Month: January 2022

Categories : COVID Healthcare Politics and RegulationsTags :

SA’s Top 10 Health Topics to Watch in 2022

On By ModernMedia
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Spotlight highlights the country’s top 10 health topics to keep an eye on in 2022.

1. COVID prosecutions
Former health minister Dr Zweli Mkhize resigned amid allegations of wrongdoing in the Digital Vibes scandal, and hit back at the findings of the Special Investigations Unit, which had also implicated a number of top health department officials. Whether Health Minister Dr Joe Phaahla  will take decisive action against those found guilty will be an important litmus test. Last year, Dr Phaahla assured the public that the department “is going to thoroughly and decisively act to ensure nothing is swept under the carpet”.

2. The NHI Bill
Public hearings on the National Health Insurance Bill will be done by the end of January, with feedback in February and final report by April 1. It then goes to the National Council of Provinces for a similar stakeholder process, and before the end of 2022 it could be signed into law.
To date, public inputs on the Bill were mostly on governance issues. A critical point this year is whether MPs will take these inputs on board and make significant changes to the bill, or whether they will simply force through the bill largely unchanged.

3. Medico-legal claims
With R74 billion in medico-legal claims against the state, the State Liability Bill is back on Parliament’s agenda. Instead of government departments paying a lump sum for successful medical negligence claims, the Bill proposes a new settlement structure of separate payments to relieve budgetary pressure on hospitals. Since the necessary final report from the South African Law Reform Commission is months away, Spotlight does not think the Bill will be passed this year – and first prize would be to prevent medico-legal claims from happening.

4. Healthcare budget cuts
Unfortunately, there is still no end in sight to continued budget cuts to healthcare. Employing more nurses could reduce medico-legal claims, but in fact there is a growing shortage of nurses. Even th Office of Health Standards Compliance is also hamstrung by inadequate funding, with only 61 inspectors to cover more than 5000 public healthcare facilities, putting off private sector inspections until next year.

5. HIV prophylaxis
With the extremely promising results of injectable pre-exposure prophylaxis (PrEP) for HIV, there is still a process to go through before it will be made available in South Africa this year. COVID has shown that processes can be sped up if there is the will, but whether there is the same drive to treat HIV remains to be seen. As such, PrEP will most likely only be available in public healthcare facilities by the end of 2023.

6. An end to the COVID pandemic
While South Africa is heading towards living with COVID as an endemic disease, it is impossible to predict what surprises the coronavirus will have in store for the world this year in the form of new variants. However, according to Director of the Medical Research Council, Professor Glenda Gray, the winter months will give us an idea of the direction the pandemic will take with a fifth wave. Vaccination will remain key to reducing its severity.

7. SA’s TB programme
COVID severely set back SA’s TB programme, but 2022 should see the arrival of a number of delayed initiatives. These include rollout of the relatively new 3HP prevention pills, the results of new X-ray detection technology and  consequent possible changes to screening and testing, and an update to the Thembisa HIV model which will now include TB.

8. The National Mental Health Policy Framework
The new National Mental Health Policy Framework and Strategic Plan are expected to be finalised this year. However, as with the NHI, funding remains a problem. Only 5% of the current health budget goes to mental health services, and it only provides for one in 10 of those in need.

9. Improved procurement legislation
As illustrated by the government’s COVID procurement debacle, an overhaul is needed. Draft Public Procurement Bill proposes a single regulatory framework for all goods and services procured by government departments and has the potential to strengthen and streamline procurement processes. However, Spotlight notes that critically important pieces of legislation can simply vanish, as did the Medical Schemes Amendment Bill of 2018.

10. No-fault compensation fund
The COVID vaccine injury no-fault compensation fund has quietly fallen off the radar, with no payouts made to date. However, the NICD again urged people to report adverse events with the vaccine.

Source: Spotlight

Categories : TransplantsTags :

Lifestyle Changes Key for Older Kidney Transplant Recipients

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Photo by Robina Weermeijer on Unsplash

Researchers discovered that deaths among kidney transplant recipients due to factors other than organ rejection is the leading cause for transplanted kidney loss. Their findings, published in Transplantation Direct, revealed that only one in four transplanted kidney losses were caused by organ rejection.

“Immunosuppression medication to prevent rejection is often the focus when caring for patients post transplant. But this study highlights the increased risk of death from cancer and infection for transplant patients, especially those who are older and have diabetes,” said Andrew Bentall, MB, ChB, MD, the study’s co-first author.

