Category: 8. Health

What can contribute to heart attack risk?

Dr Dhirendra Singhania, principal consultant of interventional cardiology at Yashoda Super Speciality Hospitals in Kaushambi, said in June 30 interview with NDTV that the ‘major causes of risk in heart attacks are steroids, lack of sleep, and hormonal therapies, especially for women’.

He said, “Everyone, whether a celebrity or a common man, if they are not following the rules of the body, they will have problems. In celebrities, they all try to maintain their body for fit appearances. Many times, we don’t know what they do to achieve that. Lack of sleep has been known as a cardiac risk factor – many celebrities are awake for almost the whole night at times.”

Highlighting the importance of approaching anti-ageing treatments with caution, and prioritising your health and safety, Dr Singhania added, “Steroids, drug overdoses, and hormonal therapies for women, such as hormone replacement therapy (HRT for menopause) and oral contraceptives, can contribute to heart attack risk.”

Be cautious with anti-ageing treatments

Before trying any anti-ageing treatments, it’s essential to consult a qualified doctor, especially if you have heart conditions or other health issues. In a May 2025 interview with HT Lifestyle, a dermatologist explained non-invasive skin treatments, the ideal age to start them, signs of ageing, and who should avoid these treatments in a complete guide. Click here to know what she said.

Note to readers: This article is for informational purposes only and not a substitute for professional medical advice. Always seek the advice of your doctor with any questions about a medical condition.

A new study from UCLA Health has uncovered how inflammation in brain blood vessels exacerbates damage in vascular dementia and demonstrated that targeting this process with a repurposed drug can promote brain repair and functional recovery in mice.

Published in Cell, the research combines laboratory and human data to pinpoint a critical signaling pathway that could lead to the first effective treatment for this understudied form of dementia.

Vascular dementia is the second leading cause of dementia. This disease co-occurs with Alzheimer’s disease in the leading cause of dementia, termed “mixed dementia.” There is no drug therapy that promotes recovery in vascular dementia. A key problem in this disease is that the brain damage expands from initial areas, to become larger over time. The UCLA team sought to identify what happens in the brain in these areas of expansion. To do this, the researchers identified all the molecules that communicate among the cells of the brain adjacent to the dementia lesions, and which ones are abnormally up or down in the disease compared to normal brain. By doing this both in laboratory models of vascular dementia and in human brain, the UCLA team was able to precisely identify the “interactome” in vascular dementia – all the molecules that signal or interact in the cells at risk.

We reasoned that the cell in the brain areas in which the disease expands will lose their normal signaling with each other. In other words, the cell-to-cell interaction is disturbed in a toxic way in vascular dementia. We set out to identify these cell-to-cell interactions or the “interactome” in vascular dementia.” 

Dr. S. Thomas Carmichael, study’s lead author and professor and chair Neurology at the David Geffen School of Medicine at UCLA

One molecular system jumped out as potentially significant. This system communicates between blood vessel cells and adjacent brain inflammatory cells, termed microglia. In vascular dementia, the CD39 (an enzyme) and the adenosine A3 receptor (A3AR) are downregulated together in these two cell types, synergistically by aging and vessel ischemic lesion. Because vascular dementia is a disease of aging, this double finding – a downregulation with both disease and aging – signaled a possibly significant role. CD39 generates through several steps the molecule adenosine, which binds to A3AR, and modifies inflammation, downregulating some of its harmful effects. 

To test this CD39/A3AR system as a possible drug target for treating vascular dementia, the group utilized a drug that is in clinical trials for psoriasis. When given to mice in a model of vascular dementia, this drug promoted repair of brain tissue and recovery of memory and gait functions.

“The most exciting finding was that delayed intervention still worked,” said lead author Dr. Min Tian, a postdoctoral scholar at UCLA Health. “This is crucial because vascular dementia is often diagnosed late. By targeting the crosstalk between blood vessels and brain cells, we’re addressing the root cause of damage, not just masking symptoms.”

While the results are promising, further studies are needed before human trials can begin. The team is now optimizing dosing and exploring biomarkers to track the therapy’s effectiveness.

