A new study led by UC San Francisco researchers finds that chronic cannabis use, whether it’s smoked or consumed in edible form, is associated with significant cardiovascular risks.
The report, published in JAMA Cardiology, found that people who regularly used marijuana in either form had reduced blood vessel function that was comparable to tobacco smokers. Vascular function in those who used cannabis by either means was reduced roughly by half compared to those who did not use it.
Decreased vascular function is associated with a greater risk of heart attack, hypertension, and other cardiovascular conditions.
The researchers recruited 55 people between October 2021 and August 2024 who were outwardly healthy and either regularly smoked marijuana or consumed edibles containing tetrahydrocannabinol (THC), the primary psychoactive compound found in cannabis.
The participants, none of whom used any form of nicotine, consumed cannabis at least three times a week for at least a year. Smokers averaged 10 years of chronic use, and those who took edibles averaged five years.
Along with decreased vascular function, marijuana smokers had changes in their blood serum that were harmful to endothelial cells, which form the inner lining of all blood and lymphatic vessels. Those who took edibles containing THC, however, did not display these changes in blood serum.
It’s unclear how THC damages blood vessels. But the researchers said it must be happening in a way that does not involve those changes to blood serum.
These results suggest smoking marijuana negatively affects vascular function for different reasons than ingesting THC does, according to first author Leila Mohammadi, MD, PhD, and senior author Matthew L. Springer, PhD.
In the study of 2268 US individuals aged 60 years and older who completed the Psychosocial and Lifestyle Questionnaires and provided blood samples in 2016, there was a strong association between engaging in social activities and a low risk of 4-year mortality. High social engagement was associated with a 42% lower mortality risk than low engagement.
Specific activities, such as charity work, engaging with grandchildren, and participation in sports or social clubs, were particularly significant predictors of a reduced risk of dying.
Also, analyses indicated that decelerated biological aging and greater physical activity levels played key roles in facilitating the beneficial relationship between social engagement and lower mortality rates.
“Staying socially active is more than a lifestyle choice. It is closely linked to healthier aging and longevity,” said corresponding author Ashraf Abugroun, MBBS, MPH, of the University of California, San Francisco. “These results underscore how participating in community life contributes to better health in older adults.”
There are two vaccines against shingles – an often painful and debilitating condition caused by the same virus that causes chickenpox – but neither are available in South Africa. Photo by Mika Baumeister on Unsplash
By Catherine Tomlinson
The only shingles vaccine on the market in South Africa was discontinued last year. A newer and better vaccine is being used in some other countries, but has not yet been registered in South Africa, though it can be obtained by those with money who are willing to jump through some hoops.
Shingles is a common and painful condition that mostly affects the elderly and people with weakened immune systems. It generally appears with a telltale red rash and cluster of red blisters on one side of one’s body, often in a band-like pattern.
“Shingles is pretty awful to get – it’s extremely painful, and some people can get strokes, vision loss, deafness and other horrible manifestations as complications,” said infectious disease specialist Professor Jeremy Nel. “Shingles really is something to avoid, if at all possible,” he added.
One way to prevent the viral infection is by getting vaccinated against it. But while two vaccines against shingles have been developed and broadly used in the developed world, neither of these are currently available in South Africa.
Two vaccines
Zostavax, from the pharmaceutical company MSD, was the first vaccine introduced to prevent shingles. It was approved for use in the United States in 2006 and in South Africa in 2011. It is 51% effective against shingles in adults over 60.
A more effective vaccine, Shingrix, that is over 90% effective in preventing shingles was introduced by GlaxoSmithKline (GSK) in the United States in 2016. It is not yet authorised for use in South Africa, but GSK has submitted paperwork for approval with the South African Health Products Regulatory Authority (SAHPRA), said the company spokesperson, Kamil Saytkulov.
The superior protection offered by Shingrix compared to Zostavax quickly made it the dominant shingles vaccine on the market. As a result, MSD discontinued the production and marketing of Zostavax. MSD spokesperson Cheryl Reddy said Zostavax was discontinued globally in March 2024. Before then, the vaccine was sold in South Africa’s private healthcare system for about R2 300, but it was never widely available in government clinics or hospitals.
