New research in rats indicates that a Mediterranean plant may be an effective treatment for ulcerative colitis, a type of inflammatory bowel disease. The findings are published in the Journal of the Science of Food and Agriculture.
Various antioxidant and anti-inflammatory medications are used to treat ulcerative colitis, but they can cause numerous side effects. To test the potential of the Arbutus unedo plant (often referred to as the strawberry tree) that is native to the Mediterranean region, investigators gave rats doses of an extract from the plant before exposing the animals to acetic acid, a chemical that induces ulcerative colitis.
The pretreatment prevented changes in the colon’s lining and led to fewer colonic lesions compared with no pretreatment. The pretreatment also caused decreased expression of various proteins that promote oxidative stress and inflammation.
“Our findings suggest that Arbutus unedo should be studied further in preventative and therapeutic approaches to gastrointestinal disorders,” said corresponding author Soumaya Wahabi, PhD, of the University of Jendouba, in Tunisia.
New research from UC Davis Comprehensive Cancer Center has uncovered an evolutionary change that may explain why certain immune cells in humans are less effective at fighting solid tumours compared to non-human primates. The findings, published in Nature Communications, could lead to more powerful cancer treatments.
The study revealed a tiny genetic difference in an immune protein called Fas Ligand (FasL) between humans and non-human primates. This genetic mutation makes the FasL protein vulnerable to being disabled by plasmin, a tumour-associated enzyme. This vulnerability seems unique to humans and is not found in non-human primates, such as chimpanzees.
“The evolutionary mutation in FasL may have contributed to the larger brain size in humans,” said Jogender Tushir-Singh, senior author for the study and an associate professor in the Department of Medical Microbiology and Immunology. “But in the context of cancer, it was an unfavourable tradeoff because the mutation gives certain tumours a way to disarm parts of our immune system.”
Tumour environment neutralises key immune protein
FasL is an immune cell membrane protein that triggers apoptosis, which activated immune cells, including CAR-T cells, make use of to kill cancer cells.
The UC Davis team discovered that in human genes, a single evolutionary amino acid change — serine instead of proline at position 153 — makes FasL more susceptible to being cut and inactivated by plasmin.
This means that even when human immune cells are activated and ready to attack the tumour cells, one of their key apoptosis tools, FasL, can be neutralised by the tumour environment, reducing the effectiveness of immunotherapies.
The findings may help explain why CAR-T and T-cell-based therapies can be effective in blood cancers but often fall short in solid tumours. Blood cancers often do not rely on plasmin to metastasise, whereas tumours like ovarian cancer rely heavily on plasmin to spread the cancer.
Plasmin inhibitors may enhance immunotherapy
Significantly, the study also showed that blocking plasmin or shielding FasL from cleavage can restore its cancer-killing power. That finding may open new doors for improving cancer immunotherapy.
By combining current treatments with plasmin inhibitors or specially designed antibodies that protect FasL, scientists may be able to boost immune responses in patients with solid tumours.
“Humans have a significantly higher rate of cancer than chimpanzees and other primates. There is a lot that we do not know and can still learn from primates and apply to improve human cancer immunotherapies,” said Tushir-Singh. “Regardless, this is a major step toward personalising and enhancing immunotherapy for the plasmin-positive cancers that have been difficult to treat.”
This lemur is called Nemesis and lives at the Duke Lemur Center
What can lemurs tell us about inflammation and aging, aka “inflammaging” in humans? That’s the question Elaine Guevara, a biological anthropologist who studies the evolution of life history and aging in primates, set out to understand.
In newly published research on age-related inflammation in ring-tailed and sifaka lemurs, Guevara discovered that perhaps we should rethink the inevitability of inflammaging in humans.
Although similar in many ways, ring-tailed and sifaka lemurs show differences in life pacing and lifespan, making useful comparisons. Because lemurs and humans are primates and share a common ancestor that lived millions of years ago, they offer valuable insights into human evolution.
“Contrary to our predictions, neither species showed age-related change in either marker of oxidative stress. Neither lemur species exhibited age-related change in inflammation; if anything, contrary to our prediction, ring-tailed lemurs showed marginal declines in inflammation with age,” Guevara said.