The study involved 5752 patients who underwent a kidney transplant between 2006 and 2018. Of those, 691 died with a functioning kidney. Researchers found that 20% of these patients died from cancer; 19.7%, infection; and 12.6%, cardiac disease.

Another 553 patients lost their transplant due to the failure of a transplanted kidney. Of these patients, 38.7% of the patients’ kidneys failed due to rejection; 18.6%, glomerular diseases; and 13.9%, tubular injury.

Two types of recipients were found to be most vulnerable after transplant. The first are younger, nondiabetic patients who develop kidney failure due to organ rejection. The second group includes older, often diabetic patients who are at risk of death due to causes not associated with organ rejection, including cancer, infections and heart disease.

Care providers need to treat these two populations differently to minimise risks, according to Dr Bentall. For younger patients, that includes focusing on immunosuppression medication to prevent rejection. For older, often diabetic patients, it is critical to address chronic health issues, such as obesity, high blood pressure and diabetes. Focusing on these lifestyle changes is critical for improving long-term outcomes for kidney transplant recipients.

“It is important for these older patients that care providers emphasise the need for ongoing lifestyle changes that address obesity, high blood pressure and diabetes. Those include losing weight, exercising and new strategies for managing diabetes,” he said. “Making those changes could potentially impact the patient’s life and kidney outcomes more than immunosuppression therapies.”

Source: Mayo Clinic

Categories : Ageing ExerciseTags :

Exercise Protects Ageing Synapses

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Photo by Barbara Olsen from Pexels

When elderly people stay active, their brains have more proteins that enhance the connections between neurons to maintain healthy cognition, according to a study published in Alzheimer’s & Dementia: The Journal of the Alzheimer’s Association.

This protective impact was found even in people whose brains at autopsy were riddled with amyloid and tau proteins, associated with Alzheimer’s and other neurodegenerative diseases.

“Our work is the first that uses human data to show that synaptic protein regulation is related to physical activity and may drive the beneficial cognitive outcomes we see,” said lead author Kaitlin Casaletto, PhD.

The beneficial effects of physical activity on cognition have been shown in mice but have been much harder to demonstrate in people.

Dr Casaletto collaborated with William Honer, MD, a professor of psychiatry at the University of British Columbia and senior author of the study, to leverage data from the Memory and Aging Project at Rush University in Chicago. The project tracked the late-life physical activity of elderly participants, who also agreed to donate their brains upon death.

“Maintaining the integrity of these connections between neurons may be vital to fending off dementia, since the synapse is really the site where cognition happens,” Dr Casaletto said. “Physical activity – a readily available tool – may help boost this synaptic functioning.”

The researchers found that elderly people who remained active had higher levels of proteins that facilitate the exchange of information between neurons. This result dovetailed with Prof Honer’s earlier finding that people who had more of these proteins in their brains when they died were better able to maintain their cognition late in life.

Surprisingly, the effects ranged beyond the hippocampus to include other brain regions associated with cognitive function.

“It may be that physical activity exerts a global sustaining effect, supporting and stimulating healthy function of proteins that facilitate synaptic transmission throughout the brain,” Prof Honer said.

The brains of most older adults accumulate amyloid and tau proteins that are the hallmarks of Alzheimer’s disease pathology. Many scientists believe amyloid accumulates first, then tau, causing synapses and neurons to fall apart.

Dr Casaletto previously found that synaptic integrity, whether measured in the spinal fluid of living adults or the brain tissue of autopsied adults, appeared to dampen the relationship between amyloid and tau, and between tau and neurodegeneration.

“In older adults with higher levels of the proteins associated with synaptic integrity, this cascade of neurotoxicity that leads to Alzheimer’s disease appears to be attenuated,” she said. “Taken together, these two studies show the potential importance of maintaining synaptic health to support the brain against Alzheimer’s disease.”

Source: University of California in San Francisco

Categories : Mental HealthTags :

Virtual Companion Helps Reduce Anxiety

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Photo by Priscilla du Preez on Unsplash

A study found that, when a companion is present virtually as an avatar, people respond with less anxiety to fear-inducing noises. This effect was found to be most pronounced in women.

Led by Professor Grit Hein, the study is published in the journal Translational Psychiatry and could have implications for the treatment and management of social anxiety.

“In a nutshell, we have shown that anxiety can also be reduced by the ‘presence’ of a virtual person, especially in socially anxious women. And women in general seem to benefit more from social presence,” Prof Hein said. She believes that this insight might have practical significance.