No registered and available vaccine
Since Zostavax has been discontinued and Shingrix remains unregistered, the only way to access a vaccine against shingles in South Africa is by going through the onerous process of applying to SAHPRA for a Section 21 authorisation – a legal mechanism that allows the importation of unregistered medicines when there is an unmet medical need.
“Access will only be available to those who are able to get Section 21 approval” and “this is a costly and time-consuming process, requiring motivation by a doctor,” said Dr Leon Geffen, director of the Samson Institute For Ageing Research.
The cost of the two-dose Shingrix vaccine imported through Section 21 authorisations is currently around R15 600, said Dr Albie de Frey, CEO of the Travel Doctor Corporation.
People who do go through the effort of getting Section 21 authorisation typically have to pay this price out of their own pockets.
“Shingrix is not covered [by Discovery Health] as it is unregistered in South Africa and is therefore considered to be a General Scheme Exclusion,” Dr Noluthando Nematswerani, Chief Clinical Officer at Discovery Health, told Spotlight.
The Department of Health did not respond to queries regarding whether Section 21 processes are being pursued for priority patients in the public sector or whether there has been any engagement with GSK regarding the price of this product.
People who receive organ transplants, for example, should be prioritised to receive the shingles vaccine as the medications they are given to suppress their immune system puts them at a high risk of developing shingles.
Why is the price of Shingrix so high?
Unlike South Africa, where companies must sell pharmaceutical products at a single, transparent price in the private sector, the United States has no such requirement. Even so, the US Centers for Disease Control and Prevention (CDC) pays $250 or R4600 for the two-dose Shingrix vaccine through CDC contracts. This is less than a third of the price charged when Shingrix is imported into South Africa.
Equity Pharmaceuticals, based in Centurion in Gauteng, is importing GSK’s Shingrix for patients that receive Section 21 authorisations to use the unregistered vaccine. It is unclear what price Equity Pharmaceuticals is paying GSK for Shingrix to be imported into South Africa under Section 21 approvals, or what Equity Pharmaceuticals’ mark up on the medicine is.
When asked about the price of Shingrix in South Africa, Saytkulov told Spotlight: “Equity Pharmaceuticals is not affiliated with GSK nor is it a business partner or agent of GSK. Therefore, we cannot provide any comments with regards to pricing of a non-licensed product, which has been authorized for importation through Section 21.”
Equity Pharmaceuticals also said it was difficult to comment on the price. “The price of a Section 21 product depends on a number of fair considerations, including the forex rate, the quantity, transportation requirements, and the country of importation. Once the price and lead time are defined for an order, the information is shared with the healthcare provider to discuss with their patient and the medical aid,” the company’s spokesperson Carel Bouwer told Spotlight
Nematswerani pointed out that “Section 21 pricing is not regulated” and that price can change due to many factors including supplier costs, product availability, and inflation.
What causes shingles?
Shingles is caused by the same highly infectious virus that causes chickenpox. Most people are infected with the varicella-zoster virus (VZV) during childhood. Chickenpox occurs when a person is first infected by VZV. When a person recovers from chickenpox, the VZV virus remains dormant in their body but can reactivate later in life as one’s immune system weakens. This secondary infection that occurs, typically in old age when the dormant virus reactivates, is called shingles.
People who were naturally infected with chickenpox, as well as those vaccinated against chickenpox with a vaccine containing a weakened form of the VZV virus, can get shingles later in life.
But, people who were vaccinated against chickenpox have a significantly lower risk of developing shingles later in life compared to those who naturally contracted chickenpox, according to the World Health Organization (WHO).
The chickenpox vaccine is available in South Africa’s private sector but is not provided in the public sector as part of government’s expanded programme on immunisation. Chickenpox is usually mild in most children, but those with weakened immune systems at risk of severe or complicated chickenpox should be vaccinated against it, said Professor James Nuttall, a paediatric infectious diseases sub-specialist at the Red Cross War Memorial Children’s Hospital and the University of Cape Town.
Who should be vaccinated against shingles?
South Africa does not have guidelines regarding who should receive the shingles vaccine and when they should receive it. The US CDC recommends that all adults over 50 receive the two-dose Shingrix vaccine. They also recommend that people whose immune systems can’t defend their body as effectively as it should, like those living with HIV, should get the vaccine starting from age 19.
