to data from human tissues. They found that patients with type 1 diabetes, where beta cells are destroyed by an autoimmune response, showed similar signs of impaired cell maturation. This suggests that the findings from the mouse study could also be relevant to humans.

“Our study confirms that intermittent fasting is beneficial for adults, but it might come with risks for children and teenagers,” says Stephan Herzig, a professor at TUM and director of the Institute for Diabetes and Cancer at Helmholtz Munich. “The next step is digging deeper into the molecular mechanisms underlying these observations. If we better understand how to promote healthy beta cell development, it will open new avenues for treating diabetes by restoring insulin production.”

Source: Technical University of Munich (TUM)

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Older Patients can Inadvertently be Put at Risk When Taken off Anticoagulants

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Photo by cottonbro studio

For patients with atrial fibrillation, the risk of stroke or heart attack from stopping anticoagulants usually outweighs the risk of bleeding, according to new findings from the University of Bath.

Clinicians often worry about the dangers of prescribing blood thinning medications to older patients, due to concerns about falls and major bleeding, however this new study suggests that for patients with the common heart condition atrial fibrillation (AF), the health risks of not taking these drugs are significantly higher than the risk of a life-threatening bleed.

AF is associated with a fivefold increase in the risk of stroke. It also increases the risk of heart attacks and death. Anticoagulants are highly effective in managing AF and preventing strokes and other complications.

Older people also tend to fall more frequently, with falls being a leading cause of injury among adults aged 65 and older. These can lead to serious injuries, such as hip fractures and head injuries.

However, the new study, published in Heart, found that contrary to popular medical belief, stopping anticoagulants for patients aged 75 and over does not change the risk of major bleeds. These findings are important for clinicians to factor into their prescribing behaviour, according to the study’s authors.

“Prescribers need to consider the increased risk to patients of coming off anticoagulants, including stroke,” said Dr Anneka Mitchell, who conducted the research from the University of Bath and is a visiting researcher at the University’s Department of Life Sciences.

Rising cases

Cases of AF are rising in all age groups but particularly among people aged 85 years and over. In this age group, the number of people diagnosed with the condition doubled in men from 11.6% to 22.1% between 2000 and 2016, and increased in women from 9.6% to 16.5%. There is no data available to show trends from 2016.

Though there is a large body of evidence to support the use of blood thinners for older people with AF, the new study is believed to be the first to measure patient outcomes when anticoagulant medication is stopped.

Dr Mitchell’s study analysed data from the UK Clinical Practice Research Datalink (a research dataset that includes anonymised patient data from some UK general practices) between 2013 and 2017, focusing on patients aged 75 and older who were newly prescribed anticoagulants.

It found that the risks of stroke and death were three times higher during periods when patients were not receiving anticoagulation therapy. The risk of heart attacks was nearly double compared with periods when patients were treated with anticoagulants.

Warfarin versus direct oral anticoagulants

Dr Mitchell believes that as well as concern about falls, many clinicians base their decisions to withhold anticoagulants on the historic experience of patients taking the anticoagulant warfarin.

This medication – the only available option for treating AF until 2012 – is associated with a complex medication regimen, along with dietary restrictions and frequent blood-tests, making treatment difficult for many older patients.

Since 2013, however, a new family of drugs called direct oral anticoagulants (DOACs) have become the first line option for most patients. DOACs are as effective and safe as warfarin – sometimes more so – and are far more straightforward to take.

Dr Mitchell said: “For example, apixaban (a DOAC) has a lower risk of significant bleeding than warfarin, so for many older patients with AF, this would be an excellent medication.

“Our findings highlight the critical need for clinicians to carefully consider the risks of stopping anticoagulation therapy in older patients. Despite concerns about bleeding, this study suggests that discontinuing anticoagulation does not significantly affect the risk of major bleeding but does increase the risk of serious events such as stroke and death.”

She added: “Both the risks and benefits of medication must be discussed fully with patients before a medic stops prescribing anticoagulants, so that both doctor and patient are making a shared and informed decision. This study underscores the importance of evaluating the consequences of deprescribing anticoagulants, particularly in older adults who are at higher risk of adverse outcomes.”