The study, “Deconstructing the Intercellular Interactome in Vascular Dementia with Focal Ischemia for Therapeutic Applications,” will be online in Cell, June 30, 2025, and includes collaborators from UCLA’s neurology, pathology, neurobiology, physiology and psychiatry departments. Funding was provided by the National Institutes of Health, Ressler Family Foundation, The Dr. Miriam and Sheldon G. Adelson Medical Research Foundation, UCLA Eli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research, including support from the Steffy Family Trust.

In radiation therapy, precision can save lives. Oncologists must carefully map the size and location of a tumor before delivering high-dose radiation to destroy cancer cells while sparing healthy tissue. But this process, called tumor segmentation, is still done manually, takes time, varies between doctors – and can lead to critical tumor areas being overlooked.

Now, a team of Northwestern Medicine scientists has developed an AI tool called iSeg that not only matches doctors in accurately outlining lung tumors on CT scans but can also identify areas that some doctors may miss, reports a large new study.

Unlike earlier AI tools that focused on static images, iSeg is the first 3D deep learning tool shown to segment tumors as they move with each breath – a critical factor in planning radiation treatment, which half of all cancer patients in the U.S. receive during their illness.

We’re one step closer to cancer treatments that are even more precise than any of us imagined just a decade ago.”

Dr. Mohamed Abazeed, senior author, chair and professor of radiation oncology at Northwestern University Feinberg School of Medicine

“The goal of this technology is to give our doctors better tools,” added Abazeed, who leads a research team developing data-driven tools to personalize and improve cancer treatment and is a member of the Robert H. Lurie Comprehensive Cancer Center of Northwestern University.

The study will be published June 30 in the journal npj Precision Oncology.

How iSeg was built and tested

The Northwestern scientists trained iSeg using CT scans and doctor-drawn tumor outlines from hundreds of lung cancer patients treated at nine clinics within the Northwestern Medicine and Cleveland Clinic health systems. That’s far beyond the small, single-hospital datasets used in many past studies.

After training, the AI was tested on patient scans it hadn’t seen before. Its tumor outlines were then compared to those drawn by physicians. The study found that iSeg consistently matched expert outlines across hospitals and scan types. It also flagged additional areas that some doctors missed – and those missed areas were linked to worse outcomes if left untreated. This suggests iSeg may help catch high-risk regions that often go unnoticed.

“Accurate tumor targeting is the foundation of safe and effective radiation therapy, where even small errors in targeting can impact tumor control or cause unnecessary toxicity,” Abazeed said.

“By automating and standardizing tumor contouring, our AI tool can help reduce delays, ensure fairness across hospitals and potentially identify areas that doctors might miss – ultimately improving patient care and clinical outcomes,” added first author Sagnik Sarkar, a senior research technologist at Feinberg who holds a Master of Science in artificial intelligence from Northwestern.

Clinical deployment possible ‘within a couple years’

The research team is now testing iSeg in clinical settings, comparing its performance to physicians in real time. They are also integrating features like user feedback and working to expand the technology to other tumor types, such as liver, brain and prostate cancers. The team also plans to adapt iSeg to other imaging methods, including MRI and PET scans.

“We envision this as a foundational tool that could standardize and enhance how tumors are targeted in radiation oncology, especially in settings where access to subspecialty expertise is limited,” said co- author Troy Teo, instructor of radiation oncology at Feinberg.

“This technology can help support more consistent care across institutions, and we believe clinical deployment could be possible within a couple of years,” Teo added.

This study is titled “Deep learning for automated, motion- resolved tumor segmentation in radiotherapy.”

For the first time, the extreme variability in dengue fever has been linked to a biological mechanism, potentially opening doors to new treatments and vaccines for the most common mosquito-borne disease worldwide. The study was published today in Proceedings of the National Academy of Sciences (PNAS) by researchers from the University of Pittsburgh, UPMC and Instituto Aggeu Magalhães in Brazil.

Cases of dengue fever, commonly known as “breakbone fever” for the excruciating joint pain that is the hallmark of the disease, have been rising around the world in recent years. More than half the global population is at risk.

There’s an urgent need for better prevention and treatment for this global threat. Dengue outbreaks can quickly overwhelm local hospitals.”