While Shingrix works better than Zostavax at preventing shingles, it has other advantages that make it a safer and better option for people with weak immune systems.
The Zostavax vaccine contains a weakened live form of the VZV virus and thus poses a risk of complications in people with severely weakened immune systems. “In the profoundly immunosuppressed, the immune system might not control the replication of this weakened virus,” explained Nel. The Shingrix vaccine does not contain any live virus and therefore does not present this risk.
In March 2025, the WHO recommended that countries where shingles is an important public health problem consider the two-dose shingles vaccine for older adults and people with chronic conditions. “[T]he vaccine is highly effective and licensed for adults aged 50 years and older, even if they’ve had shingles before,” according to the WHO. It advised countries to look at how much the vaccine costs compared to the benefits before deciding to use it.
The cost of not vaccinating against shingles
The cost of not vaccinating against shingles is high for people who develop the condition, as well as the health system.
“[T]he risk of getting shingles in your lifetime is about 20 to 30%…by the age of 80 years, the prevalence is almost 50%,” said Geffen. “Shingles is often a painful debilitating condition, with significant morbidity. It can result in chronic debilitating pain which affects sleep, mood and overall function,” he added.
Beyond preventing shingles and its complications, new evidence suggests that getting the shingles vaccine may also reduce one’s risk of developing dementia and heart disease.
In April, a large Welsh study published in Nature reported that people who got the Zostavax vaccine against shingles were 20% less likely to develop dementia seven years after receiving the vaccine compared to those who were not vaccinated.
In May, a South Korean study published in the European Heart Journal reported that people vaccinated against shingles had a 23% lower risk of cardiovascular events, such as strokes or heart disease for up to eight years after vaccination.
Losing weight via lifestyle adjustments can deliver significant long-term health benefits, without the need for surgery or anti-obesity drugs. Alongside preventing diabetes, it can help ward off chronic conditions including arterial and pulmonary diseases as well as cancers.
A University of Helsinki study tracked 23 000 individuals from Finland and the UK, aged 30 to 50 at the outset, over a period of 12 to 35 years. Health benefits were found in overweight men and women who lost an average of 6.5% of their body weight in early middle age and maintained it throughout the 12–35-year follow-up period. Weight maintenance is crucial.
“The benefits of lifestyle-based weight management are widely discussed even though studies have found it surprisingly difficult to demonstrate health benefits beyond the prevention of diabetes,” notes Professor Timo Strandberg.
The study he led is now filling this gap.
“I hope the findings will inspire people to see that lifestyle changes can lead to major health improvements and a longer life. This is particularly important today as more people are overweight than when the collection of our research data began 35 years ago.”
The study also supports the view that, for optimal health, a lifelong body mass index (BMI) under 25 is ideal.
The study was published in JAMA Network Open, the open-access journal of the American Medical Association.
People with an autism diagnosis are at a higher risk of developing Parkinson’s disease early in life, according to a large-scale study from Karolinska Institutet. The researchers believe that the two conditions can share underlying biological mechanisms.
The study, published in JAMA Neurology, is based on registry data from over two million people born in Sweden between 1974 and 1999 who were followed from the age of 20 up to the end of 2022.
The researchers interrogated a possible connection between the neuropsychiatric diagnosis Autism Spectrum Disorder (ASD), which affects an individual’s thought processes, behaviour and interpersonal communication, and early-onset Parkinson’s disease, a condition that affects locomotion and movement.
Possible dopamine involvment
The results show that people with an autism diagnosis were four times more likely to develop Parkinson’s disease than people without such a diagnosis, a correlation that remained when controlling for socioeconomic status, a genetic predisposition for mental illness or Parkinson’s disease and other such factors.
“This indicates that there can be shared biological drivers behind ASD and Parkinson’s disease,” says first author Weiyao Yin at the Department of Medical Epidemiology and Biostatistics. “One hypothesis is that the brain’s dopamine system is affected in both cases, since the neurotransmitter dopamine plays an important part in social behaviour and motion control.”
It is well-known that dopamine-producing neurons are degraded in Parkinson’s disease. Previous studies have also shown that dopamine is possibly implicated in autism, but more research needs to be done to confirm this.
