With the 2025-2026 Influenza and Respiratory Syncytial Virus seasons launching in the United States, a debated innovation recently recieved positive data on how it can passively reduce respiratory diseases.
The new study published in JAMA Internal Medicine trialled commercially available germicidal ultraviolet (GUV) appliances in senior care facilities, finding they reduced rates of viral respiratory infections by about 12.2%.
GUV appliances, which purify the air with UV-C light rays and deactivate harmful micro-organisms like viruses and bacteria.
“Some of the key advantages of germicidal ultraviolet air-treatment appliances are that they are easily installed into existing facilities and cost-effective to use,” says lead author Dr Andrew Shoubridge from Flinders University and SAHMRI’s Microbiome and Host Health Programme, in a press release on July 28, 2025.
“When used in conjunction with existing infection control measures, they could be transformative in reducing rates of seasonal respiratory viral infections and protecting residential aged care facilities against emerging pathogens.”
This randomized clinical trial tested commercially available LAF Technologies GUV appliances that are already used in a wide range of clinical and commercial settings, including hospitals.
The appliances can be mounted to ceilings or walls, fitted into ventilated AC systems, are harmless to people, and have already proven to reduce levels of airborne pathogens in laboratory and hospital settings.
Senior author of the study, Professor Geraint Rogers, conceived this world-first trial and the transformative adaptation of this technology to reduce respiratory viral outbreaks in vulnerable older Australians.
“Our study aimed to explore new ways in which to protect aged care residents from harmful outbreaks of viruses, without disrupting their day-to-day activities.
“Based on our findings, it’s difficult to see why you wouldn’t install these appliances in aged care facilities.”
Diets rich in vegetables, legumes, whole grains, and omega-3s (like fish) may reduce liver cancer risk.
Reducing processed meats, sugary beverages, saturated fats, and alcohol is crucial for liver health.
The Mediterranean diet, focused on plant-based foods and healthy fats, has shown protective effects for liver cancer.
Hepatocellular carcinoma (HCC) is the most common type of liver cancer, making up more than 80% of cases worldwide and being the sixth most common cancer and the third leading cause of cancer-related deaths. Major risk factors include having metabolic dysfunction-associated steatotic liver disease (MASLD). MASLD, previously called non-alcoholic fatty liver disease, is linked to fat buildup in the liver and other metabolic issues.
Conditions like elevated cholesterol, diabetes and high blood pressure may increase your MASLD risk. With MASLD-related hepatocellular carcinoma cases expected to rise significantly, focusing on modifiable factors like diet and lifestyle could play a key role in prevention. Because of this, researchers conducted a review of the available data to determine links between dietary habits and liver cancer risk, and the results were published in Narrative Review.
How Was This Study Conducted?
To conduct this study, researchers used reports from the International Agency for Research on Cancer (IARC) and the 2018 World Cancer Research Fund (WCRF)/American Institute for Cancer Research (AIRC), to identify foods, dietary components, and contaminants that may increase the risk of liver cancer, specifically hepatocellular carcinoma. To dig deeper, the researchers searched a medical research database for studies on certain foods and their connection to hepatocellular carcinoma, focusing on high-quality reviews and analyses.
The strength of the link between each dietary factor and hepatocellular carcinoma was evaluated based on the quality of the research.
What Did This Study Find?
Certain foods and nutrients were found to influence the risk of developing liver cancer. For example, aflatoxins (toxins from fungi in contaminated food) and alcohol are strongly linked to an increased risk, while coffee likely lowers the risk, and fish may have a limited protective effect.
The researchers also addressed several more key findings for particular foods. Let’s break them down.
Meat
When it comes to meat, while The International Agency for Research on Cancer (IARC) has classified processed meats (like bacon and sausage) as cancer-causing to humans and red meats (like beef and pork) as probably cancer-causing, the researchers reported that there wasn’t strong evidence linking overall meat consumption to liver cancer specifically.
The researchers reported that, based on data they evaluated, people who eat white meat have a 24% lower risk of hepatocellular carcinoma, and those who eat fish have a 9% lower risk of developing hepatocellular carcinoma. On the other hand, eating processed meat was linked to a 20% higher risk of liver cancer. No clear link was found between liver cancer risk and eating red meat or total meat overall.
Fat
Researchers found no clear link between overall fat intake and hepatocellular carcinoma, and there wasn’t enough evidence to say whether a low-fat diet helps mitigate cancer risk. However, eating more omega-3 fatty acids, like those in fish and flaxseeds, may be linked to a 51% reduced risk of liver cancer.
On the flip side, eating more saturated fats was linked to a 34% higher risk of liver cancer. No strong connections were found for other types of fats.
Carbohydrates
There was no clear evidence linking carbohydrate intake to hepatocellular carcinoma risk. Similarly, there wasn’t quite enough proof to draw conclusions about glycemic index, or how quickly foods raise blood sugar.
But some studies suggest that drinking sugar-sweetened beverages might double the risk of liver cancer, though other research found no such link.
Cereals, Vegetables, Fruit, Pulses and Grains
Besides the link between aflatoxins, or toxins from mold in contaminated grains and nuts, being strongly linked to a higher risk of liver cancer, there was no clear evidence connecting cereals, fruits, vegetables or vitamin C to liver cancer risk. The researchers noted that there wasn’t much research to rely on for those connections. Some studies do suggest that eating more vegetables may lower the risk, though no significant link was found for fruits. A Chinese study hinted that tomatoes might reduce liver cancer risk, but further research found no connection to lycopene, a nutrient in tomatoes.
Whole grains and fiber, particularly from grains and fruits, appear to offer protection. Regular fiber intake is associated with a 34% lower risk of liver cancer, with every 50 grams of daily fiber reducing the risk by 23%. Legumes, such as beans and lentils, may also lower the risk by 14%, with benefits seen at 8 to 40 grams per day. However, no significant links were found for refined grains or nut consumption.
Micronutrients
Certain antioxidant nutrients may help lower the risk of liver cancer. For example, vitamin E, folate, β-carotene and manganese have been linked to a reduced risk of liver cancer. On the other hand, people with low vitamin D levels may have more than double the risk of liver cancer. Additionally, higher levels of vitamin D in the blood were associated with a 47% lower risk of liver cancer.
Dietary Patterns
The Mediterranean diet, while not directly linked to reducing hepatocellular carcinoma risk, has strong evidence supporting its role in preventing weight gain, which may indirectly lower liver cancer risk. Higher adherence to the Mediterranean diet was associated with a 32% lower risk of liver cancer after adjusting for factors like body mass index, diabetes, and smoking.
Other diets, such as the DASH diet and Healthy Eating Index, also showed protective effects, but the Mediterranean diet had the strongest and most consistent results. Additionally, vegetable-based diets were linked to a lower risk of liver cancer, while Western-style diets (high in processed foods and sugar) were associated with an increased risk.