This finding, consistent with a few recent studies of other non-human primates, suggests that lemurs avoid the phenomenon of “inflammaging” widely observed in humans.
The study shows inflammaging is not a universal feature of primates, pointing to some differences that might suggest it turns out it’s not even a universal feature of humans, according to Christine Drea, a professor of evolutionary anthropology who was one of the researchers working with Guevara.
What is Inflammaging?
As we grow older, low-grade chronic inflammation sets in, which in turn can cause health problems such as heart disease, strokes, diabetes, cancer and osteoarthritis.
Why inflammaging increases with age in humans, what causes it and how it can be prevented are answers to questions that can unlock critical information to help humans live longer and healthier lives.
Collecting Data from Lemurs
Drea said the team first had to find a way to measure oxidative stress, which can be found in blood, urine and saliva. They settled on urine.
“Our role at the beginning was planning, designing, brainstorming, comparing and getting these samples,” said Drea, who has worked with the Duke Lemur Center since 1999. The Lemur Center does not allow research that will harm the animals.
The next step says Guevara is to conduct similar research with lemurs in the wild.
“There are a lot of good reasons to think that aging can be quite different in captivity and in the wild, and that in itself, is informative to evaluating the degree to which human inflammation is intrinsic versus environmental,” she said.
In the meantime, Guevara says this study serves as the first step in unravelling the question of why humans are suffering from inflammatory-related and age-related conditions and finding ways to treat them.
With a rapidly aging global population, “these insights are essential for mitigating disability and improving quality of life in later years,” she said.
But upping physical activity level still linked to 20–25% lower risk of death from any cause Switching to a more active lifestyle at any point in adulthood may extend lifespan
Being consistently physically active in adulthood is linked to a 30–40% lower risk of death from any cause in later life, while upping levels from below those recommended for health is still associated with a 20–25% lower risk, finds a pooled data analysis of the available evidence, published online in theBritish Journal of Sports Medicine.
The findings prompt the researchers to conclude that switching to a more active lifestyle at any point in adult life may extend the lifespan, and that it’s never too late to start.
Currently, it’s recommended that adults should aim for 150-300 weekly minutes of moderate intensity physical activity, or 75-150 weekly minutes of vigorous intensity physical activity, or a combination of the two, note the researchers.
But while these recommendations were based on the best evidence available, most of it captured measurements of physical activity at only one point in time, which might hide the potential impact of changing patterns during adulthood, they add.
The researchers therefore wanted to find out if differing patterns of physical activity, as well as its cumulative impact during adulthood, might be associated with a lower risk of death from all causes, and specifically from cardiovascular disease and cancer.
They scoured research databases for relevant studies that assessed physical activity at two or more points in time, and included in their review 85 studies published in English up to April 2024, with sample sizes ranging from 357 to 6,572,984 participants.
Fifty nine of the studies looked at long term patterns of physical activity across adulthood; 16 looked at the average benefits of different physical activity levels; and 11 explored the potential impact of cumulative physical activity on risk of death.
To overcome the challenges posed by different analytical methods used, the researchers carried out separate analyses for each of them.
Pooled data analysis of the study results showed that, overall, a higher level of physical activity was associated with lower risks of all the included outcomes.
Consistently active people (32 studies) had around a 30–40% lower risk of dying from any cause, while those who increased their levels of physical activity (21 studies) from below those recommended had a 20-25% lower risk of death from any cause.
Specifically, participants who switched from being physically inactive to being active were 22% less likely to die from any cause than those who remained inactive, while those who increased their leisure time physical activity levels were 27% less likely to do so.
On the other hand, swapping an active lifestyle for an inactive one wasn’t associated with a lower risk of death from any cause.
Generally, the associations observed between a high level of physical activity and a lower risk of death were more evident for cardiovascular disease than for cancer.
Compared with participants who were consistently inactive over time, those who were consistently active, overall, or only in their leisure time, were around 40% and 25% less likely to die from cardiovascular disease and cancer, respectively.
But in general, the evidence for the associations between physical activity patterns and death from a specific cause remained inconclusive, especially for death from cancer.
The pooled data suggested that people who were consistently active or who became active had lower risks of death from any cause, and specifically from cardiovascular disease, when meeting the recommended weekly physical activity levels.
