Category: 8. Health

  • AI models might spot pancreatic cancer at an early stage and predict the deadly disease’s prognosis

    AI models might spot pancreatic cancer at an early stage and predict the deadly disease’s prognosis

    A brief illustration of the main cellular processes and biological pathways that contribute to the development of Pancreatic cancer, with emphasis on the genetic mutations and cellular alterations. Credit: Current Oncology (2022). Doi: https://doi.org/10

    A brief illustration of how each diagnostic test contributes to cancer detection, progression assessment, as well as treatment decision-making, and how they complement each other in clinical settings to provide a thorough evaluation of pancreatic cancer.

    AI models have the potential not only to spot pancreatic cancer at an early stage, but also to predict the deadly disease’s prognosis, say scientists

    SHARJAH, EMIRATE OF SHARJAH, UNITED ARAB EMIRATES, June 30, 2025 /EINPresswire.com/ — Oncologists utilizing Artificial Intelligence (AI) in their tests to spot pancreatic cancer at an early stage can also gain an overall picture of how the deadly disease is bound to develop, scientists from the University of Sharjah have revealed in a new study.

    Although still at its initial stage, the AI-enabled prognosis, the scientists say, has the potential to pave the way for the provision of individualized healthcare and treatment of pancreatic cancer patients.

    The scientists, who describe their findings in Beni-Suef University Journal of Basic and Applied Sciences, arrived at the groundbreaking conclusion following a comprehensive review of pancreatic cancer-related scientific literature. https://doi.org/10.1186/s43088-025-00610-4

    Due to its high mortality rate, pancreatic cancer poses a serious health concern, with 467,409 deaths reported worldwide in 2022 and 510,992 new cases. Researchers often refer to pancreatic cancer as the ‘king’ of all cancers due to the exceptional ability of its cancerous cells to quickly spread to other parts of the body if not detected at an early stage.

    “Nevertheless, due to several factors, including the lack of distinct molecular markers and clinical symptoms, the disease tends to be detected at an advanced stage, rendering surgical interventions futile,” the authors warn. ”For this reason, early detection and precise stratification of pancreatic cancer stages are crucial for enhancing therapeutic outcomes.”

    In their study, the scientists provide what they claim to be “a concise overview” of how AI is used in the diagnosis, prognosis, and treatment of pancreatic cancer.

    “Utilizing AI for preliminary testing can significantly enhance the prognosis of those who have been diagnosed with pancreatic cancer,” they write. “Advances in AI-driven image analysis have the potential to transform computer-aided diagnostic systems, aiding doctors in establishing precise and reliable assessments.”

    The researchers’ extensive review of the literature dwells on numerous aspects of AI and its multiple uses in handling cases of pancreatic cancer.

    One important aspect for the scientists is multicomics, which requires the combination and analysis of different data types, along with professionals and scientists, to acquire a thorough and deep understanding of a complex and deadly disease like pancreatic cancer.

    They note that “it is crucial to recognize the significance of AI in multiomics domains. The healthcare industry is at the forefront of a new era, driven by technological and scientific improvements, facilitated by the integration of AI in healthcare.

    “This progress can only be made through the efforts of clinicians, scientists, data analysts, and technicians. Although computer systems have several limits, they are anticipated to contribute to substantial breakthroughs soon, owing to their amazing processing powers.”

    The authors endow AI models with a high ability to spot pancreatic tumors at their earliest stages, helping doctors to correctly assess the risks for patients, and then provide the associated healthcare and draw plans for long-term treatment.

    They call for a better grasp and control of these models, as they are not easy to operate and understand. They show that the plethora of AI-based solutions about pancreatic cancer detection, prognosis, and treatment have “made clinical use a bit sophisticated, whereby without understanding and clear interpretation, doctors cannot critically evaluate the output of these algorithms in terms of their applicability and reliability.”

    Despite the sophistication associated with AI applications, the authors report that researchers have been exerting considerable efforts to develop a variety of approaches to make them accessible to healthcare professionals and at the same time gain the confidence of patients about their effectiveness.