Impacting the lives of older patients

Dr Anita McGrogan who led the research team from the Department of Life Sciences at Bath, said: “Older patients were poorly represented in clinical trials that evaluated the efficacy and safety of DOACs before these products were licensed, and those who were included were healthier than many people in the target group for prescribing. Because of this, the safety of these medications for people aged 75-plus was not evaluated, and many chose to avoid prescribing them for older people.

“This study has produced important results that will have an impact on patients in the future. It has filled the information gap by looking at anonymous data on 20 167 people aged over 75 years, collected by GPs. It clearly demonstrates the value of using big data to investigate important clinical questions, especially in vulnerable populations.”

Dr Tomas Welsh, an academic geriatrician at Royal United Hospitals Bath and research & medical director at ReMind, hopes the new research will provide both clinicians and patients with better evidence to inform their decisions regarding anticoagulants. He noted that, until now, clinicians advising patients to stop taking blood thinners were unable to quantify the increased risk of stroke.

“These data help patients and clinicians have a firmer grasp of the risks that they are being exposed to,” he said.

Dr Welsh also stressed that new-generation blood thinners were not always the right course of action for frail, older people.

“Suspending any medication or reducing the use of multiple medications in a frailer older patient is always a nuanced and individual discussion,” he said.

Source: University of Bath

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Mitochondria may Hold the Key to Curing Diabetes

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Cells with nuclei in blue, energy factories in green and the actin cytoskeleton in red. Credit: NIH

A new study has revealed that abnormalities in mitochondria, the powerhouses of the cell, can affect the development and maturation of pancreatic beta cells, eventually leading to them no longer being able to produced. This opens to the door to possibly restoring their function – and reversing the course of type 2 diabetes.

Mitochondrial defects are associated with the development of diseases such as type 2 diabetes. Several studies have shown that insulin-producing pancreatic β-cells of patients with diabetes have abnormal mitochondria and are unable to generate energy. Yet, these studies were unable to explain why the cells behaved this way.

In a study published in Science, University of Michigan researchers used mice to show that dysfunctional mitochondria trigger a response that affects the maturation and function of β-cells.

“We wanted to determine which pathways are important for maintaining proper mitochondrial function,” said first author Emily M. Walker, PhD, a research assistant professor of internal medicine.

To do so, the team damaged three components that are essential for mitochondrial function: their DNA, a pathway used to get rid of damaged mitochondria, and one that maintains a healthy pool of mitochondria in the cell.

“In all three cases, the exact same stress response was turned on, which caused β-cells to become immature, stop making enough insulin, and essentially stop being β-cells,” Walker said. 

“Our results demonstrate that the mitochondria can send signals to the nucleus and change the fate of the cell.”

The researchers also confirmed their findings in human pancreatic islet cells.

Mitochondrial dysfunction affects several types of cells

Their results prompted the team to expand their search into other cells that are affected during diabetes.  

Losing your β-cells is the most direct path to getting type 2 diabetes. Through our study we now have an explanation for what might be happening and how we can intervene and fix the root cause.”

-Scott A. Soleimanpour, M.D.

“Diabetes is a multi-system disease – you gain weight, your liver produces too much sugar and your muscles are affected. That’s why we wanted to look at other tissues as well,” said Scott A. Soleimanpour, M.D., director of the Michigan Diabetes Research Center and senior author of the study.

The team repeated their mouse experiments in liver cells and lipid cells and saw that the same stress response was turned on. Both cell types were unable to mature and function properly.

“Although we haven’t tested all possible cell types, we believe that our results could be applicable to all the different tissues that are affected by diabetes,” Soleimanpour said.

Reversing mitochondrial damage could help cure diabetes

Regardless of the cell type, the researchers found that damage to the mitochondria did not cause cell death. 

This observation brought up the possibility that if they could reverse the damage, the cells would function normally.

To do so, they used a drug called ISRIB that blocked the stress response. They found that after four weeks, the β-cells regained their ability to control glucose levels in mice.

“Losing your β-cells is the most direct path to getting type 2 diabetes. Through our study we now have an explanation for what might be happening and how we can intervene and fix the root cause,” Soleimanpour said.