Limitations and Considerations
This study highlights important links between dietary habits and liver cancer risk, but comes with several limitations. The role of diet in modulating hepatocellular carcinoma risk is still not well understood, and the findings rely heavily on systematic reviews and meta-analyses, which may exclude newer or smaller studies and introduce publication bias. Additionally, the complexity of dietary patterns and interactions between nutrients makes it challenging to isolate the effects of individual components.
Factors like physical activity, socioeconomic status and access to healthcare may also confound the results, making it difficult to attribute risk solely to diet. Moreover, the lack of long-term interventional studies and limited exploration of emerging dietary patterns, such as intermittent fasting, leave gaps in understanding the broader implications of diet on HCC risk.
How Does This Apply To Real Life?
With liver cancer being one of the most common and deadly cancers worldwide, understanding how diet and lifestyle play a role is crucial. Making certain food choices, like eating more vegetables, legumes, whole grains and omega-3-rich foods like fish, may help lower your risk. Incorporating foods rich in omega-9 monounsaturated fats (MUFAs) and omega-3 polyunsaturated fats (PUFAs) is also beneficial for liver health, as the authors note. That means snacking on foods like olives, avocados, almonds and hazelnuts can offer some benefits for your liver health.
Cutting back on processed meats, sugar-sweetened beverages, saturated fats and alcohol is equally important. Additionally, adopting dietary patterns like the Mediterranean diet, which emphasizes whole, plant-based foods and healthy fats, has shown promise in reducing liver cancer risk indirectly by preventing weight gain and improving metabolic health.
Making some tweaks to your diet can be a slow and steady process—you don’t have to overhaul everything at once. Consider including a few Mediterranean diet meals in your routine each week, if you aren’t already. Even simple suppers like our No-Cook White Bean & Spinach Caprese Salad and this 20-minute Vegan Coconut Chickpea Curry can be easy picks to add plenty of veggies and flavor to your day.
Our Expert Take
This study published in Narrative Reviews sheds light on the important connection between dietary habits and the risk of developing liver cancer (hepatocellular carcinoma), particularly in the context of rising cases linked to metabolic disorders like MASLD. The findings suggest that making certain food choices such as increasing intake of vegetables, legumes, whole grains and omega-3-rich foods like fish may play a role in reducing HCC risk. At the same time, limiting processed meats, sugar-sweetened beverages, saturated fats, and alcohol is crucial. Additionally, the study highlights the importance of limiting exposure to aflatoxins, toxic substances found in contaminated foods like cereals, maize, rice, nuts, and spices.
By making small, intentional changes to your diet and lifestyle, you can take meaningful steps to protect your liver and overall health. Remember, every small positive choice, whether it’s adding more veggies to your plate, swapping a cocktail for a mocktail or enjoying fish as a protein choice, each decision brings you closer to a healthier future.
Influenza viruses like bird flu can mix and match their genomes, and this has played a role in at least three of the last four flu pandemics. Influenza viruses are shifty entities. They accumulate small genetic changes on a regular basis, necessitating yearly updates to the flu vaccines because the prior year’s strain may not look much like the following year’s. But they can also make sudden leaps by incurring big genetic changes that may allow them to jump from one animal species to another or to humans.
A seemingly ingenious and sneaky way for viruses to make these leaps is by swapping genetic material with other flu strains. Called reassortment, this exchange happens when a person or animal is infected with two types of flu virus at the same time. While replicating inside the host cell, the viruses can grab bits of each other’s genetic code and incorporate them into their own gene sequences.
More than 100,000 people in Wisconsin are living with epilepsy, and the experience can be different for every person.
Movies and television often depict seizures as large, full-body convulsions. “And that certainly happens to a lot of our patients,” clinical pharmacist Dr. Barry Gidal told WPR’s “Wisconsin Today.”
But seizures vary from patient to patient, Gidal said, because the brain is such a complex organ.
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“A seizure is this sudden, massive electrical activity — like a storm that takes place in the brain … For a lot of our patients, it’s very subtle. They may stop talking, or get really confused, or look like they’re spacing out.”
As a pharmacy professor at UW-Madison, Gidal specializes in treatment research for adult epilepsy, a seizure disorder. He also sees patients in a clinical setting to manage their medications and reduce side effects and interactions.
“I would encourage people struggling with epilepsy, even if their seizures are under pretty good control — which, in my mind, means being seizure-free — but are having side effects, to seek out an epilepsy center,” Gidal said. “Go have a different set of eyes see if you’re a candidate for different clinical studies or the newest medicines.”
Despite progress in epilepsy research, Dr. Gidal said he is worried about its future because of widespread cuts to research funding.
“It’s not just the clinical studies — some of the basic science work takes years. We’ve got to understand the basic science if we want to come up with an idea for a new medicine. If the funding stops, that’s only going to impede things in progress,” Gidal said.
Gidal talked with host Kate Archer Kent about the cutting edge of epilepsy treatment and the challenge of affordability for patients.
The following interview has been edited for clarity and brevity.
Kate Archer Kent: What excites you about the hive of epilepsy research right now?
Barry Gidal: As a pharmacist, you would probably expect me to say “the new drugs.” But I think, for me, it’s two areas: one is genetics. As we learn more about what is actually happening that’s causing the problem, there’s great research that, I hope, is able to continue looking at things like gene therapy. These are in the very nascent, early stages. Also, electrical devices that can do different types of stimulation within the brain to abort seizures are really getting started. Some of them are already making it to the clinic.
KAK: I also understand that cannabis can be used in the treatment of epilepsy. What are you finding there?
BG: We use the term medical marijuana a lot. It’s very non-specific. If you look at the cannabis plant, it doesn’t just have one thing in it. Everybody thinks THC, or maybe CBD. But there’s hundreds of different chemicals. Some may be good for our brains, some may not be, but the only cannabinoid that’s been studied and now FDA approved for epilepsy is a purified form of cannabidiol, or CBD. And that’s really led to a lot of interesting new avenues of research. The purified, FDA approved form of CBD will work in a lot of different types of patients, in different types of seizures. So it’s really pretty exciting, but it’s not cannabis. It’s one molecule out of that plant.
KAK: In your research, you also learned that some over-the-counter CBD products are not correctly labeled. Can you tell us more about that?
BG: Yeah, that’s correct. That’s some work that came out of our lab and some other collaborations a couple years ago now. I mentioned there’s an FDA approved prescription form of CBD, but you can go anywhere and buy different CBD oils or tinctures — and that’s not the same thing. Here within the state of Wisconsin, we looked at lots of different over-the- counter forms of CBD that were being sold without a prescription, and we found lots of contamination. We found a lot of them had far less CBD than what the label indicated. A lot of them were contaminated with THC, which would be of concern if you’re giving this to your child to try to treat seizures or anything else. In a different study we found contamination with some heavy metals like lead. So in the over the counter world, there’s lots of concerns about the product’s purity.