But being consistently physically active and clocking up more than the recommended maximum weekly amount of moderate to vigorous intensity exercise was associated with only a small additional reduction in risk.
Maintaining or increasing physical activity at levels below the recommended weekly amount, however, was associated with appreciable health benefits, indicating that some physical activity is always better than none, say the researchers.
And an average volume of physical activity that met the recommended weekly amount was also associated with a 30–40% lower risk of death from all causes. But more research is needed to confirm this, they add.
The researchers acknowledge some limitations to their findings, including that most of the studies included in the pooled data analyses relied on subjective assessments of physical activity, which may not always have been accurate.
And there were only a few studies that looked at cumulative amounts of physical activity, or cancer deaths.
Nevertheless, the findings have important public health implications, insist the researchers.
“First, our results emphasised the importance of [physical activity] across adulthood, indicating that initiating [it] at any point in adulthood may provide survival benefits.”
They add: “As being consistently active provides greater health benefits than being previously active (ie, no longer maintaining activity), this highlights the importance of sustained [physical activity] over time.
“Future [physical activity] interventions may not only target inactive people, but also support active people to maintain their activity.”
Weizmann Institute scientists have discovered hundreds of molecules that promote nerve regeneration in mice – and may even encourage growth in brain neurons
Top: Overexpression of genes from the B2-SINE family in retinal ganglion neurons led to accelerated growth after injury. Bottom: Ganglion cells after injury without B2-SINE overexpression. Credit: Weizmann Institute of Science
Unlike the brain and spinal cord, peripheral nerve cells, whose long extensions reach the skin and internal organs, are capable of regenerating after injury. This is why injuries to the central nervous system are considered irreversible, while damage to peripheral nerves can, in some cases, heal, even if it takes months or years. Despite decades of research, the mechanisms behind peripheral nerve regeneration remain only partially understood.
In a new study published in Cell, researchers from Prof Michael (Mike) Fainzilber’s lab at the Weizmann Institute of Science discovered that a family of hundreds of RNA molecules with no known physiological function is essential to nerve regeneration. Remarkably, the study showed that these molecules can stimulate growth not only in the peripheral nervous system of mice but also in their central nervous system. These findings could pave the way for new treatments for a variety of nerve injuries and neurodegenerative diseases.
For a peripheral nerve to regenerate, it must maintain communication between the neuron’s cell body and its long extension – the axon – which in humans can reach more than a meter in length. In a series of studies over the past two decades, Fainzilber’s lab has revealed key components of this communication: proteins that act like postal couriers, delivering instructions for the production of growth-controlling factors and other proteins, from the cell body to the axon. These molecular couriers also help assess the distance between the cell body and the axon tip, allowing the neuron to modulate its growth accordingly. Yet one central issue remained: What triggers the regenerative growth after injury, and why does this not happen in central nervous system cells?
“While the growth acceleration observed in our study is not yet sufficient to address clinical paralysis, it is definitely significant”
In the new study, Dr Indrek Koppel of Fainzilber’s lab, in collaboration with Dr Riki Kawaguchi of the University of California, Los Angeles (UCLA), examined a specific kind of gene expression in the peripheral nerves of mice following injury. The researchers were surprised to find that one day after damage, the neurons increased the expression of an entire family of short genetic sequences called B2-SINEs, whose role was previously unknown. These sequences do not encode any proteins, and because they are known for “jumping” around the genome, meaning that they can appear at the wrong place or time, they have a bad reputation. But the researchers found that after injury, the neurons began expressing many B2-SINE RNA transcripts, in parallel with other processes preparing the cell for regeneration and repair.
However, B2-SINE is an enormous family, comprising some 150 000 sequences scattered throughout the mouse genome. The initial analysis could not determine which of these were responsible for promoting growth. Dr. Eitan Erez Zahavi, also of Fainzilber’s lab, who led the new study alongside Koppel, used bioinformatics tools to identify 453 B2-SINE sequences that are highly expressed after injury, promoting nerve growth. Collaborating with international research teams, the scientists showed that this overexpression after injury is unique to peripheral nerve cells and does not occur in the central nervous system.