Priscila Castanha, Ph.D., MPH, lead author, assistant professor of infectious diseases and microbiology at Pitt’s School of Public Health

The course of the disease varies widely from person to person. Some are asymptomatic; others experience dengue’s painful flu-like symptoms and then recover within days or weeks. “But 5% have serious bleeding, shock and organ failure-they can be critically ill within two days,” said senior author Simon Barratt-Boyes, Ph.D., professor of infectious diseases and microbiology at Pitt Public Health and immunology at Pitt School of Medicine.

For decades, epidemiologic studies have documented a puzzling phenomenon: In countries with ethnically diverse populations-like Brazil, Colombia, Haiti and Cuba-people of African ancestry tend to have milder cases of dengue, while people of European ancestry have more severe disease. But no one could explain why.

In this study, the team used a model they developed with samples of human skin that had been donated by individuals who had undergone elective skin-reduction surgeries after profound weight loss. The participants consented to contributing their tissues to this study.

“We used skin because it is an immunologic organ and the body’s first line of defense against dengue infection,” said Barratt-Boyes. When maintained in culture under proper conditions, the tissue samples used in this model can survive and carry out their normal immune functions for days, providing a unique opportunity for scientific study, he added, “because the skin is where the story begins with all mosquito-borne diseases.”

The study focused on samples from individuals who had self-identified as having European or African ancestry. First, the researchers objectively measured the ancestral geographic origins written into the skin samples’ DNA by analyzing genetic markers known as single nucleotide polymorphisms. The team then injected each sample with dengue virus, observed the samples’ subsequent immune responses over a 24-hour period and compared them.

The team found that the inflammatory response was much greater in skin from people with higher proportions of European ancestry. And unfortunately, in severe dengue, this immune response is prone to “friendly fire.” The virus infects inflammatory cells, actually recruiting them to spread the infection instead of fighting it off. This dynamic is believed to be what is so damaging to blood vessels and organs in severe cases of dengue fever.

In the samples from donors of European ancestry, the team saw this friendly fire in action as myeloid cells mobilized to confront the virus, then themselves became infected. The turncoat cells then moved out of the skin and spread out into the dish-similar to how they would spread within the body, traveling through the bloodstream and into lymph nodes.

The team further showed that the problem was not the skin itself-it was indeed the inflammatory response. In the samples from individuals with higher proportions of African ancestry, the researchers added inflammatory molecules called cytokines, and the friendly fire ensued. Then, when the team blocked the inflammation within those same samples, the virus’s rate of infection in the cells plummeted.

“It makes sense that, in parts of the world where ancient populations were exposed to deadly mosquito-borne viruses-like the one that causes yellow fever, which is related to dengue viruses and has been around for a very long time-those with a limited inflammatory response had an advantage,” said Barratt-Boyes. “They then passed that advantage down to their descendants.” Ancient Europeans’ descendants, however, lack that ancestral exposure and the evolutionary adaptation it made possible.

The authors hope that, eventually, the mechanism they’ve identified could be exploited for precision medicine approaches to things like risk assessment, triage in an outbreak, therapies and vaccines. In future studies, they hope to describe this mechanism in further detail, including which specific gene variants contribute to protection from severe dengue. The current study’s broader analysis of geographic ancestry could be an important first step to that end.

“Ancestry does affect biology. Evolution has made its mark on everyone’s DNA,” said Castanha.

Other authors on the study are Michelle M. Martí, M.S., Parichat Duangkhae, Ph.D., Jocelyn M. Taddonio, M.S., Kristine L. Cooper, M.S., Megan Wallace, M.S., Gwenddolen Kettenburg, M.S., Geza Erdos, Ph.D., Hasitha Chavva, M.S., Aleena Alex, M.S., Pharm. D., J. Peter Rubin, M.D., Simon C. Watkins, Ph.D., Louis D. Falo, Jr., M.D., Ph.D., and Jeremy J. Martinson, Ph.D., all of Pitt; and Ernesto T. A. Marquesa, M.D., Ph.D., of Pitt and Instituto Aggeu Magalhães.

This research was supported by Pitt, the Institute for Precision Medicine, the Richard K Mellon Foundation for Pediatric Research and the National Cancer Institute (P30CA047904). 