KAK: Has that made you more cautious about using CBD protocols for a patient, or is the concern just in over-the-counter options?
BG: I think prescription CBD most clearly has a role and should be considered as an alternative. Right now we add prescription CBD onto somebody’s already existing anti-seizure medicine regimen. The over-the-counter stuff is “buyer beware” because I’m concerned about what other stuff is in there. Also, because of what we learned in clinical trials about the dosages that work to treat seizures, you can’t achieve the right doses without the prescription product. We also need to be mindful because CBD can cause some drug interactions. That’s my other concern — people using over-the-counter products without talking with their physician, pharmacist, nurse practitioner, etc., because it may interact with other medicines that they are taking.
KAK: If a patient is struggling to cover the costs of the medications in managing their seizures and someone’s insurance won’t cover a particular medication, are you able to work with them to find something that will work?
BG: Sadly, insurance coverage is an issue. Most neurologist offices are pretty adept at either getting prior authorizations, coupons or manufacturer rebates that are available for the drugs themselves. But it’s not easy, and it is time consuming. I also encourage patients to find a good pharmacy and a pharmacist that you can work with. A lot of times they know about some patient assistance programs that maybe the physician doesn’t. Pharmacists are willing to work with patients to try to come up with ways to help make this more affordable for patients. But yes, it’s a constant struggle.
KAK: You’ve spent so much of your career immersed in this neurological disorder. What gives you hope about epilepsy?
BG: Number one, it’s the patients. I know our patients’ lived experience, what they struggle with. It’s an opportunity to make a difference. But also the scientific and clinical community — nationally, here in the state and internationally. This is just a really amazing group of people that are really committed to helping with this disease and helping our patients. I refer to this as my extended family. They are very mission focused. (They’ll say) “let’s find a cure,” or “let’s find the most effective treatment that we can,” and “how can we also improve our patients’ quality of life?”
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At-home laser hair removal devices have been popular for their convenience, safety, relative comfort and results. If you’re curious about trying one out yourself, you may be wondering if the portable gadgets are actually effective. “Yes, at-home laser hair removal can work for some people with long-term consistent use—but they’re much less powerful than professional treatments,” says Dr. Chelsea Hoffman,board-certified dermatologist at Hudson Dermatology and Laser Surgery.
At-home laser hair removal is convenient and relatively painless, but it can take time and … More consistency to see results.
ILLUSTRATION: FORBES / PHOTO: BRAUN
At-home laser hair removal devices generally cost between $150 and $450. They feature different laser types with multiple intensity levels, and they’re meant to target specific skin tones. (For more on at-home hair removal, check out our guide to the best laser hair removal devices and our in-depth review of the Nood Flasher 2.0.)
Is At-Home Laser Hair Removal Safe?
“Yes. When used as directed, FDA-cleared at-home laser devices are generally considered safe,” says Hoffman. “Side effects are typically mild and may include temporary redness, swelling, or irritation.” However, it’s important to follow skin tone guidelines, perform a small spot test first, and avoid use on tattoos, moles or broken skin. People with darker skin tones should use devices specifically designed for their skin type, as certain devices can increase the risk for burns or hyperpigmentation, according to Hoffman.
The first at-home laser hair removal devices became FDA-approved in the late 2000s, and they have slowly become more readily available. They work by targeting pigment (melanin) in the hair using either diode laser or intense pulsed light (IPL) technology to slow and reduce hair growth over time. “Using a principle called selective photothermolysis—a scientific way of saying light is used to safely heat and destroy a specific target—these devices send light into the hair shaft, which then travels down to the root (or follicle),” says Hoffman. “The light is converted into heat that damages the tiny blood vessels feeding the follicle. Without that blood supply, the follicle loses its ability to grow new hair.” These treatments work best when there’s a contrast between skin and hair color—typically lighter skin with darker hair—and they don’t work well on very light, blonde, or gray hairs.
Is At-Home Laser Hair Removal Permanent?
“No hair removal should be thought of as truly permanent, but rather as hair reduction,” says Hoffman. If used consistently, at-home devices can help decrease hair growth over time. Like with many beauty treatments, though, results vary and long-term, regular maintenance is typically needed. In-office treatments are much more likely to deliver more complete and longer-lasting results—and typically in far fewer sessions, according to Hoffman. The problem is that in-office treatments are usually significantly more expensive, costing up to $600 per session and requiring three to eight treatments.
Can You Do At-Home Laser Hair Removal When Pregnant?
It’s generally recommended to avoid laser treatments—both at home and in-office—during pregnancy, just to be safe. “While there’s no strong evidence that laser hair removal is harmful during pregnancy, we don’t have enough data to confirm that it’s completely safe, either,” says Hoffman. “Hormonal changes in pregnancy can also make hair growth more unpredictable, potentially reducing the effectiveness of treatment during that time.”
Why Trust Forbes Vetted
The Forbes Vetted beauty team has researched, reported on and tested a variety of beauty and grooming devices, including the best LED face masks, the best hair straighteners and the best electric razors for men.
Molly Calhoun, the author of this piece, is an experienced lifestyle journalist who has written about fashion, beauty, home and entertainment for 20 years. Some of her recent work for Forbes Vetted includes the best hair dryers, the best retinol creams and the best neck firming creams. She has done both at-home and in-office hair removal.
Forbes Vetted deputy editor Jane Sung oversaw the publishing of this piece. She is a beauty industry veteran who has covered lifestyle topics for two decades.
Calhoun consulted Dr. Chelsea Hoffman, board-certified dermatologist at Hudson Dermatology and Laser Surgery, for her expertise on laser hair removal and the effectiveness and limitations of at-home treatments.
New research from New Zealand shows the promise of a patient-tailored follow-up model following curative surgery, as the number of colorectal cancer (CRC) cases rises and health care systems experience increasing strain. 1 The study’s participants expressed general satisfaction with the care they were receiving, but they also indicated that if important obstacles like access, continuity, and technology use are removed, they would be open to alternatives like remote monitoring or general practitioner (GP) visits.
A New Zealand study finds patients are open to remote and general practitioner-led care when it is tailored to their needs. | Image credit: Ahmet Aglamaz – stock.adobe.com
This qualitative study is published in ANZ Journal of Surgery.
“This is the first qualitative study to explore the perspectives of colorectal cancer patients on their current follow-up and their opinions of alternative follow-up in New Zealand,” wrote the researchers of the study. “The key finding is that patients are open to a range of modalities, with preferences being patient-specific. A ‘one size fits all’ model of follow-up care is unlikely to be suitable for a New Zealand population.”
CRC places a growing burden on health systems worldwide, as rising incidence rates and longer survivorship increase demand for follow-up care.2 Traditional oncology-led models are often resource-intensive and may not fully meet the diverse needs of survivors, particularly those facing geographic, socioeconomic, or logistical barriers to care.