“We hope that our results will eventually help to bring greater clarity to the underlying causes of both ASD and Parkinson’s disease,” says Dr Yin.
Medical checkups are vital
Depression and the use of antidepressants are common in people with autism, as are antipsychotic drugs, which are known for being able to cause Parkinson’s-like symptoms. When the researchers adjusted for these factors, the correlation between ASD and the later development of Parkinson’s disease was less salient, but the risk was still double.
The researchers point out that they only analysed early-onset Parkinson’s disease before the age of 50 and that the average age of participants by the end of the study was 34. The incidence of Parkinson’s disease was therefore very low. Future studies will need to examine if the elevated risk persists into older age.
“The healthcare services need to keep people with ASD – a vulnerable group with high co-morbidity and a high use of psychotropics – under long-term observation,” says last author Sven Sandin, statistician and epidemiologist at the Department of Medical Epidemiology and Biostatistics. “At the same time, it’s important to remember that a Parkinson’s diagnosis before the age of 50 is very rare, including for people with autism.”
Researchers have discovered how an ion channel in the brain’s neurons has a kind of ‘molecular memory’, which contributes to the formation and preservation of lifelong memories. The researchers have identified a specific part of the ion channel at which new drugs for certain genetic diseases could be targeted.
Learning from past experiences and forming memories depend on the reshaping of connections between neurons in the brain. Synapses are strengthened or weakened throughout life in such a way that the brain is, in a certain sense, constantly being reshaped at the cellular level. This phenomenon is called synaptic plasticity.
There are several processes contributing to synaptic plasticity in the nervous system. One of these processes has to do with a type of molecules called calcium ion channels, which have long been of interest to researchers at Linköping University, LiU.
“I want to uncover the secret lives of these ion channel molecules. Calcium ion channels have very important functions in the body – by opening and closing, they regulate, among other things, nerve-to-nerve signalling. But beyond that, these molecules also have a kind of memory of their own, and can remember previous nerve signals,” says Antonios Pantazis, associate professor at the Department of Biomedical and Clinical Sciences at LiU, who led the study published in Nature Communications.
How can a molecule remember?
The focus of this study was on a specific type of ion channel, the CaV2.1 channel, which is the most common calcium ion channel in the brain. The ion channel is located at the synapse, at the very end of the neuron. When an electrical signal passes through the neuron, the ion channel open, setting in motion a process leading to neurotransmitter being released towards the receiving neuron in the synapse. In this way, CaV2.1 channels are the gatekeepers of synaptic, neuron-to-neuron communication.
Prolonged electrical activity reduces the number of CaV2.1 channels that can open, resulting in less transmitter release, so the receiving neuron receives a weaker message. It is as if the channels can ‘remember’ previous signalling, and in doing so, make themselves unavailable to open by subsequent signals. How this works at the molecular level has been unknown to scientists until now.
The Linköping researchers have now discovered a mechanism for how the ion channel can ‘remember’. The channel is a large molecule made up of several interconnected parts, which can move relative to each other in response to electrical signals. They discovered that the ion channel can take almost 200 different shapes depending on the strength and duration of an electrical signal; it is a very complex molecular machine.
“We believe that during sustained electrical nerve signalling, an important part of the molecule disconnects from the channel gate, similar to the way the clutch in a car breaks the connection between the engine and the wheels. The ion channel can then no longer be opened. When hundreds of signals occur over long enough time, they can convert most channels into this ‘declutched memory state’ for several seconds,” says Antonios Pantazis.
Target for future drugs
If the ion channel can ‘remember’ for just a few seconds, how does it contribute to lifelong learning? This type of collective memory in the ion channels can accumulate over time and reduce the communication between two neurons. This then leads to changes in the receiving neuron, lasting for hours or days. Eventually, it results in much longer-lived changes in the brain, such as the elimination of weakened synapses.
“In this way, a ‘memory’ that lasts for a few seconds in a single molecule can make a small contribution to a person’s memory that lasts for a lifetime,” says Antonios Pantazis.
Increased knowledge of how these calcium ion channels work can in the long term contribute to the treatment of certain diseases. There are many variants of the gene that produces the CaV2.1 channel, CACNA1A, that are linked to rare but serious neurological diseases, that often run in families. To develop drugs against these, it helps to know which part of the large ion channel you want to affect and in what way its activity should be changed.