    They predict a promising future for upcoming AI tools, which they believe can be employed with much less sophistication due to the emergence of a new frontier in artificial intelligence called explainable AI that will make the tools easily accessible for clinical adoption.

    They reveal that cancer researchers are “creating and applying explainable AI methods, including feature relevance ratings, infographics, and natural language explanations to interpret AI predictions.”

    They highly commend the new Machine Learning models to identify pancreatic cancer at an early stage, with implications for a significant reduction in the morbidity and mortality rates.

    The application of methods employing the Internet of Things have recently caught the attention of oncological researchers who, according to the authors, are expected to revolutionize pancreatic cancer detection, prognosis, and treatment.

    “AI ought to help oncologists create personalized treatment regimens by combining patient-specific data. It is being utilized to predict how patients react to therapies like immunotherapy, chemotherapy, radiation therapy, and surgery,” they write.

    In their recommendations, the authors call for more AI-based pancreatic cancer research to eventually build “semi-autonomous models that reduce clinician stress, boost productivity, or be fully autonomous.”

    LEON BARKHO
    University Of Sharjah
    +971 501654376
    email us here

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  • Alzheimer’s Might Not Actually Be a Brain Disease, Says Expert : ScienceAlert

    Alzheimer’s Might Not Actually Be a Brain Disease, Says Expert : ScienceAlert

    The pursuit of a cure for Alzheimer’s disease is becoming an increasingly competitive and contentious quest with recent years witnessing several important controversies.

    In July 2022, Science magazine reported that a key 2006 research paper, published in the prestigious journal Nature, which identified a subtype of brain protein called beta-amyloid as the cause of Alzheimer’s, may have been based on fabricated data.

    One year earlier, in June 2021, the US Food and Drug Administration had approved aducanumab, an antibody-targeting beta-amyloid, as a treatment for Alzheimer’s, even though the data supporting its use were incomplete and contradictory.

    Some physicians believe aducanumab never should have been approved, while others maintain it should be given a chance.

    Related: New Link Connects Herpes to Alzheimer’s. Here’s What We Know.

    With millions of people needing an effective treatment, why are researchers still fumbling in this quest for a cure for what is arguably one of the most important diseases confronting humankind?

    Illustration of beta-amyloid plaques (yellow) amongst neurons. (Science Photo Library/Canva)

    Escaping the beta-amyloid rut

    For years, scientists have been focused on trying to come up with new treatments for Alzheimer’s by preventing the formation of brain-damaging clumps of this mysterious protein called beta-amyloid.

    In fact, we scientists have arguably got ourselves into a bit of an intellectual rut concentrating almost exclusively on this approach, often neglecting or even ignoring other possible explanations.

    Regrettably, this dedication to studying the abnormal protein clumps has not translated into a useful drug or therapy. The need for a new “out-of-the-clump” way of thinking about Alzheimer’s is emerging as a top priority in brain science.

    My laboratory at the Krembil Brain Institute, part of the University Health Network in Toronto, is devising a new theory of Alzheimer’s disease.

    Based on our past 30 years of research, we no longer think of Alzheimer’s as primarily a disease of the brain. Rather, we believe that Alzheimer’s is principally a disorder of the immune system within the brain.

    The immune system, found in every organ in the body, is a collection of cells and molecules that work in harmony to help repair injuries and protect from foreign invaders.

    When a person trips and falls, the immune system helps to mend the damaged tissues. When someone experiences a viral or bacterial infection, the immune system helps in the fight against these microbial invaders.

    The exact same processes are present in the brain. When there is head trauma, the brain’s immune system kicks into gear to help repair. When bacteria are present in the brain, the immune system is there to fight back.

    Bright green cells with orange spots in between them
    White blood cells of the immune system activated to fight a bacterial infection. Green shows expression of molecules in their surfaces, and orange shows synthesis of molecules inside the cells. (Dlumen/Canva)

    Alzheimer’s as autoimmune disease

    We believe that beta-amyloid is not an abnormally produced protein, but rather is a normally occurring molecule that is part of the brain’s immune system. It is supposed to be there.

    When brain trauma occurs or when bacteria are present in the brain, beta-amyloid is a key contributor to the brain’s comprehensive immune response. And this is where the problem begins.