The study used a qualitative research design to explore patient perspectives on follow-up care after curative-intent CRC surgery.1 Researchers conducted semi-structured interviews with 13 patients with ages ranging from 41 to 86 years. Participants were selected based on their experience with post-surgical CRC follow-up, and interviews were designed to gain insights into their experiences with current care models, openness to alternative approaches, and perceived barriers and enablers to effective follow-up. In doing so, the researchers aimed to provide patient-centered, real-world insights to inform the development of a more personalized and accessible follow-up care framework.
Findings from the study revealed that most patients were satisfied with their current follow-up care and described feelings of reassurance and positivity around their oncology visits. Participants expressed openness to alternative follow-up methods, particularly remote appointments, which they valued for their convenience and efficiency. However, some voiced concerns about the lack of physical examination, difficulty using technology, and hesitancy to raise concerns without face-to-face interaction. GP-led follow-up was deemed potentially beneficial but raised concerns about rushed visits, misdiagnosis, and lack of continuity in care.
Barriers to follow-up included travel distance, disability, caregiving or work obligations, and limited access to transportation. Enablers included strong social support networks and reliable transport.
However, the researchers acknowledged some limitations. First, social desirability bias was a concern. Second, the exclusion of non–English speakers and patients limited generalizability. Additionally, one patient lost to follow-up could have provided insights into barriers to care. Lastly, having a single researcher conduct and analyze all interviews may have introduced bias.
Despite these limitations, the researchers believe the study enforces that as survivorship becomes more complex, personalized strategies will be essential for effective follow-up after CRC surgery.
“Some barriers to follow-up could be overcome by alternative modalities,” wrote the researchers. “The patient-led framework can help guide advancements in colorectal cancer follow-up.”
References
1. Srikumar G, McLaughlin S, McGuinness MJ, et al. Follow-up strategies in colorectal cancer: what do patients prefer? ANZ J Surg. Published online July 30, 2025. doi:10.1111/ans.70269
2. Steinzor P. Colorectal cancer shared care model gains support from clinicians. AJMC®. July 14, 2025. Accessed July 30, 2025. https://www.ajmc.com/view/colorectal-cancer-shared-care-model-gains-support-from-clinicians
Elevated plasma glucose levels upon hospital admission, known as acute hyperglycemia, are prevalent among patients experiencing acute myocardial infarction (AMI), affecting up to 50% of cases, depending on the defined glycemic threshold and presence of diabetes [1,2,3,4]. Acute hyperglycemia has been recognized as a significant independent predictor of both in-hospital morbidity and mortality in patients with AMI, regardless of diabetes status [4, 5]. Notably, for every 18 mg/dL (1 mmol/L) rise in glucose levels above 200 mg/dL, there is an associated 5% increase in hospital mortality risk for patients with AMI with diabetes and a 4% increase for those without diabetes [6]. However, the adverse effects of glucose dysregulation extend beyond acute hyperglycemia to include fluctuations in glycemic values, with acute glucose changes in both directions [7]. Indeed, increasing evidence suggests that hypoglycemia and, more recently, glycemic variability (GV) in hospitalized patients with AMI are emerging concerns closely linked to prognosis, thus highlighting their importance as potential therapeutic targets. In AMI, acute fluctuations in glucose levels appear to have more detrimental effects on the development of major cardiovascular complications compared to acute hyperglycemia.
This review will delve into the clinical and prognostic significance of hypoglycemia and GV in patients with AMI, while also exploring current insights into the potential mechanisms underlying the association between these glucose dysregulations and adverse outcomes. Ultimately, we advocate for the incorporation of hypoglycemia prevention and GV reduction as standard treatment objectives during AMI management.
To address these objectives, relevant literature was identified through a comprehensive search of the PubMed, MEDLINE, and Scopus databases. The search was conducted using combinations of the following keywords: “acute myocardial infarction,” “hypoglycemia,” “glycemic variability,” “blood glucose fluctuations,” “prognosis,” “cardiovascular outcomes,” and “continuous glucose monitoring.” Additional studies were identified through manual searches of reference lists from key articles and systematic reviews. Included studies encompassed original clinical research, meta-analyses, and expert consensus statements published in English between January 2000 and May 2025. Priority was given to studies involving hospitalized adult patients with AMI. Studies focusing on glucose abnormalities outside the context of AMI or involving non-human models or performed before 2000 were excluded unless they contributed mechanistic insight relevant to the topic.
Hypoglycemia in AMI
Hypoglycemia is a clinical condition characterized by an abnormally low level of blood glucose [8]. Establishing a single plasma glucose level indicative of hypoglycemia is challenging, as the glycemic threshold for symptom development varies depending on the individual’s diabetes status and their chronic glycemic control [9, 10]. Nonetheless, hypoglycemia is typically defined as a blood glucose concentration below 70 mg/dL (3.9 mmol/L), with a critical alert value below 54 mg/dL (3.0 mmol/L), which can lead to severe neurological consequences, including potentially fatal outcomes, if not promptly addressed [11]. Hypoglycemia may manifest with or without typical adrenergic symptoms such as sweating, palpitations, trembling, and tingling. Additionally, hypoglycemia is most commonly induced iatrogenically as a result of anti-hyperglycemic therapy, particularly with insulin, or less commonly, it may occur spontaneously, possibly due to a more serious underlying disease [4, 12,13,14].
Incidence of hypoglycemia in AMI
Data from the Cooperative Cardiovascular Project, encompassing a substantial American community-based sample of 141,680 elderly patients hospitalized with AMI from 1994 to 1996, revealed that approximately 15% of patients had admission glucose values lower than 110 mg/dL. However, this frequency varied, ranging from 2% among patients without diabetes to 40% among those with diabetes [15]. In a subsequent analysis of a database comprising 23,613 patients with AMI admitted to 40 hospitals across the United States between 2000 and 2005, the incidence of critical hypoglycemia (below 60 mg/dL) during hospitalization was approximately 6%. One-third of hypoglycemic events occurred spontaneously, while the majority followed insulin administration [13]. Another study, involving a post hoc analysis of two large trials with 30,536 patients with AMI, reported admission hypoglycemia (below 70 mg/dL; < 3.9 mmol/L) in 1.5% of patients, with an additional 5% experiencing hypoglycemic events within the subsequent 24 h after admission [16]. More recently, among 34,943 patients with AMI from two registries, the Korea Acute Myocardial Infarction Registry (KAMIR) and the Korea Working Group on Myocardial Infarction (KorMI), 1.2% had admission glucose levels below 70 mg/dL (< 3.9 mmol/L) [4]. Hypoglycemia is even more prevalent among AMI patients with diabetes. In the Diabetes Mellitus Insulin Glucose Infusion in Acute Myocardial Infarction 2 (DIGAMI 2) trial, hypoglycemic episodes were observed in 12% of all patients with diabetes [17]. Furthermore, the likelihood of hypoglycemia increases to up to 8% when considering only patients with ST-elevation myocardial infarction (STEMI) [18].