“Our work pinpoints which part of the protein should be targeted when developing new drugs,” says Antonios Pantazis.
A real-world study based on information from an electronic health records–derived database reveals limited benefits of adding bevacizumab to first-line chemotherapy for patients with ovarian cancer, consistent with previous clinical trials. The findings are published by Wiley online in CANCER, a peer-reviewed journal of the American Cancer Society.
Bevacizumab is a monoclonal antibody against vascular endothelial growth factor A that acts to inhibit malignant cell growth and blood vessel formation. It’s approved as a treatment for various types of cancer. In clinical trials of patients with ovarian cancer, adding bevacizumab to first-line chemotherapy did not prolong overall survival compared with chemotherapy alone, but this treatment strategy did improve overall survival in analyses limited to patients with high-risk prognostic factors—such as those with advanced disease and those who had residual cancer present after surgery. A final long-term analysis did not find an overall survival benefit associated with bevacizumab in the full patient cohort.
To investigate whether these findings also hold true in real-world clinical practice, researchers examined the electronic health records of 1,752 patients with stage III or IV ovarian cancer who initiated chemotherapy with or without bevacizumab in 2017–2023 and were followed for a median time of 1.5 years.
Among patients with high-risk prognostic factors, the median time to next treatment was significantly longer for those receiving chemotherapy plus bevacizumab compared with those receiving chemotherapy alone: 13.6 versus 11.7 months. (Time to next treatment is used to assess the duration of clinical benefit by measuring the time between initiating a treatment and starting the next line of therapy). In these patients, there was also a trend towards longer median overall survival for the combination therapy: 31.1 versus 27.4 months. Among patients without high-risk prognostic factors, outcomes did not differ with the addition of bevacizumab. Benefits therefore seemed limited to special subpopulations, mirroring the findings from clinical trials.
“Our results were similar to results from clinical trials,” said lead author Linda R. Duska, MD, MPH, of the University of Virginia School of Medicine. “Our findings suggest that clinicians should consider a patient’s risk factors before using bevacizumab with first-line chemotherapy in the treatment of advanced ovarian cancer.”
Despite clinicians recommending that many patients with diabetes take statins, nearly one in five opt to delay treatment. In a new study, researchers from Mass General Brigham found that patients who started statin therapy right away reduced the rate of heart attack and stroke by one third compared to those who chose to delay taking the medication. The results, which can help guide decision-making conversations between clinicians and their patients, are published in the Journal of the American Heart Association.
“I see patients with diabetes on a regular basis, and I recommend statin therapy to everyone who is eligible,” said senior author Alexander Turchin, MD, MS, of the Division of Endocrinology at Brigham and Women’s Hospital, a founding member of the Mass General Brigham healthcare system. “Some people refuse because they want to first try lifestyle interventions or other drugs. But other interventions are not as effective at lowering cholesterol as starting statin therapy as soon as possible. Time is of the essence for your heart and brain health.”
Heart attacks and strokes remain the leading cause of complications and mortality for patients with diabetes. Statin therapy reduces risk of these cardiovascular events by preventing plaque buildup in the blood vessels.
The researchers used an artificial intelligence method called Natural Language Processing to gather data from the electronic health records of 7239 patients at Mass General Brigham who ultimately started statin therapy during the nearly 20-year study period. The median patient age was 55, with 51% being women, 57% white, and a median HbA1c of 6.9.
Nearly one-fifth (17.7%) of the patients in the study declined statin therapy when it was first recommended by their clinicians, then later accepted the therapy (after a median of 1.5 years) upon repeated recommendation by their clinician. Of those who delayed, 8.5% had a heart attack or stroke. But for patients who started statins immediately, the rate of those cardiovascular events was just 6.4%.
“Clinicians should recognize the increased cardiovascular risk associated with delaying statin therapy for patients with diabetes and use this information to guide shared decision-making conversations with their patients,” said Turchin.
People with a certain heart valve abnormality, mitral annular disjunction, are at increased risk of severe heart rhythm disorders, even after successful valve surgery. This is according to a new study from Karolinska Institutet and Karolinska University Hospital in Sweden published in the European Heart Journal. The condition is more common in women and younger patients with valve disorder and can, in the worst case, lead to sudden cardiac arrest.