    Because of striking similarities between the fat molecules that make up both the membranes of bacteria and the membranes of brain cells, beta-amyloid cannot tell the difference between invading bacteria and host brain cells, and mistakenly attacks the very brain cells it is supposed to be protecting.

    This leads to a chronic, progressive loss of brain cell function, which ultimately culminates in dementia – all because our body’s immune system cannot differentiate between bacteria and brain cells.

    When regarded as a misdirected attack by the brain’s immune system on the very organ it is supposed to be defending, Alzheimer’s disease emerges as an autoimmune disease.

    There are many types of autoimmune diseases, such as rheumatoid arthritis, in which autoantibodies play a crucial role in the development of the disease, and for which steroid-based therapies can be effective. But these therapies will not work against Alzheimer’s disease.

    The brain is a very special and distinctive organ, recognized as the most complex structure in the Universe.

    A senior man and woman looking at a book together
    Alzheimer’s is arguably one of the most important diseases confronting humankind. (Robert Kneschke/Canva)

    In our model of Alzheimer’s, beta-amyloid helps to protect and bolster our immune system, but unfortunately, it also plays a central role in the autoimmune process that, we believe, may lead to the development of Alzheimer’s.

    Though drugs conventionally used in the treatment of autoimmune diseases may not work against Alzheimer’s, we strongly believe that targeting other immune-regulating pathways in the brain will lead us to new and effective treatment approaches for the disease.

    Other theories of the disease

    In addition to this autoimmune theory of Alzheimer’s, many other new and varied theories are beginning to appear. For example, some scientists believe that Alzheimer’s is a disease of tiny cellular structures called mitochondria – the energy factories in every brain cell.

    Mitochondria convert oxygen from the air we breathe and glucose from the food we eat into the energy required for remembering and thinking.

    Some maintain that it is the end-result of a particular brain infection, with bacteria from the mouth often being suggested as the culprit. Still others suggest that the disease may arise from an abnormal handling of metals within the brain, possibly zinc, copper, or iron.

    It is gratifying to see new thinking about this age-old disease. Dementia currently affects more than 50 million people worldwide, with a new diagnosis being made every three seconds.

    Often, people living with Alzheimer’s disease are unable to recognize their own children or even their spouse of more than 50 years.

    Alzheimer’s is a public health crisis in need of innovative ideas and fresh directions.

    A young person kissing an older lady on the cheek
    Often, people living with Alzheimer’s disease are unable to recognize their own children. (akurtz/Canva)

    For the well-being of the people and families living with dementia, and for the socioeconomic impact on our already stressed health-care system coping with the ever-escalating costs and demands of dementia, we need a better understanding of Alzheimer’s, its causes, and what we can do to treat it and to help the people and families who are living with it.The Conversation

    Donald Weaver, Professor of Chemistry and Director of Krembil Research Institute, University Health Network, University of Toronto

    This article is republished from The Conversation under a Creative Commons license. Read the original article.

    An earlier version of this article was published in September 2022.

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  • Green Tea May Lower Dementia Risk

    Green Tea May Lower Dementia Risk

    • Green tea may have more beneficial plant compounds for dementia than other teas.
    • Drinking 2.5 cups of green tea per day was associated with a 25% reduced risk of dementia.
    • Other foods with the same antioxidants as green tea include dark chocolate and berries.

    Brain health has become a popular topic as scientists continue to study the brain in more depth. And while there is still much to learn about the brain, one thing we do know is that dementia is on the rise. We recently reported on a study that suggests that new dementia cases may double from half a million to a million per year by the year 2060. Since we know more about the brain and how to take care of it than we did just a few years ago, this estimation is pretty astonishing.

    Dementia is a general term for a loss of memory, language, problem-solving skills and other abilities that are severe enough to interfere with everyday life. Alzheimer’s disease is the most common type of dementia. 

    We know that nutrition plays a large role in brain health. There’s even a diet designed specifically to provide brain-healthy nutrients, called the MIND diet. Scientists also consider specific foods to see if there is any correlation between them and decreased disease risk. This is what researchers from Japan did regarding green tea and dementia risk. They recently published their findings in The Journal of Nutrition, Health and Aging. Let’s break down what they found.