Prognostic relevance of hypoglycemia in AMI
Similar to the well-established link between acute hyperglycemia and heightened morbidity and mortality in patients with AMI, the presence of hypoglycemia has been associated with a poorer prognosis. Numerous observational studies have demonstrated that hypoglycemia during hospitalization for AMI is closely correlated with increased mortality rates. In one of the earliest studies focusing on the clinical significance of glycemia in AMI, Pinto et al. [18] reported a U-shaped relationship between admission glucose levels and adverse outcomes. Specifically, the incidence of death or recurrent AMI within 30 days in STEMI patients was higher in cases of hypoglycemia (10.5%) or hyperglycemia (7.2%) compared to euglycemia (4.2%). A similar distribution of 30-day mortality rates based on admission glucose levels was observed by Lee et al. [4] in a large cohort of patients with AMI. This trend was evident across the entire population as well as among patients with and without diabetes analyzed separately. Notably, hypoglycemia was associated with an almost fivefold higher risk of mortality in patients without diabetes and an almost threefold higher risk in those with diabetes. This discrepancy may be attributed to the greater prognostic impact of spontaneous hypoglycemia, which is more common in patients without diabetes, compared to iatrogenic hypoglycemia. Indeed, a retrospective cohort study by Kosiborod et al. [19] revealed that in patients hospitalized with AMI, hypoglycemia was linked to increased mortality only in those experiencing spontaneous hypoglycemia (18% vs. 9% of patients not experiencing hypoglycemia). Conversely, iatrogenic hypoglycemia following insulin therapy was not associated with a higher mortality risk (10%). Consistent with this, an analysis from the DIGAMI 2 trial, which focused on the safety and efficacy of insulin use in hyperglycemic patients with diabetes during AMI, concluded that hypoglycemic episodes occurring within the first 24 h after admission do not elevate the risk of cardiovascular mortality, re-infarction, or stroke during hospitalization or in the subsequent three years.
The association between hypoglycemia during hospitalization for AMI and adverse outcomes has also been observed in long-term follow-up studies. Retrospective analyses of patients admitted for acute coronary syndromes revealed that hypoglycemia was an independent predictor of all-cause mortality up to three years post-hospitalization [20].
Possible mechanisms underlying the association between hypoglycemia and worse prognosis in AMI (Fig. 1). Hypoglycemia sets off a cascade of events that may elucidate its prognostic significance during hospitalization for AMI and in the aftermath of the acute event. The occurrence of hypoglycemia triggers an increase in plasma adrenaline levels, which subsequently elevate heart rate and systolic blood pressure, and an increase in left ventricular systolic function [21, 22], resulting in a 50%-100% rise in cardiac output [23, 24]. This substantial increase in cardiac workload and oxygen demand can be particularly detrimental in the context of acute myocardial ischemia. Additionally, acute hypoglycemia promotes endothelial dysfunction by increasing circulating levels of interleukins, cytokines, and reactive oxygen species. Notably, endothelin-1, a potent vasoconstrictor released by endothelial cells, has been shown to increase by up to 70% during hypoglycemia [25]. High-sensitivity C-reactive protein (hs-CRP) elevation during AMI is a widely observed finding. A prospective study of 2,064 patients showed that hs-CRP predicts in-hospital outcomes and two-year mortality in patients with AMI with and without diabetes [26]. Moreover, in patients with diabetes, the same risk of adverse events as in patients without diabetes is associated with higher hs-CRP levels. This suggests that the inflammation-related risk during AMI overlaps with the chronic inflammatory state associated with diabetes [26]. Also acute hypoglycemia may induce inflammation, as evidenced by significant elevations in hs-CRP levels and other proinflammatory cytokines, including tumor necrosis factor-alpha (TNF-α), interleukin (IL)-1β, IL-6, and IL-8, following hypoglycemic episodes [27, 28].
Fig. 1
Biochemical and clinical effects of hypoglycemia in acute myocardial infarction. ABP Arterial blood pressure, CK Cytokines, HR Heart rate, hs-CRP High sensitivity-C reactive protein, IL Interleukin, LVEF Left ventricular ejection fraction, NSVT Non-sustained ventricular tachycardia, ROS Reactive oxygen species, TNF Tumor necrosis factor, VW Von Willebrand
Numerous studies have demonstrated that acute hypoglycemia enhances platelet aggregation and clot activation, leading to a prothrombotic and procoagulant state [29, 30]. In patients with diabetes, acute hypoglycemia induces a significant increase in serum VIII factor levels [31]. Additionally, Von Willebrand factor is released from endothelial cells and platelets in response to low blood glucose, promoting platelet aggregation [32, 33]. Consequently, episodes of hypoglycemia appear to amplify many of the pathophysiological pathways already involved in acute myocardial ischemia, which are closely linked to prognosis [34].
Another mechanism through which hypoglycemia may impact outcomes in patients with AMI is its pro-arrhythmic effect. In patients hospitalized with STEMI undergoing primary percutaneous coronary intervention (PCI), hypoglycemia has been associated with a significantly higher frequency of ventricular arrhythmias, including ectopic ventricular beats and non-sustained ventricular tachycardias [35, 36]. Moreover, in various clinical contexts, hypoglycemia has been linked to an increased susceptibility to cardiac arrhythmias such as bradycardia, atrial fibrillation, and ventricular ectopic beats [37, 38]. Additionally, hypoglycemia has been implicated in QT interval prolongation, with a strong correlation observed between hypoglycemia, peak adrenaline blood levels, and QT lengthening, independent of extracellular potassium levels [38,39,40].
Finally, aside from a causal relationship between hypoglycemia and worse outcomes in AMI, hypoglycemia may also be considered an epiphenomenon of severe organ dysfunction, similarly as it has been proposed in septic shock [41]. The higher frequency of hypoglycemia during STEMI, the most severe form of AMI, and the association of adverse prognosis with spontaneous rather than iatrogenic hypoglycemia, suggest that low blood glucose levels may reflect greater severity of the ongoing acute event, identifying critically ill patients [4, 13, 14].
Glycemic variability in AMI
Glycemic variability is often overlooked in routine clinical practice but plays a crucial role in glycemic control. It encompasses fluctuations in blood glucose levels or related parameters of glucose regulation over a specific period. This concept includes two main types of measurements: short-term and long-term GV. Short-term variability encompasses fluctuations within a single day (within-day) as well as variations between different days (between-day), ranging from peak to trough levels. Long-term GV involves serial measurements over an extended period, including assessments of glycosylated hemoglobin and fasting and postprandial glucose levels [6, 42, 43].