Every year, tens of thousands of people with signs of Parkinson’s disease go unnoticed until the incurable neurodegenerative condition has already progressed.

Motor symptoms, such as tremors or rigidity, often emerge only after significant neurological damage has occurred. By the time patients are diagnosed, more than half of their dopamine-producing neurons may already be lost. This kind of diagnostic delay can limit treatment options and slow progress on early-stage interventions. While there are existing tests to detect biomarkers of Parkinson’s, including cell loss in the brain and inflammatory markers in blood, they typically require access to specialists and costly equipment at major medical centers, which may be out of reach for many.

Led by Jun Chen, an associate professor of bioengineering at the UCLA Samueli School of Engineering, researchers have developed a seemingly simple yet effective tool: a smart, self-powered magnetoelastic pen that could help detect early signs of Parkinson’s by analyzing a person’s handwriting.

The highly sensitive diagnostic pen, described in a UCLA-led study and published as a cover story in the June issue of Nature Chemical Engineering, features a soft, silicon magnetoelastic tip and ferrofluid ink – a special liquid containing tiny magnetic particles. When the pen’s tip is pressed against a surface or moved in the air, the pen converts both on-surface and in-air writing motions into high-fidelity, quantifiable signals through a coil of conductive yarn wrapped around the pen’s barrel. Although not intended for writing, the pen is self-powered leveraging changes in the magnetic properties of its tip and the dynamic flow of the ferrofluid ink to generate data.

To test the pen’s diagnostic potential, the team conducted a pilot study with 16 participants, three of whom had Parkinson’s disease. The pen recorded detailed handwriting signals, which were then analyzed by a neural network trained to detect motor patterns associated with the disease. The model was able to distinguish participants with Parkinson’s from healthy individuals with an average accuracy of 96.22%.

Detection of subtle motor symptoms unnoticeable to the naked eye is critical for early intervention in Parkinson’s disease. Our diagnostic pen presents an affordable, reliable and accessible tool that is sensitive enough to pick up subtle movements and can be used across large populations and in resource-limited areas.”

Jun Chen, study’s corresponding author

The researchers anticipate that this pen could transform early detection of Parkinson’s and other neurodegenerative conditions. Rather than waiting for symptoms to become disruptive, primary care physicians or geriatric specialists could administer a quick handwriting test during routine visits and use the data to inform earlier referrals or treatment.

Wei Wang, a professor who holds the Leonard Kleinrock Term Chair in Computer Science, and Song Li, a chancellor’s professor in bioengineering, are also authors on the paper. Other authors include graduate students Guorui Chen, Zhaoqi Duan, Kamryn Scott and Xun Zhao; research scientists Zeyang Liu; and postdoctoral scholars Trinny Tat and Yihao Zhou – all members of Chen’s Bioelectronics Research Group. They were joined by graduate student Junkai Zhang, who is advised by Wang. Chen is also a member of the California NanoSystems Institute at UCLA.

The study was funded by the U.S. Office of Naval Research, the National Institutes of Health, the National Science Foundation, the American Heart Association, the Science Hub for Humanity and Artificial Intelligence at UCLA, UCLA Samueli and a Caltech/UCLA joint NIH grant.

Researchers discovered a previously unappreciated mechanism by which CMV, a herpes virus that infects the majority of the world’s adult population, enters cells that line the blood vessels and contributes to vascular disease. In addition to using molecular machinery that is shared by all herpes viruses, CMV employs another molecular “key” that allows the virus to sneak through a side door and evade the body’s natural immune defenses.

The finding might explain why efforts to develop prophylactic treatments against CMV have, so far, been unsuccessful. This research also highlights a new potential avenue for the development of future antiviral drugs and suggests that other viruses of the herpes family, such as Epstein-Barr and chickenpox, could use similar molecular structures to spread from one infected cell to the next while avoiding immune detection.

“If we don’t know what weapons the enemy is using, it is hard to protect against it,” said senior author Jeremy Kamil, Ph.D., associate professor of microbiology and molecular genetics at Pitt. “We found a missing puzzle piece that represents one possible reason why immunization efforts against CMV have been unsuccessful.”