The study recruited 208 men and women, who were all exposed to fear-inducing sounds alternating with neutral ones – either alone or in the company of another person. Women had female companions, men had male companions. The researchers determined the level of the participants’ anxiety response through changes in skin conductance. Moreover, the participants had to rate the sounds on a scale.

But the series of experiments differed in one key aspect: One group had a real person at their side during the experiment whereas the second group completed the task in a virtual reality – accompanied by an avatar that was an image of the real companion.

“Earlier experiments have shown that the presence of a third party can significantly reduce fear responses. In such situations, social support thus has a stress-buffering effect,” said Prof Hein.

However, not all people are equally sociable: for some, the presence of others might actually trigger apprehension or anxiety. They fear that their companion might notice their anxious responses, such as trembling, flushing or sweating, causing them stress in the first place. Thus far it was unclear whether an avatar is also capable of triggering such a response.

The results of Prof Hein’s study have now provided clarity in this regard. They show that:

  • women respond much more strongly to fear-inducing sounds than men do.
  • the presence of another person reduces anxiety, especially in women. This is especially true for women without social anxiety disorder.
  • the presence of a virtual person also reduces the anxiety response in women – regardless of the level of social anxiety they experience. So a virtual agent may increase feelings of safety in women suffering from social anxiety disorder.
  • social anxiety does not have a comparable effect on men.

“Our findings provide new insights into the individual differences that influence the social modulation of the autonomic human anxiety responses,” the authors concluded in their study. The researchers’ next aim is to study long-term effects and replicate the findings in real life.

Future studies should systematically explore the effect of the gender of the present person, they suggested. This would also allow scientifically sound evidence to be provided as to how men respond when they have a woman at their side in fear-inducing situations and vice versa.

Source: News-Medical.Net

Categories : Diseases, Syndromes and Conditions Injury & TraumaTags :

A New Treatment for Chronic Tendon Disease

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Photo by Nino Liverani on Unsplash

The Achilles tendon can endure a load nearly 8 times body weight during exercise, rendering it vulnerable to injury despite its strength, which can be worsened by a failure to properly heal, forming bone instead of new tendon. A new study found that by inhibiting blood vessel formation, the anomalous bone growth can be prevented.

Due to the unique nature of tendons, failing to consult a doctor soon after an injury can lead to chronic tendon disease, which is characterised by pain, swelling, and movement problems. Tendon heterotopic ossification (HO) is a rare type of chronic tendon disease where new bone grows the tendon, causing even more damage. Famous athletes have had to retire early from sports due to a lack of a radical solution for Achilles tendon injuries.

Using single-cell sequencing technology, a team led by Professor Ouyang Hongwei found that changes in the tissue microenvironment of tendon HO alterations in gene expression and in tendon stem progenitor cells. These findings were published in Bone Research, providing a novel treatment for tendon heterotopic ossification.

The researchers firstly found that the tendon specific transcription factor MKX decreased significantly in heterotopic ossified human tendon, and deletion of MKX led to spontaneous ossification of mouse tendon, suggesting that MKX plays a critical role in tendon HO.

Further studies revealed that MKX knockout mouse tendon cells expressed high levels of genes related to blood vessel formation, resulting in vascular invasion and remodelling of the tendon extracellular matrix. This also resulted in abnormal activation of genes related to bone and cartilage in tendon stem cells. These data indicated that inhibition of blood vessel formation may improve the tendon tissue microenvironment and prevent HO progression.

Armed with this knowledge, Prof Ouyang and his colleagues searched for drugs that can inhibit the angiogenesis process. They found that local injection of a small molecule inhibitor known as BIBF1120 significantly inhibited the neovascularisation of tendon after injury, thus alleviating the progression of tendon HO.

Source: MedicalXpress

Categories : Medical Research & TechnologyTags :

New Coating Makes the Nanomedicine Go Down

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Upon injection into the blood, nanomedicines (blue spheres) are immediately attacked by proteins of the immune system called complement proteins (orange). Complement proteins cause rapid destruction of the nanomedicine, and also induce an anaphylaxis-like reaction. By attaching complement-degrading proteins (yellow ninjas made of protein) to the surface of nanomedicines, Penn researchers have largely solved this problem, potentially allowing more diseases to be safely treated by nanomedicine. Credit: University of Pennsylvania

In nanomedicine, immune reactions against the nanoparticles that contain the medicine or vaccine, reducing its effectiveness. Researchers have now come up with a new method to prevent the body from treating nanomedicines like foreign invaders, by covering those nanoparticles with a coating to suppress the immune response.