Traditionally, self-monitoring of blood glucose has been the preferred method for evaluating GV [44]. However, continuous glucose monitoring (CGM) systems have become increasingly favored in recent years and are now considered the gold standard for assessing short-term GV [45, 46]. In the clinical context of AMI and other critical conditions, short-term GV is often defined using various metrics, leading to variability in its assessment. The most used metrics are the standard deviation (SD), defined as the variation over the mean glucose concentration, and the coefficient of variation (CV), defined as SD divided by the mean glucose concentration. Standard deviation is deeply related to the mean glucose level: CV should be preferred in patients who have higher mean glucose level, because they will have higher SD. Furthermore, CV is a metric relative to the mean, which makes it a better reflection of hypoglycemic fluctuations than SD alone. Another measure of within-day variability is the mean amplitude glycemic excursion (MAGE), which describes the average glycemia above one SD from the 24-h mean glycemia; the mean of daily differences (MODD) is considered to be the best metric of between-day GV and is obtained based on the differences between two glucose measurements at the same time within a 24-h period. Referring to GCM, continuous overall net glycemic action (CONGA) is another short-term GV metric assessed by the differences between glucose levels calculated ad regular time intervals and then on the SD of these differences [43]. The heterogeneity in reporting GV was largely due to the previous lack of standardized definitions, which was addressed by a consensus established in 2017 [46]. Therefore, more recent literature is expected to report GV more consistently, particularly when based on CGM data.
Incidence of high GV in AMI
In a retrospective study involving 18,563 patients hospitalized with AMI between 2000 and 2008, who underwent > 3 blood glucose determinations within the first 48 h, it was found that 50% of patients experienced a glucose level excursion of at least 64 mg/dL, with half of them having a glucose excursion exceeding 127 mg/dL [47]. In a more recent prospective study of 222 patients hospitalized with AMI, acute GV—defined as a MAGE > 70 mg/dL (> 3.9 mmol/L), detected through CGM systems within the first 48 h after admission—was observed in 36% of cases [48]. Similarly, a study involving 237 STEMI patients undergoing primary PCI reported a GV rate of 33%, defined as MAGE > 66 mg/dL within the first 72 h [49]. Notably, in all these studies, patients with higher GV were more likely to have diabetes, receive insulin treatment for acute hyperglycemia, and consequently present with higher admission glucose levels. However, when only patients with STEMI without diabetes were considered, a MAGE > 60 mg/dL during the first 72 h was observed in 34% of them [50].
Prognostic relevance of GV in AMI
In the context of AMI, Su et al. [48] investigated the correlation between GV, determined by CGM systems, and a composite endpoint of cardiovascular death, recurrent AMI, and acute heart failure at 1 year. Patients with a MAGE ≥ 70 mg/dL had a threefold higher rate of this composite endpoint compared to those with a MAGE below this threshold (24% vs. 8%). Elevated MAGE levels predicted major cardiovascular events (hazard ratio 2.4) even after adjusting for the Global Registry of Acute Coronary Events (GRACE) risk score. Another study examined the association between GV and mid-term major cardiac events (median follow-up 17 months) in 327 patients with diabetes hospitalized with acute coronary syndromes [51]. Interestingly, increased GV, defined as a standard deviation of glycemia ≥ 49 mg/dL and assessed during hospitalization using point-of-care measurement of capillary glucose values, emerged as the strongest independent predictor of cardiovascular death, recurrent AMI, and acute heart failure (odds ratio [OR] 2.2), surpassing even left ventricular ejection fraction < 40% (OR 1.7) and a GRACE score > 140 (OR 1.1). However, some previous studies have failed to establish a clear association between GV and outcomes in patients with AMI. In a re-analysis of the Hyperglycemia and Its Effect After Acute Myocardial Infarction on Cardiovascular Outcomes in Patients with Type 2 Diabetes (HEART2D) study, Siegelaar et al. [52] demonstrated that a reduction in GV through insulin treatment did not lower cardiovascular events in patients with diabetes hospitalized with AMI. Additionally, a report from the DIGAMI-2 trial exploring the prognostic implications of GV during the first 48 h of hospitalization for AMI in patients with diabetes receiving insulin-glucose infusion found no correlation between GV and the 1-year risk of the composite endpoint of death, re-infarction, or stroke [53].
Zhang et al. [49] observed in 237 STEMI patients monitored by CGM systems for 72 h after primary PCI that MAGE levels correlated with enzymatic infarct size and the incidence of in-hospital cardiac death, re-infarction, repeat target vessel revascularization, or recurrent angina. Thus, accumulating evidence suggests that elevated GV should be considered a prognostic parameter for short-term and long-term risk stratification of patients hospitalized with AMI. Another study that enrolled 417 patients with acute coronary syndrome analyzed glycemic variability with CGM. It evaluated MAGE (defined as a variability of plasma glucose level of at least 52 mg/dl) and its relationship with major adverse cardio-cerebral events (MACCEs) showing a higher rate of MACCEs in patients who had wider MAGE; this finding was also confirmed in a multivariate analysis demonstrating that an increased MAGE is an independent predictive factor of poor prognosis [54]. Furthermore, a systematic review that included 11 studies with more than 3,500 patients confirmed that increased GV is related to a poor prognosis in patients with acute coronary syndromes, independently by metrics implied [55].
In 2018, we evaluated acute-to-chronic glycemic ratio at admission in patients with AMI. We measured admission glycemia and estimated the average chronic glucose level based on glycosylated hemoglobin (HbA1c). Our prospective study, using multivariate and reclassification analyses, demonstrated that acute-to-chronic glycemic ratio was a better predictor of in-hospital morbidity and mortality than admission glycemia alone, and it was associated with a parallel increase in peak troponin I values [56]. Furthermore, as noted in a 2021 review, GV continues to significantly impact cardiovascular outcomes [57]. As anticipated by a Delphi consensus, CGM has proven valuable for diagnosis and prognosis in high-risk diabetic patients. The cited studies underscore CGM’s role in detecting GV and supporting better glycemic control [58, 59].
In conclusion, recent evidence supports a strong association between GV and clinical outcomes in patients hospitalized with AMI, suggesting that GV may serve as a valuable prognostic marker. However, it remains unproven whether interventions specifically targeting GV can improve outcomes in this clinical context. Further research is warranted to establish whether reducing GV can yield meaningful clinical benefits in this high-risk population.
Possible mechanisms underlying the association between high GV and worse prognosis in AMI (Fig. 2). In the past two decades, experimental studies have shed light on the detrimental effects of GV. In vitro exposure of human umbilical vein endothelial cells to both constant and intermittent high glucose mediums has been shown to stimulate the overproduction of reactive oxygen species (ROS) by the mitochondrial respiratory chain. The resulting heightened oxidative stress and increased cellular apoptosis were more pronounced when the culture was exposed to intermittent, rather than constant, high glucose medium. Interestingly, at the same level of hyperglycemia, the severity of endothelial dysfunction and oxidative stress were directly correlated with the magnitude of glucose level increase [60]. Clinical studies have also corroborated these findings. For instance, acute glucose fluctuations, but not sustained hyperglycemia, have been positively correlated with the urinary excretion rate of free-8-isoprostaglandine F2, a marker of oxidative stress, in patients with type-2 diabetes treated with oral anti-hyperglycemic agents [61]. Similarly, oscillating glucose over a 24-h period was found to be more damaging to endothelial function than stable constant high glucose, irrespective of diabetic status [62]. Interestingly, a study involving 37 consecutive patients with AMI who underwent optical coherence tomography (OCT) revealed plaque rupture in 24 patients and no rupture in 13 at the culprit coronary site. The study found that MAGE, measured via CGM, was significantly higher in patients with plaque rupture compared to those without. Additionally, levels of a specific monocyte sub-population (CD14brightCD16+) were significantly elevated in the rupture group. Notably, the prevalence of this monocyte subset showed a significant positive correlation with MAGE [63].