In the United States, approximately one in every 200 babies is born with congenital CMV infection. Of the babies infected, one in five will have birth defects, such as hearing loss, or go on to have long-term health challenges. For most adults, CMV infections are asymptomatic. But a CMV infection during pregnancy presents significant health risks to the unborn child and could be deadly for people who are immunosuppressed, including organ transplant recipients.

Because of the large size of its genome and its complicated molecular machinery, CMV long evaded attempts to develop prophylactic treatments. Similar to other herpes viruses, CMV relies on a protein called gH to enter cells of the vessel lining. But unlike other herpes viruses, which use a protein partner called gL to facilitate infection, the new study found that CMV replaces gL with another partner called UL116 and recruits a protein called UL141. The resulting complex of gH-UL116-UL141, called GATE by the authors, then becomes an alternative tool for breaking into cells lining the blood vessels and causing internal damage while simultaneously preventing the body’s own immune system from recognizing the signs of infection.

The newly discovered GATE could become a potential vaccine target for CMV and other herpes viruses.

“Previous attempts to generate a CMV vaccine have failed, but that was before we identified the GATE complex. We hope that new strategies targeting GATE will improve our chances to combat CMV infection, and also perhaps cleanse our bodies of this lifelong infection,” said Chris Benedict, Ph.D., associate professor at La Jolla Institute for Immunology and co-senior author of the study with Kamil and LJI professor, president & CEO Erica Ollmann Saphire, Ph.D., MBA. “If we can develop antiviral drugs or vaccines that inhibit CMV entry, this will allow us to combat the many diseases this virus causes in developing babies and immune-compromised people.”

Other authors of this research are Michael Norris, Ph.D., of the University of Toronto; Lauren Henderson, Mohammed Siddiquey, Ph.D., both of Louisiana State University Health Shreveport; and Jieyun Yin, Ph.D., Kwangsun Yoo, Ph.D., Simon Brunel, Ph.D., Michael Mor, Ph.D., and Erica Ollmann Saphire, Ph.D., all of La Jolla Institute for Immunology.

This research was supported by the National Institutes of Health (grants AI11685, AI139749, AI101423 and T32HL155022) and by ARPA-H APECx contract 1AY1AX000055.

Some ups and downs in blood sugar are natural. What we want to avoid are large fluctuations in blood sugar, either too high or too low. Avoiding these fluctuations isn’t always easy—glucose variability can occur for a variety of reasons, like taking too much or too little medication, dehydration, stress, illness and overeating foods high in carbohydrates. 

Rebecca Jaspan, M.P.H., RD, CEDS, CDCES, describes the process, “Rises in blood sugar are normal for people with and without diabetes. Particularly when we eat, blood sugar rises, the hormone insulin is released and helps move the sugar from the blood into cells to produce energy.  When there is a disturbance in this insulin process, either from insulin resistance or not making enough insulin, the sugar stays in the blood and causes prolonged high blood sugar, which can be detrimental to health over time.” Here are seven habits diabetes experts recommend to help keep your blood sugar from spiking.

1. Not Addressing Your Stress 

Stress is inevitable, but chronic stress that is not addressed can hurt your health. Jaspan says, “High stress is one factor that can increase blood sugar. When we are stressed, the stress hormones cortisol and adrenaline are released, which can raise blood sugar and disrupt normal insulin function. This ‘fight or flight’ response keeps sugar in the blood longer rather than it moving into cells.” Lauren Plunkett, RDN, CDCE, a registered dietitian, certified diabetes care and education specialist and a person living with type 1 diabetes, adds, “When emotional stress is constant, it becomes chronic and this can lead to health problems over time.”

2. High-Intensity Exercise 

Exercise, a healthy habit, is important for increasing insulin sensitivity, i.e., how your body uses insulin. Regular exercise improves circulation, heart and respiratory health, and is a pivotal part in maintaining a healthy weight, increasing energy and mood, and building and maintaining bone and muscle.

Exercise improves blood sugar and can even cause it to dip below normal. However, for some people, strenuous exercise may cause blood sugar to rise. This occurs when adrenaline is released. Adrenaline can raise blood sugar by stimulating your liver to release glucose.