Mitral annular disjunction, MAD, is a heart abnormality in which the mitral valve attachment ‘slides’. In recent years, the condition has been linked to an increased risk of severe cardiac arrhythmias. Until now, it has not been known whether the risk of arrhythmias disappears if MAD is surgically corrected.
MAD is often associated with a heart disease called mitral valve prolapse, which affects 2.5% of the population and causes one of the heart’s valves to leak. This can lead to blood being pumped backwards in the heart, causing heart failure and arrhythmias. The disease can cause symptoms such as shortness of breath and palpitations.
Followed patients after surgery
In the current study, researchers at Karolinska Institutet investigated the risk of cardiac arrhythmias in 599 patients with mitral valve prolapse who underwent heart surgery at Karolinska University Hospital between 2010 and 2022. Sixteen percent of the patients also had the cardiac abnormality MAD.
“We have been able to show that people with MAD have a significantly higher risk of suffering from ventricular arrhythmias, a dangerous type of heart rhythm disorder that in the worst case can lead to cardiac arrest in a subset of patients,” says Bahira Shahim, associate professor at the Department of Medicine, Solna, Karolinska Institutet and cardiologist at Karolinska University Hospital
People with MAD were more likely to be female and were on average eight years younger than those without MAD. They also had more extensive mitral valve disease. Although the surgery was successful in correcting MAD, these patients had more than three times the risk of ventricular arrhythmias during five years of follow-up compared to patients without preoperative MAD.
“Our results show that it is important to closely monitor patients with this condition, even after a successful operation,” says Bahira Shahim.
Investigating new hypotheses
The study has led to new hypotheses that the researchers are now investigating further. One hypothesis is that MAD causes permanent changes in the heart muscle over time. Another is that MAD is a sign of an underlying heart muscle disease. The researchers are now continuing to study scarring in the heart using MRI (magnetic resonance imaging) and analyse tissue samples from the heart muscle.
For 30% of people with major depressive disorder (MDD), antidepressants don’t work. When infused at a low dose, ketamine shows remarkable efficacy as a rapidly acting antidepressant, with effects observed within hours even in patients who have been resistant to other antidepressant treatments. One drawback is that consistent infusions of ketamine are needed to maintain symptoms at bay, which could result in side effects, such as dissociative behaviours and the possibility of addiction, and stopping treatment can result in relapse.
In a new study published in Science, Lisa Monteggia’s and Ege Kavalali’s labs show that it is feasible to substantially extend the efficacy of a single dose of ketamine from its current duration of up to a week to a longer period of up to two months.
“The premise of this study, which was led by Zhenzhong Ma, a fantastic research assistant professor, was based on a testable mechanistic model that we developed that accounts for ketamine’s rapid antidepressant action,” Monteggia said.
Previously, researchers in the field had determined that ketamine’s antidepressant effect requires the activation of a key signalling pathway called ERK, but only ketamine’s long-term effects – not its rapid effects – are abolished when ERK is inhibited. As a fast-acting antidepressant, ketamine relies on ERK-dependent synaptic plasticity to produce its rapid behavioural effects. Ma and colleagues hypothesised that they could maintain ketamine’s effects for longer periods by enhancing ERK activity.
In the recent paper, Ma discovered that ketamine’s antidepressant effects could be sustained for up to two months by using a drug called BCI, which inhibits a protein phosphatase and results in increased ERK activity. By inhibiting the phosphatase, the authors retained ERK’s activity and augmented the synaptic plasticity that drives ketamine’s prolonged antidepressant effects.
lthough the use of BCI makes the application of these results to the clinic difficult, Monteggia said that the results provide a proof of principle that ketamine’s antidepressant action can be sustained by targeting intracellular signaling. She and Kavalali, the William Stokes Professor of Experimental Therapeutics and the chair of the Department of Pharmacology, have worked on the project since its inception and hope that it will foster other studies looking to identify specific molecules to enhance and sustain the action of a single dose of ketamine.
Ultimately, this work will be a stepping stone toward improving MDD patients’ lives by reducing the burden of treatment.