Fig. 2
Biochemical and clinical effects of high glycemic variability in acute myocardial infarction. Ly Lymphocyte, NT-proBNP N-terminal pro B-type Natriuretic Peptide, ROS Reactive oxygen species; urinary 8 isoPG F2 = urinary 8 iso-prostaglandin F2
However, no relationship was found between GV and oxidative stress markers in a small cohort of patients with type 1 diabetes [64]. In a separate small observational study, an increased mean daily difference in blood glucose blood levels was directly correlated with increased NT-proBNP levels, although this association has not yet been linked to adverse clinical outcomes [65].
Experimental models of diabetic heart disease have demonstrated that glucose fluctuations exacerbate ischemia/reperfusion injury by increasing the generation of ROS [66]. Clinical evidence supports these findings. In patients with AMI, high GV has been associated with electrocardiographic and angiographic indicators of impaired myocardial reperfusion [67]. For instance, in STEMI patients undergoing primary PCI and monitored by CGM systems, a lower rate of electrocardiographic ST-segment resolution was observed in those with high GV. Moreover, high GV was linked to angiographic no-reflow and lower myocardial blush grades in STEMI patients treated with primary PCI [54]. Additionally, a negative correlation was found between high GV and the myocardial salvage index, as assessed by cardiac magnetic resonance imaging, in reperfused STEMI patients [68].
Another potential mechanism linking GV to outcomes in patients with AMI involves platelet activity. A recent study in patients with type 2 diabetes on clopidogrel therapy demonstrated that those with high residual platelet activity also exhibit higher GV [69]. Additionally, high GV has been associated with increased production of thromboxane B2, a marker of in-vivo platelet activation [70]. These findings suggest a greater propensity for thrombotic complications in patients with AMI with elevated GV.
Gaps in knowledge and future perspectives
Despite the well-established link between persistent high GV and an increased occurrence of both macrovascular and microvascular complications in patients with diabetes, the precise role of GV during the acute phase of AMI remains incompletely understood.
Although international consensus reports [46, 71] recommend standardized metrics for assessing short-term GV, their limited use in research and clinical practice, coupled with an incomplete understanding of GV’s biological effects on ischemic myocardium, continue to challenge the establishment of a clear causal link between GV and clinical outcomes in AMI. Moreover, it is uncertain how GV during the acute phase of AMI contributes, in terms of prognostic significance, compared to acute hyperglycemia. Notably, as acute hyperglycemia typically resolves promptly with insulin therapy during AMI, patients with the highest blood glucose levels upon hospital admission also tend to experience the greatest variability in glucose levels during normalization. Thus, GV in the initial hours of AMI may reflect the flip side of stress-induced hyperglycemia. The complexity is further compounded by the observation that elevated blood glucose levels at admission may not necessarily indicate true stress hyperglycemia, particularly in individuals with diabetes who may already have chronically elevated glucose levels. This ambiguity makes it challenging to determine the independent prognostic role of GV in this clinical context. Particularly in patients with diabetes, the swift correction of chronically elevated glucose levels may inadvertently lead to iatrogenic increases in GV, potentially resulting in adverse clinical outcomes.
In this regard, hypoglycemia represents another underappreciated but harmful facet of glucose dysregulation during AMI. Episodes of hypoglycemia, particularly when occurring as a consequence of aggressive glucose-lowering strategies, may exert proarrhythmic effects, trigger sympathoadrenal activation, and exacerbate myocardial ischemia. The prognostic implications of hypoglycemia—especially when superimposed on a background of high GV—remain largely undefined in the context of AMI. It is also unclear whether the cardiovascular risk associated with hypoglycemia differs between spontaneous and iatrogenic episodes, and how such events interact with the overall glycemic profile during hospitalization. Additionally, the detection of hypoglycemia is often limited by intermittent glucose monitoring, potentially leading to underestimation of its frequency and clinical impact. These gaps in evidence further highlight the need for CGM and refined clinical protocols to identify and mitigate harmful glycemic excursions on both ends of the spectrum. To this end, metrics like MAGE, by capturing both high and low glucose swings, may better inform pharmacological strategies particularly when aiming to minimize hypoglycemic risk without compromising glycemic control. Therefore, GV, through MAGE, might be more effective in tailoring individualized treatment plans.
Nevertheless, some studies have identified GV as an independent predictor of outcomes in patients with AMI, even after accounting for admission glycemia as a confounding factor, suggesting an additional prognostic contribution. However, this observation warrants confirmation, particularly when assessing “true” stress hyperglycemia rather than solely relying on the absolute glycemic value at admission. There are two ongoing clinical trials focused on exploring the prognostic role of GV in patients with AMI, according to available data from ClinicalTrials.gov as of the latest update on May 19th, 2025. The characteristics of these two studies are summarized in Table 1. Future research is essential to definitively clarify the clinical significance of high GV and its therapeutic management in patients with AMI.
Table 1 Characteristics of ongoing clinical trials focused on glucose variability (GV) in acute myocardial infarction
Finally, while hypoglycemia and GV are increasingly recognized as significant prognostic factors in AMI, their targeted management remains underexplored. Current treatment strategies largely focus on hyperglycemia control, often neglecting the harmful effects of glucose excursions on both ends of the spectrum. Among the potential interventions, glucose-insulin-potassium (GIK) infusions have been extensively studied. GIK was initially proposed to provide metabolic support to the ischemic myocardium by optimizing substrate utilization, limiting infarct size, and minimizing GV. Early trials showed promising results, particularly when administered early after symptom onset [72]. However, subsequent large randomized studies, including the CREATE-ECLA trial, failed to demonstrate a consistent benefit in reducing mortality or major cardiac events [73]. Moreover, concerns about fluid overload and hypoglycemia have limited its widespread adoption. In parallel, glucagon-like peptide-1 (GLP-1) receptor agonists have gained attention due to their cardioprotective properties and low risk of inducing hypoglycemia. Experimental studies have suggested that GLP-1 agonists may improve left ventricular function post-AMI and reduce infarct size, particularly when administered acutely [74]. Their ability to attenuate GV without triggering hypoglycemic episodes adds to their therapeutic appeal in this setting. For example, a study by Read et al. [75] showed that GLP-1 infusion is able to reduce ischemic left ventricular dysfunction after supply ischemia during coronary balloon occlusion in patients undergoing elective PCI and mitigates stunning. Given the complex interplay between glycemic control and cardiovascular outcomes, further investigation is warranted to determine whether strategies like GIK or GLP-1 agonist therapy can meaningfully reduce hypoglycemia, GV, and their associated risks. Integrating such targeted approaches into AMI treatment protocols may ultimately improve both short- and long-term patient outcomes.