In addition, Jaspan says, “The body needs more glucose for energy during this type of exercise, causing the liver to release glucose into the bloodstream.” This rise is usually short, and “not necessarily unhealthy,” and “a completely normal part of our physiology,” adds Plunkett. If you have insulin resistance and diabetes, Jaspan recommends incorporating a variety of exercises and focusing on low- and medium-intensity exercises such as walking, Pilates and moderate weight training.

3. Taking Certain Medications 

Several classes of medications can cause blood sugar to rise. Medications like glucocorticoids, antipsychotics, heart medications (statins, beta blockers, diuretics), immunosuppressive drugs and hormone treatments are associated with changes in glucose metabolism and the incidence of high blood sugar or diabetes. If you have diabetes, make sure your care provider is aware of all the medications you’re taking. And don’t start or stop taking any medications without speaking to your provider first. 

4. Not Paying Attention to Hydration 

When you are not adequately hydrated, glucose becomes more concentrated in your blood, which can cause your levels to rise. To stay hydrated, women should aim for 11.5 cups (91 ounces) of fluids per day and men 15.5 cups (125 ounces) of fluids per day. This accounts for 20% of your fluid intake from the food you consume. However, your individual fluid needs can vary based on climate, sweat, physical activity and illness. Determine if you are adequately hydrated by examining your urine. It should be light yellow. 

5. Eating Large Amounts of Sugar-Free Foods 

The American Diabetes Association cautions people with diabetes to carefully read labels, as sugar-free and no-sugar-added claims do not necessarily mean that a food is carbohydrate-free or lower in carbohydrates. Carbohydrates are the macronutrients that impact blood sugar the most. Therefore, if you overeat sugar-free foods, your blood sugar may rise too high. 

Keep in mind that “When we eat, our food has an absorption rate that lasts for several hours. Blood glucose rises and typically falls during this time, and the rate of absorption is a result of meal composition. If blood glucose rises while eating and continues to rise between meals, it might be time to talk with a dietitian trained in preventing insulin resistance through lifestyle,” says Plunkett. 

6. Skipping Out on Sleep 

It’s tempting to stay up late to binge a thrilling new show or listen to your favorite podcast, but sleep and diabetes have a bidirectional relationship. Not enough sleep can cause blood sugar to rise. High blood sugar often interrupts sleep, especially if you are making frequent bathroom trips in the middle of the night. In a cohort study, researchers evaluated the risk of developing diabetes and sleep duration. They discovered that people who slept less than six hours per night had a greater risk of developing type 2 diabetes. ,

Research also demonstrates that people with diabetes who have inadequate sleep duration or sleep quality have higher fasting blood sugar, hemoglobin A1C, and experience more insulin resistance. Ideally, aim for seven to nine hours of sleep per night. Try to be consistent and shoot for the same bedtime and wakeup time daily. 

7. Getting Too Much Sun 

Frequent sun exposure can increase the chances of getting burned. Sunburn is often accompanied by pain, which can increase stress hormones and, as a result, increase your blood sugar.

Other Habits That Can Increase Blood Sugar:

• Skipping breakfast 
• Drinking too much coffee 
• Using a nose spray 
• Not taking care of your teeth 

Our Expert Take 

Blood glucose is supposed to rise and fall throughout the day. The problem occurs when blood sugar is elevated for long periods, increasing the risk of developing diabetes or complications of diabetes for those people who have it. Knowing where your blood sugar should be and which behaviors elevate it higher than normal is important. Many habits that increase blood sugar, such as too much stress, inadequate hydration and lack of sleep, can be remedied with simple lifestyle modifications. If you are unsure where to start or what your blood sugar should be, reach out to a certified diabetes educator or your health care provider.

The current landscape of public health in the United States is marked by a far-reaching attack on foundational scientific principles and institutions, threatening decades of progress in combating preventable diseases. Recent actions by the Trump administration, such as the abrupt dismissal of the Advisory Committee on Immunization Practices (ACIP) members and the appointment of individuals who have publicly expressed skepticism about established vaccine science, have generated profound concerns in the medical and public health communities. 