The team is working on further dissecting the cellular pathways that are disrupted and hope that they will be able to replicate their results in cell samples from diabetic patients.

Source: Michigan Medicine – University of Michigan

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Global Action Needed to Solve the Medical Oxygen Crisis

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Photo by engin akyurt on Unsplash

Targets for universal access, national roadmaps and more affordable and accessible care are vital to help fill the medical oxygen gap affecting more than half of the world’s population, according to a new global report.

The Lancet Global Health Commission report details for the first time how future investment in strengthening medical oxygen systems could have a huge impact by saving millions of lives and improving pandemic preparedness.

Almost 400 million children and adults require medical oxygen every year. More than five billion people, 60 per cent of the world’s population, don’t have access to safe and affordable medical oxygen services.

The Commission, co-chaired by Makerere University in Uganda, the International Centre for Diarrheal Disease Research (icddr,b) in Bangladesh, Murdoch Children’s Research Institute (MCRI) in Australia, Karolinska Institute in Sweden and the Every Breath Counts Coalition in the US was launched in 2022 against the backdrop of the COVID-19 pandemic. The Commission was tasked with submitting actionable recommendations for governments, industry, global health agencies, donors and the healthcare workforce.

MCRI Dr Hamish Graham said the COVID-19 pandemic had put a spotlight on the longstanding global inequities in accessing medical oxygen.

“Oxygen is required at every level of the healthcare system for children and adults with a wide range of acute and chronic conditions,” he said. Previous efforts, including the major investments in response to the COVID-19 pandemic, largely focused on the delivery of equipment to produce more oxygen, neglecting the supporting systems and people required to ensure it was distributed, maintained, and used safely and effectively.”

Dr Graham said channelling investments into national oxygen plans and bolstering health systems, including wider use of pulse oximeters (a small device that measures how much oxygen is in the blood), would help solve the medical oxygen crisis.

“We urgently need to make high-quality, pulse oximeters more affordable and widely accessible,” he said. Pulse oximeters are available in 54 per cent of general and 83 per cent of tertiary hospitals in low- and middle-income countries, with frequent shortages and equipment breakdowns.

“Concerningly, in these countries the devices are performed for only 20 per cent of patients presenting to general hospitals and almost never for those at primary healthcare facilities. We see the greatest inequities in small and rural government health facilities and across Sub-Saharan Africa.”

Dr Graham said the importance of medical oxygen must also be recognised and integrated into broader national strategies and pandemic preparedness and response planning.

“Governments should bring together public and private sector partners with a stake in medical oxygen delivery, including health, education, industry, energy and transport to design a system and set up a governance structure that supports the new Global Oxygen Alliance (GO₂AL) and replenishing The Global Fund with a strong oxygen access mandate,” he said.

Source: Murdoch Childrens Research Institute

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Calorie Labels on Menus could Make Eating Disorders Worse

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Photo by Thought Catalog on Unsplash

Calorie labels on restaurant menus are negatively impacting people with eating disorders, according to a new study published in the BMJ Public Health.

The review, which is the first of its kind, is led by researchers at King’s College London. It found that individuals who have been diagnosed with an eating disorder changed their behaviours if presented with a menu featuring calorie labels.

This included avoiding restaurants, triggering eating disorder thoughts and paying more attention to calorie labels as identified by eye tracking research.

The research found that some people with eating disorders reported that seeing menu labels reinforced their eating disorder beliefs.

The study evaluated existing research to help build a picture of how nutritional labels on menus impact people with a lived experience of eating disorders or disordered eating. It reviewed 16 studies from the UK, US, Canada and Saudi Arabia which included 8,074 participants in total.

The study highlights that people with eating disorders can feel that eating disorders are perceived as less important in the light of obesity prevention policies.

However, physical health cannot be measured by a single indicator such as weight. Some argue that calorie labels can be seen as a blunt instrument to fix a complicated problem and that people with eating disorders could be losing out.

Food labelling came into force in England in 2022. Restaurants, take-aways and cafes with 250 employees or more must display the calories of the food and drink they sell on menus, online menus and take-away platforms. The measure was an attempt to curb rising obesity levels. The United States and Canada have also made calorie displays mandatory, however, few policies targeting obesity have considered the potential impact on eating disorders.