As soon as they are injected into the bloodstream, unmodified nanoparticles are swarmed by complement proteins, triggering an inflammatory response and preventing the nanoparticles from reaching their treatment targets. Penn Medicine researchers, whose findings are published in Advanced Materials, have devised a coating for nanoparticles that suppresses complement activation.

Nanoparticles are tiny capsules, typically made from proteins or fat-related molecules, that contain certain types of treatment or vaccine. The best-known examples of nanoparticle-delivered medicines are mRNA COVID vaccines.

“It turned out to be one of those technologies that just works right away and better than anticipated,” said study co-senior author Jacob Brenner, MD, PhD.

RNA- or DNA-based therapies generally need delivery systems to get them through the bloodstream into target organs. Harmless viruses often have been used as carriers or “vectors” of these therapies, but nanoparticles are increasingly considered safer alternatives. Nanoparticles also can be tagged with antibodies or other molecules that make them hone in precisely on targeted tissues.

The complement attack problem has been a serious impediment to nanomedicine. Circulating complement proteins treat nanoparticles as if they were bacteria, immediately coating nanoparticle surfaces and summoning macrophages to engulf them. Researchers have attempted to reduce the problem by pre-coating nanoparticles with camouflaging molecules, such as forming a watery, protective shell around nanoparticles using polyethylene glycol (PEG).

But nanoparticles camouflaged with substances like PEG still draw at least some complement attack. In general, nanoparticle-based medicines that move through the bloodstream (mRNA COVID vaccines are injected into muscle, not the bloodstream) have had a very low efficiency in getting to their target organs, usually under 1%.

In the study, the researchers came up with a new approach to protect nanoparticles, based on natural complement-inhibitor proteins that circulate in the blood, attaching to human cells to help protect them from complement attack.

In vitro tests using standard PEG-protected nanoparticles with one of these complement inhibitors, called Factor I, provided dramatically better protection from complement attack. In mice, the same strategy prolonged the half-life of standard nanoparticles in the bloodstream, allowing a much larger fraction of them to reach their targets.

“Many bacteria also coat themselves with these factors to protect against complement attack, so we decided to borrow that strategy for nanoparticles,” said co-senior author Jacob Myerson, PhD, a senior research scientist in the Department of Systems Pharmacology and Translational Therapeutics at Penn.

In a set of experiments in mouse models of severe inflammatory illness, the researchers also showed that attaching Factor I to nanoparticles prevents the hyper-allergic reaction that otherwise could be fatal.

Further testing will be needed before nanomedicines incorporating Factor I can be used in people, but in principle, the researchers said, attaching the complement-suppressing protein could make nanoparticles safer and more efficient as therapeutic delivery vehicles so that they could be used even in severely ill patients.

The researchers now plan other protective strategies for medical devices, such as catheters, stents and dialysis tubing, which are similarly susceptible to complement attack. They also plan to investigate other protective proteins.

“We’re recognising now that there’s a whole world of proteins that we can put on the surface of nanoparticles to defend them from immune attack,” Dr Brenner said.

Source: University of Pennsylvania School of Medicine

Categories : Ethics and Law Mental HealthTags :

‘No NGOs Were Ready’, Life Esidimeni Inquest Reveals

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Photo by Tingey Injury Law Firm on Unsplash

The former Gauteng deputy director-general for mental health services, Hannah Jacobus, has the process to move Life Esidimeni patients was rushed. She was being cross-examined by the State’s Advocate Willem Pienaar.

The much-delayed inquest meant to determine any criminal liability for the deaths of 144 mental health patients in the 2016 Life Esidimeni disaster continued virtually on Monday.

Jacobus’ role was in downscaling of patients at Life Esidimeni for cost savings, and says there was no indication of it closing at the time. When its closure was announced, these downscaling plans were not implemented and there was no timeframe given for when patients were to move out.

The former deputy DG admitted to writing false licences for NGOs, under pressure from then head of Gauteng mental health services, Dr Makgoba Manamelashe. However, Jacobus maintained that while she assessed their suitability, she ultimately did not issue any licences.

Dr Manamela signed licences authorising inexperienced‚ underfunded‚ poorly equipped NGOs to look after patients with profound mental illnesses.

After the Gauteng health department terminated the contract with Life Esidimeni, NGOs were used to care for the 1712 patients.