The periphery leads, the center follows
The researchers then tested whether B2-SINEs from peripheral nerve cells could also stimulate neuronal growth in the central nervous system. They induced retinal neurons in mice to overexpress RNA molecules of the B2-SINE type and observed faster regeneration after injury. A similar experiment in the mouse motor cortex – the brain region that controls muscle movement via long axons projecting to the spinal cord – showed that neurons expressing high levels of B2-SINE also regenerated faster than control neurons.
“There are still no effective treatments to accelerate nerve cell growth and regeneration,” Fainzilber notes. “While the growth acceleration observed in our study is not yet sufficient to address clinical paralysis, it is definitely significant. Of course, the path from basic research to clinical application is long, and we must make sure that enhancing growth mechanisms does not, for example, increase the risk of cancer.”
One final mystery remained: How do B2-SINE RNA molecules actually promote regeneration? With help from Prof Alma L. Burlingame’s group at the University of California, San Francisco, the researchers discovered that these RNAs promote a physical link between the molecular “couriers” carrying instructions for producing growth-associated proteins and the ribosomes that read these instructions and carry them out. This means that production of the critical factors takes place closer to the cell body rather than to the tip of the axon. The researchers believe that this signals to the neuron that it is “too small,” triggering a growth response.
“There are over a million sequences called Alu elements in the human genome, the human equivalent of B2-SINEs in mice,” says Fainzilber. “These molecules had been previously shown to bind to ribosomes and mail couriers, but why this happens was unknown. We’re now trying to determine whether Alu or other noncoding RNA elements are involved in nerve regeneration in humans.”
“Recovery from peripheral nerve injuries, or from systemic diseases like diabetes that affect these nerves, can be very slow,” he adds. “That’s why we’re now testing a therapy that might speed up regeneration by mimicking B2-SINE activity. This therapy involves small molecules that connect the couriers to ribosomes while keeping them close to the nerve cell body, promoting faster growth. We are conducting this research in collaboration with Weizmann’s Bina unit for early-stage research with applicative potential.”
Beyond promoting peripheral nerve regeneration, the new study also hints at an even broader prospect: regeneration in the central nervous system. “We are currently working with UCLA on a study showing that the mechanism we discovered plays a role in recovery from stroke in mouse models,” Fainzilber says. “Additionally, we’re collaborating with Tel Aviv University, Hebrew University and Sheba Medical Center to study its possible role in ALS, a progressive neurodegenerative disease. Neurodegenerative conditions affect many millions of people worldwide. While the road ahead is long, I truly hope we’ll one day be able to harness our newly discovered regeneration mechanism to treat them.”
Science Numbers
After injury, the axon of a peripheral nerve cell regrows at a rate of around 1 millimetre a day.
In the largest clinical trial to date, pramipexole was found to be substantially more effective than a placebo at reducing the symptoms of treatment resistant depression (TRD) over the course of nearly a year, when added to ongoing antidepressant medication.
The trial, supported by National Institute for Health and Care Research (NIHR) and published in The Lancet Psychiatry,included 150 patients with treatment resistant depression, with equal numbers receiving 48 weeks of pramipexole or a placebo, alongside ongoing antidepressant medication.
Overall, the group taking pramipexole experienced a significant and substantial reduction in symptoms by week twelve of treatment, with the benefits persisting over the course of a year. However, there were also significant side effects, such as nausea, sleep disturbance and dizziness, with around one in five people on pramipexole dropping out of the trial as a result.
Professor Michael Browning, from the Department of Psychiatry, University of Oxford, and workstream lead in Mood Disorders for the NIHR Mental Health-Translational Research Collaboration (MH-TRC) Mission, who led the trial, said: ‘Effectively treating people who have not responded to first-line interventions for depression is a pressing clinical problem and there has long been an urgent need to find new treatments.
‘These findings on pramipexole are a significant breakthrough for patients for whom antidepressants and other treatments and therapies have not worked.
‘Pramipexole is a medicine licensed for Parkinson’s disease and works by boosting the brain chemical dopamine. This differs from the majority of other antidepressant medications which act on brain serotonin and may explain why pramipexole was so helpful in this study.
‘We now need more research focusing on reducing the side effects of pramipexole, evaluating its cost-effectiveness, and comparing it with other add-on treatments.’