The eating disorder charity Beat estimates that at least 1.25 million people in the UK have an eating disorder. The number of people admitted to hospital with an eating disorder has risen approximately 7% each year since 2005 – 2006.

Senior author Dr Tom Jewell, Lecturer in Mental Health Nursing at King’s College London, said: “Our study highlights that people with lived experience of eating disorders are frustrated at being left out of the conversation around calorie labels.”

Striking a balance between the positive and harmful impacts of calorie labels on menus is vital in any public health policies.Dr Tom Jewell, Senior author and Lecturer in Mental Health Nursing at King’s College London

“Policymakers should consider the impact on both obesity and eating disorders when making decisions about nutrition labelling. A recent review found that calorie labelling has a modest effect on people’s behaviour but this needs to be counterbalanced with the potential harm it does for people with eating disorders.”

Co-author Dr Nora Trompeter, Research Fellow University College London, said: “Our study provides an important addition to the evidence base around calorie labels.”

Typically, there is a lot of focus on whether policies are effective in reducing obesity, but it is also critical to investigate whether these policies inadvertently harm people with eating disorders.

“Our review also shows that more research is needed to fully understand the impact of calorie labels on individuals with eating disorders. For example, none of the studies included young people.”

Source: King’s College London

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‘Healthy’ Vitamin B12 Levels not Enough to Ward off Neuro Decline

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Meeting the minimum requirement for vitamin B12, needed to make DNA, red blood cells and nerve tissue, may not actually be enough – particularly if for older adults. It may even put them at risk for cognitive impairment, according to a study published in Annals of Neurology.

The research found that older, healthy volunteers, with lower concentrations of B12, but still in the normal range, showed signs of neurological and cognitive deficiency. These levels were associated with more damage to the brain’s white matter – the nerve fibres that enable communication between areas of the brain – and test scores associated with slower cognitive and visual processing speeds, compared to those with higher B12.

The UC San Francisco researchers, led by senior author Ari J. Green, MD, of the Departments of Neurology and Ophthalmology and the Weill Institute for Neurosciences, said that the results raise questions about current B12 requirements and suggest the recommendations need updating.

“Previous studies that defined healthy amounts of B12 may have missed subtle functional manifestations of high or low levels that can affect people without causing overt symptoms,” said Green, noting that clear deficiencies of the vitamin are commonly associated with a type of anaemia. “Revisiting the definition of B12 deficiency to incorporate functional biomarkers could lead to earlier intervention and prevention of cognitive decline.”

Lower B12 correlates with slower processing speeds, brain lesions

In the study, researchers enrolled 231 healthy participants without dementia or mild cognitive impairment, whose average age was 71. They were recruited through the Brain Aging Network for Cognitive Health (BrANCH) study at UCSF.

Their blood B12 amounts averaged 414.8pmol/L, well above the U.S. minimum of 148pmol/L. Adjusted for factors like age, sex, education and cardiovascular risks, researchers looked at the biologically active component of B12, which provides a more accurate measure of the amount of the vitamin that the body can utilize. In cognitive testing, participants with lower active B12 were found to have slower processing speed, relating to subtle cognitive decline. Its impact was amplified by older age. They also showed significant delays responding to visual stimuli, indicating slower visual processing speeds and general slower brain conductivity.

MRIs revealed a higher volume of lesions in the participants’ white matter, which may be associated with cognitive decline, dementia or stroke.

While the study volunteers were older adults, who may have a specific vulnerability to lower levels of B12, co-first author Alexandra Beaudry-Richard, MSc, said that these lower levels could “impact cognition to a greater extent than what we previously thought, and may affect a much larger proportion of the population than we realize.” Beaudry-Richard is currently completing her doctorate in research and medicine at the UCSF Department of Neurology and the Department of Microbiology and Immunology at the University of Ottawa.

“In addition to redefining B12 deficiency, clinicians should consider supplementation in older patients with neurological symptoms even if their levels are within normal limits,” she said. “Ultimately, we need to invest in more research about the underlying biology of B12 insufficiency, since it may be a preventable cause of cognitive decline.”

Source: University of California – San Francisco