Dr Manamela admitted to Solidarity advocate Dirk Groenewald that the NGOs to which she gave authority did not comply with the legal requirements. In 2017,  it was found that patients were transferred to NGOs that had been issued “unlawful and knowingly fraudulent” licences.

Many NGOs were subsequently found to be entirely unprepared for the patients they received, some lacking sufficient food, water, medication, staff or blankets.  According to Jacobus, the process have only been completed by 2020 according to the downscaling schedule.

“From December 2015 to the end of March 2016 [is not] a sufficient period to determine and appoint suitable NGOs to receive mental healthcare [patients]. No NGOs were ready by the end of March. We needed more time,” she said.

Source: Times Live

Categories : Diseases, Syndromes and ConditionsTags :

Study Shows New Possibilities of Treating Rare Ossifying Disease

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Source: National Cancer Institute on Unsplash

Fibrodysplasia ossificans progressiva (FOP) is a rare disease characterised by anomalous bone growth at the site of even minor injuries. It results in what some term a “second skeleton,” which locks up joint movement and even making breathing difficult. However, new research shows that forming extra-skeletal bone might not be the only driver of the disease. Impaired muscle tissue regeneration allows unwanted bone to form instead of muscle regeneration after injury.

This study was published in NPJ Regenerative Medicine.

“While we have made great strides toward better understanding this disease, this work shows how basic biology can provide great insights into appropriate regenerative medicine therapies,” said the study’s lead author, Foteini Mourkioti, PhD. “From the lab, we’re now able to show that there is potential for a whole new realm of therapies for patients with this devastating condition.”

About 15 years ago, researchers discovered that a mutation in the ACVR1 gene was responsible for FOP. In that study, the team found that the mutation changed cells within muscles and connective tissues, causing them to behave like bone cells and create new, extraneus bone.

“However, while investigations of how the FOP mutation alters the regulation of cell fate decisions have been extensively pursued in recent years, little attention has been paid to the effects of the genetic mutation on muscle and its impact on the cells that repair muscle injuries,” Shore said. “We were convinced that pursuing research in this area could provide clues not only for preventing extra bone formation but also for improving muscle function and regeneration, bringing new clarity to FOP as a whole.”

The researchers studied muscle from mice with the same mutation in the ACVR1 gene that people with FOP have. They focused on two specific types of muscle tissue stem cells: fibro-adipogenetic progenitors (FAPs) and muscle stem cells (MuSCs). Typically, muscle injury repair requires a careful balance of these two cell types. Injured tissue responds by an expansion of FAP cells, which are assigned to recruit muscle stem cells that will regenerate the damaged muscle tissue. After about three days, FAPs die off, their job done. At the same time, MuSCs transition toward a more mature, differentiated state, called muscle fibre, essential to organised movement of our muscles.

In the mice with the ACVR1 mutation being studied, apoptosis – the process through which FAP cells die as a part of proper muscle regeneration – had slowed significantly, leading to a high presence of FAPs past their usual lifespan, altering their balance with the MuSCs. The injured tissue also showed a diminished capacity for muscle stem cell maturation and, as a result, muscle fibres were considerably smaller in mice carrying the ACVR1 mutation compared to muscle fibres in mice lacking the mutation.

“The prolonged persistence of diseased FAPs within the regenerating muscle contributes to the altered muscle environment in FOP, which reduces muscle regeneration and allows the over-abundant FAPs to contribute to the formation of extra-skeletal bone,” Mourkioti said. “This provides a completely new perspective on how excess extra-skeletal bone is formed – and how it could be prevented.”

The current targets for treating FOP focus on slowing extra-skeletal bone growth. This research may provide a pivotal new direction. “We propose that therapeutic interventions should consider promoting the regenerating potential of muscles together with the reduction of ectopic bone formation,” the authors wrote. “By addressing both stem cell populations and their roles in the origin of FOP, there is the possibility of greatly enhanced therapies.”

Source: University of Pennsylvania School of Medicine

Categories : Metabolic DisordersTags :

Newly Discovered Hormone Implicated in Development of Diabetes

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Image by Nataliya Vaitkevich on Pexels

A newly discovered hormone named fabkin helps regulate metabolism and may play an important role in the development of both type 1 and type 2 diabetes, according to a new study published in Nature.

Fabkin levels were abnormally high in mice and human patients with either type 1 or type 2 diabetes, and blocking the activity of fabkin prevented the development of both forms of diabetes in the animals. Fabkin likely plays a similar role in humans and the hormone complex could be a promising therapeutic target, according to the researchers.