Previous research into using the drug for depression had shown promise, but there had been limited data on its long-term outcomes and side effects until now.
Current guidelines for people with treatment resistant depression recommend adding new treatments, such as lithium or antipsychotics, to ongoing antidepressant treatment, but these have limited effectiveness and do not work for everyone.
Phil Harvey, 72, from Oxfordshire, was diagnosed with depression 20 years ago and tried different tablets and counselling but nothing worked. Eventually he had to take a year off work before retiring. He started on the trial in 2022.
He said: ‘Within a few weeks I felt the effects, it was amazing. I kept a diary which they gave us on how my mood was, motivation and how it improved. It was dragging me out of this dark black hole that I’ve been in for years.’
Participants were recruited from across the country, including as part of the NIHR-funded MH-TRC Mission mood disorder clinics, which are hosted at Oxford but located across the country. The clinics efficiently, and largely remotely, assess patients with difficult to treat mood disorders and offer them enrolment in research studies. The network can also support primary care services by providing assessment and treatment advice for patients who have not responded to initial treatment.
Mothers of newborn babies, turned away at public clinics in Johannesburg because they are not South African, say their children are missing out on lifesaving vaccines.
In recent months, vigilante group Operation Dudula has been taking control of clinic queues across Johannesburg, chasing away immigrants or telling them to stand separately from South Africans. It is alleged that some healthcare staff have been participating.
This is despite a 2023 ruling in the Gauteng High Court that pregnant and lactating women and young children should be granted free health care services regardless of their nationality.
The court ordered the Gauteng Department of Health to change its policy denying immigrants healthcare, and to place notices on the walls at all healthcare facilities stating lactating women and children may not be denied access. This order is not being consistently complied with.
GroundUp visited the Jeppe Clinic last week and saw no such notice. There was a small group of Operation Dudula members pulling immigrants out of the queue and telling them to stand to one side.
Jane Banda, a Malawian national, was at the clinic. She has been struggling to get her seven-week-old baby vaccinated, but has been blocked every time by Operation Dudula. She fears her baby’s health may be at risk if she continues to miss essential vaccinations.
Aisha Amadu, an asylum seeker from Malawi, who has a two-year-old baby, had an appointment at Jeppe Clinic last week but was chased away by Operation Dudula.
Grace Issah, also from Malawi, has a 14-week-old baby who was due for a vaccine two weeks ago. But she has been chased away from clinics in Jeppe, Bez Valley and Hillbrow.
“I feel like giving up because it seems there is nothing that I can do. My husband has no money for private doctors,” she said.
Several other women said they have also been denied access to clinics in Malvern, Kensington, Rosettenville and Soweto.
The Socio-Economic Rights Institute (SERI) launched a case in the Gauteng High Court in 2024, on behalf of Kopanang Afrika Against Xenophobia (KAAX), the Inner City Federation, Abahlali BaseMjondolo, and the South African Informal Traders Forum.
The group is seeking an interdict to declare the actions of the vigilante group, which include denying healthcare to immigrants, unlawful. The matter was heard in June, and judgment was reserved.
Mike Ndlovu from KAAX says it is a constitutional right for everyone in South Africa to be able to access healthcare.
“What Operation Dudula and a few complicit nurses are doing is unconstitutional, a criminal act, and a betrayal of our democracy. Denying healthcare is a violation of basic human rights,” said Ndlovu.
Ndlovu called on healthcare workers to remember their professional duty: to care without discrimination.
Operation Dudula’s actions have been condemned by the South African Human Rights Commission.
Department of Health spokesperson Foster Mohale said the department is aware of the action by Operation Dudula, but denied that department staff members are involved.
“The health facility managers have been advised to alert the law enforcement agencies whenever they experience these protests because that is a security issue to enforce the law,” Mohale said.
Mohale did not respond to questions about whether the department has complied with the 2023 court order to put up the notices.
Zandile Dabula, spokesperson for Operation Dudula, did not respond to a request for comment. But Veli Ngobese, a member of the movement who was at Jeppe clinic on the day GroundUp visited, said: “We are targeting all people from outside the country. We want Home Affairs to start afresh. Foreign nationals who come into the country should come and invest because the ones we see are selling amagwinya [vetkoek], pushing trolleys, and selling peanuts, and we are the ones paying taxes.”