Health and Human Services Secretary Robert F. Kennedy Jr. has publicly questioned vaccine safety, notably by halting US funding to Gavi, the global vaccine alliance, accusing it of “ignoring the science,” without significant evidence, a move experts describe as “stunning and calamitous” and potentially costing “hundreds of thousands of children’s lives a year.” This politicization of public health measures, coupled with the spread of misinformation, risks eroding public trust and undermining critical immunization programs.

Amidst this contentious environment, a recent study published in JAMA Network Open titled “All-Cause Mortality and Life Expectancy by Birth Cohort Across US States,” by Holford et al. (2025), which analyzed 179 million deaths in the US across states and birth cohorts over more than a century, offers important insights into the social value of sustained public health investments. 

This study emphasizes the utility of analyzing cohort life expectancy, a measure that more accurately reflects the “lived experiences of populations” by tracking how early-life exposures and risk factors shape health outcomes as a group ages. The cohort perspective highlights how public health interventions’ impacts can follow individuals throughout their lives.

The study, alongside other sources, underscores a period of “large gains in life expectancy” and an “unprecedented decline in mortality” in the United States during the 20th century. Between 1900 and 1950, every US state experienced a substantial increase in life expectancy. These gains continued into the 1970s. This remarkable achievement was not accidental but resulted from a combination of deliberate public health actions and medical innovations:

• Public health improvements: Significant strides were made in public health infrastructure, including improvements in sanitation and the provision of clean water.
• Medical advances: The introduction of life-saving medical treatments, such as antibiotics like sulfa drugs and penicillin, dramatically reduced deaths from infectious diseases.
• Vaccine programs: The widespread implementation of vaccination programs played a pivotal role. 

These benefits spread globally as well, with a time lag, as poorer countries sought to catch up. Measles vaccination alone accounted for 93.7 million lives saved—over 60 percent of the total 154 million lives saved by vaccination between 1974 and 2024. DTP-containing vaccines saved an estimated 40 million lives globally over the past 50 years.

In the US, routine childhood vaccinations for children born between 1994 and 2023 are estimated to have prevented 1.1 million deaths, 32 million hospitalizations, and 508 million illnesses, resulting in nearly $3.7 trillion in societal cost savings. The eradication of smallpox through vaccines is highlighted as a monumental achievement. These factors essentially ended the childhood mortality gap. In 1900, a newborn could expect to live to 48 years of age, but if they survived childhood, life expectancy dramatically increased to 61. By 1980, life expectancy at birth and after childhood were equal.

However, other critical factors in the broader public health initiatives include behavioral changes, such as the decline in cigarette smoking, that have further contributed to improved health outcomes for older adults. This included broader access to healthcare, which further supported these gains.

PHNOM PENH – Ten cases of H5N1 avian influenza have been detected in Cambodia so fa this year. The two most recent patients are a mother and son from Siem Reap province.

On Sunday, June 29, the Ministry of Health announced that two additional cases of avian influenza were found in the same area as a 41-year-old woman who had tested positive for the H5N1 virus, as confirmed by the National Institute of Public Health the previous Monday.

An active field investigation to identify suspected cases and those exposed in Lbeuk village, of Puok district’s Donkeo commune — where the 41-year-old woman resides — revealed two more confirmed H5N1 cases: a 46-year-old woman and a her 16-year-old son.

The institute confirmed that both individuals tested positive for the H5N1 virus. They are the 9th and 10th cases of bird flu recorded in Cambodia in 2025.

“These two cases reside approximately 20 metres from the home of the 41-year-old patient. Currently, both patients are in stable condition and are being treated with Tamiflu under close medical supervision,” the ministry stated.

Interviews revealed that at the homes of the patients, as well as their neighbours and around the village, there were sick or dead chickens and ducks. The patients had reportedly handled and come into contact with the ill poultry, which they then prepared and ate.

National and subnational rapid response teams from the health ministry, in cooperation with provincial agriculture department officials and local authorities, are actively investigating the outbreak. They are also responding with technical protocols, identifying sources of infection in both animals and humans, locating suspected cases and those exposed, preventing further community transmission, distributing Tamiflu to close contacts, and launching a health education campaign for villagers.

The 41-year-old woman, the first H5N1 case in the village, had also handled sick and dead poultry at her own home and her neighbour’s, and prepared them as food five days before falling ill.