“For many decades, we have been searching for the signal that communicates the status of energy reserves in adipocytes to generate appropriate endocrine responses, such as the insulin production from pancreatic beta cells,” said senior author Gökhan S. Hotamisligil. “We now have identified fabkin as a novel hormone that controls this critical function through a very unusual molecular mechanism.”

Many hormones are involved in the regulation of metabolism, such as insulin and leptin. Fabkin is different from traditional hormones in that it is not a single molecule with a single defined receptor. Instead, fabkin is composed of a functional protein complex consisting of multiple proteins, including fatty acid binding protein 4 (FABP4), adenosine kinase (ADK) and nucleoside diphosphate kinase (NDPK). Through a series of experiments, the researchers determined that fabkin regulates energy signals outside of cells. These signals then act through a family of receptors to control target cell function. In the case of diabetes, fabkin controls the function of beta cells in the pancreas that are responsible for insulin production.

Hotamisligil and colleagues previously discovered that a protein known as FABP4 is secreted from fat cells during lipolysis, the process in which lipids stored within fat cells are broken down, typically in response to starvation. Since then, many studies showed links between circulating FABP4 and metabolic diseases including obesity, diabetes, cardiovascular disease, and cancer. However, the mechanism of action was unknown.

In the new study, the researchers showed that when FABP4 is secreted from fat cells and enters the bloodstream, it binds with the enzymes NDPK and ADK to form the protein complex now identified as fabkin. In this protein complex, FABP4 modifies the activity of NDPK and ADK to regulate levels of molecules known as ATP and ADP, which are the essential units of energy in biology. The researchers discovered that surface receptors on nearby cells sense the changing ratio of ATP to ADP, triggering the cells to respond to the changing energy status. As such, fabkin is able to regulate the function of these target cells.

The pancreas’ beta cells are a target of fabkin and the hormone is a driving force behind the development of diabetes, the researchers showed. When fabkin in mice was neutralised with an antibody, the animals did not develop diabetes. When the antibody was given to obese, diabetic mice, they reverted to a healthy state.

“The discovery of fabkin required us to take a step back and reconsider our fundamental understanding of how hormones work.” said lead author Kacey Prentice. “I am extremely excited to find a new hormone, but even more so about seeing the long-term implications of this discovery.”

Source: Harvard University

Categories : COVIDTags :

Over 50s Have Greater Risk of Reduced Mobility after COVID

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Photo by Bennett Tobias on Unsplash

Adults over 50 with mild or moderate COVID have increased risk of worsening mobility and physical function, even if hospitalisation is not required to treat the virus, new research has found.

The study, published in JAMA Network Open, highlights the burden of COVID among middle-aged and older adults who are not hospitalised, and suggests that even those who experienced even mild COVID have lasting, troublesome symptoms.

Researchers surveyed more than 24 000 people over the age of 50 from across Canada during the initial phase of the lockdown in 2020 to determine the effect of a COVID diagnosis on their mobility. 

The team looked at mobility issues including difficulty getting up from sitting in a chair, ability to walk up and down stairs without assistance and walking two to three neighbourhood blocks, as well as changes in participants’ ability to move around the home, engage in housework and physical activity.

“We found that even those with mild and moderate illness due to COVID experienced adverse changes in mobility and physical function compared to individuals without COVID,” said co-author Professor Susan Kirkland.

“These findings are worth noting because they indicate that the negative effects of COVID are much broader and impact a wider range of older adults than those who are hospitalised for COVID.”

Participants with COVID had nearly double the odds of worsening mobility and physical function, although most had mild or moderate symptoms. Of the 2748 individuals with confirmed, probable or suspected COVID, 94% were not hospitalised.

Individuals with confirmed or probable COVID had double the odds of worsening ability to engage in household activities and participate in physical activity than those without COVID. Similar results were found for those with suspected COVID.

“Our results showed there was a higher risk for mobility problems in people who were older, had lower income, those with three or more chronic conditions, low physical activity and poorer nutrition,” said co-author, assistant professor Marla Beauchamp.

“However, those factors alone did not account for the mobility problems we observed among people with COVID. Rehabilitation strategies need to be developed for adults who avoid hospitalisation due to COVID but still need support to restore their mobility and physical function.”

The researchers concluded that there is a need to further understand the long-term impacts of COVID and consider “the development and implementation of effective intervention and management approaches to address any persistent deficits in mobility and functioning among those living in the community.”

Source: Dalhousie University