He said the group will be conducting daily protests until immigrants stop going to clinics.
A groundbreaking study by researchers at Rutgers Health has uncovered a way to precisely identify and target trauma sites in the body within minutes of injury. The findings, published in the journal Med (Cell Press), could revolutionise emergency care by enabling real-time diagnostics and site-specific treatments delivered within minutes of injury.
A team of scientists, led by Renata Pasqualini and Wadih Arap at the Rutgers Cancer Institute discovered something new about how the body reacts to injury. When cells are damaged, like in a major bone break, calcium levels shift, which causes certain proteins to change shape. These changed proteins, called the “traumome,” are only found in injured tissues and show up right after an injury happens. This discovery opens up a new way to treat injuries directly, without affecting healthy parts of the body.
“The moment trauma occurs, specific proteins undergo structural changes, creating a molecular footprint of injury,” said Arap. “This opens the door to delivering diagnostics or therapies directly to the site – without affecting healthy tissues.”
This discovery has relevance in emergency treatment because many medicines can affect healthy organs when they’re given too soon. With this new approach, doctors could deliver treatments like imaging agents, clotting factors or antibiotics directly to the injured area, which would help the body heal faster with fewer side effects.
“Our long-term vision is a simple injection that autonomously finds and treats injury sites,” said Pasqualini. “This could be transformative for battlefield medicine and emergency trauma care, where every second matters.”
The team used advanced testing on a pig model with major injuries to find tiny protein pieces called peptides. These peptides are like guides that can find and stick to the specific proteins altered by injury. One of these peptides stands out because it can attach to a protein that changes shape when calcium levels rise after an injury. This makes it possible to use special scans, like PET or MRI, to see exactly where the injury is in the body.
The trauma-targeting peptide worked the same way in rats, which shows that this injury “signature” is similar in all mammals, including humans.
The work was supported by the Defense Advanced Research Projects Agency (DARPA), an agency of the U.S. Department of Defense, underscoring its strategic value in both civilian and military medical applications. “Non-compressible bleeding remains a leading cause of death among soldiers before they reach a hospital, and localised treatment could dramatically improve survival rates, which was the original impetus of this research,” said Jon Mogford, a study co-author and former DARPA official.
The next phase of research will involve linking therapeutic agents to the trauma site-homing peptides and testing them in animal models before moving to early human clinical trials. The team envisions translational applications ranging from battlefield medicine to civilian trauma response and possibly even sports injuries or surgical recovery.
“We are actively developing peptide-linked drugs and imaging agents based on this discovery,” said Arap. “The traumome concept may also have applications beyond trauma, including in surgery, inflammation and tissue regeneration.”
In South Africa, men are four to five times more likely to die by suicide than women. The silence around men’s mental health has become a national crisis. Momentum Health is confronting the uncomfortable truth: traditional ideas of masculinity are costing South African men their lives. The need for a more inclusive and proactive approach to men’s health is urgent.
With men accounting for a staggering 37.6 suicides per 100 000 people2 and depression affecting over 27% of South Africans3, the economic and human cost of ignoring men’s overall wellbeing has reached a breaking point. Mental health-related absenteeism alone costs the economy billions every year, a price tag that extends far beyond financial metrics into affected families and communities.
“We’ve long lived in a society that praises men for physical strength but punishes them for emotional vulnerability. While this is slowly changing, it’s not happening fast enough to make real impact,” says Damian McHugh, Chief Marketing Officer at Momentum Health. “This is why we’re challenging South Africa to redefine what strength really means. True strength is not silently suffering; it’s having the courage to reach out before crisis hits.”
A New Narrative for Men’s Health
In many communities across South Africa, men delay seeking medical help until conditions become critical and avoid mental health services despite growing internal struggles.
“When we tell boys to ‘man up’ we’re essentially telling them to disconnect from their emotional and mental wellbeing,” McHugh explains. “At Momentum Health, we believe real strength lies in connection to yourself, to professional support and to your community. That is why our approach integrates physical, mental, emotional and financial wellbeing, rather than treating them as separate issues.”