The ministry again urged the public to remain vigilant about bird flu, as H5N1 continues to pose a serious threat to public health in Cambodia.

Anyone experiencing fever, cough, runny nose or difficulty breathing, along with a history of contact with sick or dead poultry in the 14 days before symptoms began, should avoid gatherings and crowded places and immediately seek medical advice and treatment at the nearest health centre or hospital without delay.

On June 27, officers from the Provincial Livestock and Animal Health Office of the Siem Reap agriculture department, in cooperation with the National Animal Health and Production Research Institute (NAHPRI), implemented veterinary measures at the site of an earlier outbreak in Puok district and commune’s Chambak He village.

The team culled 45 eggs and 16 chickens, and disinfected coops and the surrounding area. Additionally, samples were collected from two whole chickens for further testing.

In the world of wellness and weight loss, Ozempic is one heck of a heavyweight name. Ozempic (semaglutide) is a well-known prescription drug that’s used to treat the blood sugar of people with type 2 diabetes. Ozempic is given as an injection under your skin, and it is also used to lower the risk of cardiovascular events (heart attack, stroke, or death) in people who have type 2 diabetes and heart disease.But what if a widely used medication for weight management and type 2 diabetes could also ease migraine – a neurological disorder that affects around 15% of people worldwide, and is characterized by debilitating headaches that can be accompanied by nausea, light sensitivity, and fatigue?

Ozempic (semaglutide), a GLP-1 receptor agonist, is emerging as a strong contender to provide relief to migraine sufferers.In a small study, the drug liraglutide reduced monthly migraine episodes by nearly half among people with obesity who experience the headache-inducing condition.How? Read on to know.

The research:

A study led by Simone Braca, a neurologist at Federico II University in Naples, Italy, explored the effects of liraglutide on 31 people suffering from chronic migraines and obesity. All participants had previously tried at least two migraine prevention medications without success.

What is Liraglutide?

Liraglutide is a drug made by Novo Nordisk, the same company that produces semaglutide, known as Ozempic for diabetes and Wegovy for weight loss. Both drugs mimic a hormone called GLP-1, which helps control blood sugar and suppress appetite.In this study, liraglutide was tested on the patients for 12 weeks. By the end of the trial, the average number of migraine days each month dropped from about 20 to just under 11 – a nearly 50% reduction. One participant even stopped having migraines entirely. While some individuals lost weight, the reduction in migraines did not appear to be linked to the amount of weight lost, indicating that liraglutide’s impact on migraines was separate from its weight-loss effects.

The findings:

The results of the study were shared in June at the Congress of the European Association of Neurology and published in the journal Headache. The researchers concluded, “Our findings show that liraglutide may be effective in the treatment of unresponsive high-frequency or chronic migraine in patients with obesity.” GLP-1 drugs have been available for about 20 years, and newer ones like semaglutide and tirzepatide are more successful at helping with weight loss and blood sugar control compared to diet and exercise alone. Additionally, some studies suggest GLP-1s might help people with substance use disorders.Chronic migraines are complicated, but one potential cause is increased pressure inside the skull. Since previous research has shown that GLP-1s can lower this pressure, the researchers believed these drugs could help treat migraines.

What is migraine?

Migraines are intense headaches often accompanied by nausea and sensitivity to light and sound. They can come with warning signs and be triggered by factors such as hormonal changes, certain foods or drinks, stress, and even exercise. Common symptoms include throbbing pain in one area, nausea, and sensitivity to light (photophobia) and sound (phonophobia). Medications can help manage migraines.

The road ahead:

The researchers noted this was just a preliminary study and not meant to draw definitive conclusions. Important questions remain, such as whether newer GLP-1 drugs like semaglutide would also effectively relieve migraine-related pressure. Lanfranco Pellesi, a headache specialist from the University of Southern Denmark, who did not participate in the study, pointed out that without a control group, some of the observed reduction in headaches might be due to the placebo effect. However, he mentioned that the findings are promising enough to warrant a randomized controlled trial to further investigate this hypothesis. Given the challenges in treating migraines, discovering new therapeutic options could be extremely valuable.