UNITED NATIONS, July 30 (Xinhua) — An estimated 80,000 children are at high risk of cholera as the rainy season begins across West and Central Africa, a UN spokesperson said Wednesday.
Active outbreaks in the Democratic Republic of the Congo and Nigeria raise the threat of cross-border transmission to neighboring countries, said Farhan Haq, deputy spokesperson for the UN secretary-general, at a daily briefing.
Chad, the Republic of Congo, Ghana, Cote d’Ivoire and Togo are also grappling with ongoing epidemics, Haq cited UNICEF. Niger, Liberia, Benin, the Central African Republic and Cameroon remain under surveillance due to vulnerability, he added.
Since the start of the outbreaks, UNICEF has been delivering health, water, hygiene and sanitation supplies to treatment facilities and communities, said the spokesperson.
Besides supporting cholera vaccination in the affected areas and encouraging families to seek treatment and improve hygiene practices, urgent and scaled-up efforts are needed to prevent further spread and contain the disease across the region, he said.
To augment the emergency response across the region over the next three months, UNICEF West and Central Africa urgently requires 20 million U.S. dollars to provide support in health, water and sanitation, risk communication and community engagement, Haq said. ■
New HIV vaccines have shown promise in studies with lab animals and human volunteers, pointing to a potential way of preventing the lifelong viral disease.
These experimental vaccines are built upon mRNA technology and several triggered potent immune responses in these early tests, while also causing few side effects.
Scientists described the new vaccines in a pair of studies published Wednesday (July 30) in the journal Science Translational Medicine. The first study tested a few vaccines in rabbits and monkeys, and the promising results of that work led to further development of the shots and the subsequent human trial. The trial included over 100 healthy human volunteers and tested three vaccines similar to those tested in animals.
The effort “marks significant progress in the global effort to develop a safe and effective HIV vaccine that prevents infection,” said Seth Cheetham, director of the Australian mRNA Cancer Vaccine Centre and deputy director of the BASE mRNA manufacturing facility at the University of Queensland.
“While drugs for HIV treatment and prevention have transformed the lives of people living with HIV, an effective vaccine is still urgently needed,” Cheetham, who was not involved in the work, told Science Media Exchange.
Over the past decade, the annual rate of new human immunodeficiency virus (HIV) infections has fallen significantly, according to the World Health Organization, but, each year, many hundreds of thousands still occur. Globally, an estimated 1.3 million people acquired HIV in 2024, including about 120,000 children. An HIV vaccine could be transformative if, in just a few doses, it could raise the immune system’s ability to block the virus from taking hold in the first place.
Related: Nearly 3 million extra deaths by 2030 could result from HIV funding cuts, study suggests
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Currently, preventive medications for HIV must be taken on an ongoing basis — either daily, every other month or twice yearly. This can pose a particular challenge in areas with limited health care resources and infrastructure. Many scientists think a vaccine will be the key to ending the HIV/AIDS epidemic worldwide, because such a tool could efficiently stymie new infections and curb further spread of the disease.
But crafting an HIV vaccine is very challenging. The virus expertly evades the immune system by donning disguises, and it mutates rapidly, constantly switching up its look. Ideally, HIV vaccines will trigger the production of elusive “broadly neutralizing antibodies” — proteins that target relatively immutable bits of the virus that look similar across many strains and can block infections, thus offering wide-ranging protection.
Scientists are exploring different strategies to trigger that protection. On that front, the researchers behind the new studies turned to messenger RNA (mRNA), a molecule that serves as instructions for cells to make proteins. They designed their experimental vaccines to carry directions for a complex of proteins found on the surface of HIV. Called the “envelope trimer,” this complex enables the virus to grab the surface of human immune cells and invade those cells.
Once injected into the body, the vaccines prompt cells to build one of two versions of the envelope trimer: one that exits the cell and floats away, and another that stays bound to the surface of the cell. The free-floating version has been targeted in prior HIV vaccines studies, but previously hasn’t produced adequate neutralizing antibodies, the study authors noted.
They think this is because, on the surface of a real HIV particle, the base of the trimer is embedded inside the virus and thus hidden from view. They anticipated that the latter version of the trimer — the one that stays stuck to the cell — would trigger better neutralizing responses that take aim at other parts of the complex, rather than the base.
That turned out to be the case in both the animal study and the early clinical trial.
For the human trial, the researchers recruited 108 healthy people ages 18 to 55, split them into three groups, and gave each group one of three mRNA vaccines. One vaccine encoded a free-floating trimer, while the latter two encoded different bound versions of the structure. Each participant received three doses of their assigned vaccine: one at the initial visit, another two months later, and a final dose six months after the first.
As in the animal tests, the bound trimers elicited stronger signs of protection than the free-floating trimer did. The bound-trimer vaccines produced neutralizing antibodies in 80% of those vaccinated, while the free-floating-trimer vaccine triggered the same response in only 4% of the recipients.
Related: In a 1st, HIV vaccine triggers rare and elusive antibodies in humans
The bound-trimer vaccines also “generated strong memory responses, meaning the body would be better prepared to fight off HIV even long after vaccination,” Cheetham noted. This would be thanks to antibody-producing memory B cells, which persist for a long time to help mount quick immune responses against germs they’ve encountered in the past, either through infection or vaccination.
The human trial was primarily designed to look at the safety of the vaccines, and they were “well tolerated overall.” They triggered mostly mild and transient side effects, such as fatigue, achiness, headache, chills, nausea and injection-site pain. However, hives, also called urticaria, were seen in seven participants, which the authors noted was “a far higher frequency than reported with COVID-19 mRNA vaccines.” Several of the affected individuals experienced the skin reaction for months.
“While most adverse reactions were mild and treatable, several people experienced a skin reaction,” Cheetham said. “If these side effects can be reduced in next-generation versions and the results hold up in larger real-world studies in the community, mRNA vaccines could be a transformative tool in the fight against HIV.”
The trial had several other limitations. First, it was open-label, meaning the researchers and vaccine recipients knew which shots were being given, which can potentially bias the results. In addition, the vaccines were not specifically designed to make broadly neutralizing antibodies that can handle many strains but rather neutralizing antibodies that can tackle only select strains.
Nonetheless, the trial results provide insight into the safety and efficacy of mRNA vaccines that code for HIV envelope trimers, the researchers noted. It should inform future efforts to refine these vaccines so they trigger more broadly protective antibody responses.
This article is for informational purposes only and is not meant to offer medical advice.