This holistic approach sets Momentum Health apart from conventional healthcare models that focus only on symptoms instead of the whole person.
The New Frontline for Men’s Mental Health
According to the 2025 Digital Report for South Africa5, 78.9% of the population are now online, with mobile connectivity exceeding 193% due to multiple device ownership. Recognising that many men would rather engage privately through an app than visit a therapist’s office, Momentum Health has deployed technology to meet men where they are.
“Technology is a powerful equaliser,” says McHugh. “It breaks down barriers of stigma, geography, and access. By meeting men in the digital spaces, they already inhabit, we’re not just offering support, we are changing the way mental health care is delivered.”
The Hello Doctor platform lets men chat privately with health experts right on their phones. It gives them a safe, non-judgmental space to talk about their mental health without feeling embarrassed. This service isn’t just offering help; it’s changing the way mental health care works in South Africa.
Health and Wealth: Two Sides of the Same Coin
The link between health and financial wellbeing is clear. Poor health can derail financial goals, while financial stress can strain mental and emotional resilience. Momentum Health’s integration of financial and health services addresses a critical reality: mental health struggles and financial problems can create a devastating downward spiral.
“You cannot separate these aspects of wellbeing and expect sustainable outcomes. When we say, ‘your health is your wealth,’ we are talking about a fundamental truth: without mental and physical resilience, financial success becomes meaningless,” says McHugh.
Creating a Culture of Support
South African men must take a proactive stance, not just for themselves, but for their families, their communities and future generations.
“This is not about perfection. It is about progress,” says McHugh. “And this is not just about saving lives, though that alone would be enough, it is about transforming what it means to be a man in today’s society.”
Findings support use of P2Y12 therapy instead of aspirin for long term prevention
Source: Wikimedia CC0
Giving a P2Y12 inhibitor anti-clotting drug to patients with coronary artery disease is associated with lower rates of cardiovascular death, heart attack and stroke compared with traditional aspirin, with no increased risk of major bleeding, finds a study published by The BMJ.
P2Y12 inhibitors are often given to patients alongside aspirin (“dual therapy”) after percutaneous coronary intervention (PCI) – a procedure to widen or unblock a coronary artery – to help prevent cardiovascular events including heart attack and stroke.
After several months, patients are usually switched from dual therapy to lifelong aspirin, but some trials have suggested that a P2Y12 inhibitor may be more effective for long term prevention than aspirin.
To explore this further, researchers analysed individual patient data from five randomised clinical trials involving 16 117 patients (average age 65; 24% women) who were assigned to a P2Y12 inhibitor (clopidogrel or ticagrelor) or aspirin after completing dual therapy following PCI.
After an average follow-up period of around 4 years, P2Y12 inhibitor therapy was associated with a 23% lower risk of an outcome that combined cardiovascular death, heart attack, or stroke, compared with aspirin, with no significant difference in major bleeding. This means that for every 46 patients taking a P2Y12 inhibitor instead of aspirin after dual therapy, one cardiovascular death, heart attack, or stroke would be prevented.
When considering outcomes individually, P2Y12 inhibitor therapy reduced heart attacks and stroke compared with aspirin. However, all-cause death, cardiovascular death, and stent thrombosis were similar between the treatments.
The researchers acknowledge that some changes in the original design of some trials were needed to create uniform data, and that certain characteristics of individual trial populations may reduce the generalisability of the findings.
But they say no significant difference in major bleeding between groups was seen, and results were consistent after further analyses accounting for factors such as age, sex, geographical region, smoking, previous heart attack or stroke, underlying conditions and medication history, suggesting they are robust.
“Overall, this study supports preferential P2Y12 inhibitor monotherapy prescription over aspirin due to reductions in major adverse cardiac and cerebrovascular events (MACCE) without increasing major bleeding in the medium term,” say researchers in a linked editorial.
However, they note that “medium term efficacy does not necessarily extend lifelong, which is the duration we advise patients to continue these medications.”
As such, they suggest that “a large-scale globally representative trial directly comparing different monotherapy strategies (including discontinuation) with extended follow-up would benefit our understanding of the long-term impact of P2Y12 inhibitor monotherapy across the treatment class for secondary prevention following PCI.”