    How Was This Study Conducted?

    Researchers drew data from a long-running Japanese study called the Murakami study. This study included 13,660 people, about 52% women with an average age of 59. 

    Some of the demographics adjusted for during statistical analysis included sex, age, BMI, physical activity, smoking status, alcohol consumption, education level, marital status and medical history. Participants also filled out food frequency questionnaires asking how much and how often certain foods and beverages were consumed, including tea and coffee.  Baseline data was collected between 2011 and 2013, and the average follow-up time for each participant was 11.5 years. 

    For tea and coffee, participants were given the following options for their intake: <1 cup per week, 1-2 cups per week, 3-4 cups per week, 5-6 cups per week, 1 cup per day, 2-3 cups per day, 4-6 cups per day, 7-9 cups per day, and 10 cups per day. Options were also given for canned and bottled tea and coffee, and amounts were calculated into the total intake. 

    It’s important to note that “a cup” can be interpreted as different amounts in studies and, in this case, is not equal to our American-sized measuring cup. For this reason, researchers calculated consumption into milliliters per day and then placed participants into one of four quartiles (categories). Q1 drank <94 mL of green tea per day, Q2 drank 94-299 mL/day, Q3 drank 300-599 mL/day and Q4 drank ≥ 600 mL/day. 

    Because they were looking specifically for associations between tea and dementia risk, researchers also gathered data regarding dementia from Japan’s long-term care insurance (LTCI) database. In the LTCI, physicians assess the degree of dementia and classify patients into six ranks ranging from no dementia (0) to severe dementia-related behavioral impairment and cognitive impairment requiring treatment (V)—basically using Roman numerals, plus the number 0. Those with rank II (moderate dementia-related behavioral disturbances and cognitive dysfunction with mild dependence) or higher are considered to have dementia.

    What Did This Study Show?

    After running statistical analyses, researchers found that those in the higher quartiles for green tea intake had a lower risk of dementia. Specifically, those in the highest quartile, who drank at least 600 mL (or 20 fluid ounces) per day, had a 25% lower risk of dementia compared to those in the first quartile. 

    They also broke it down by cups of green tea consumed. Participants saw about a 5% reduction in dementia risk for each cup increase in green tea. For example, if someone averaged a cup of green tea a day, they may decrease their risk of dementia by 5%. For someone who drinks 2 cups a day, the reduction in risk goes to 10%. Keep in mind, though, that these cups are not what we consider a measuring cup amount—they’re actually closer to about ½ cup. As an example, Q4 drank at least 600 mL of green tea a day, which is equal to about 2.5 American measuring cups, and reduced their risk of dementia by 25% compared to those in Q1.

    Because there is some evidence that coffee may decrease dementia risk, researchers were curious to know if those who drank both coffee and green tea might lower their risk even more. Turns out, unlike those who drank a lot of green tea, adding high levels of coffee in addition to green tea did not have the same effects as green tea alone, and showed no reduction in dementia risk. 

    Researchers propose a couple of possible reasons for this. First, drinking both green tea and coffee in high doses might have a sort of overdose effect, especially regarding caffeine. As an example, green tea contains 20 mg of caffeine per 100 mL dose, and coffee contains 60 mg of caffeine for the same amount. During the combined portion of this trial, participants in Q4 consumed at least 600 mL/day of green tea and 300 mL/day of coffee, which averages out to 300 mg of caffeine per day. And some were drinking well beyond these amounts. The current recommendation for caffeine is no more than 400 mg/day, so those in Q4 were definitely near or beyond that amount.

    Researchers also note that coffee and tea contain different plant compounds and that they may counteract each other. But they seemed to lean more into the caffeine theory.

    There are a few limitations to this study. One is that participants’ cognitive status was not assessed at baseline. So there’s a chance that those who had lower cognitive function at the start of the study drank less green tea. If this is true, then the association between green tea and reduced risk of dementia would be weaker. Also, because green tea consumption was estimated based on self-reports, it leaves room for bias and inaccuracies. Lastly, the type of dementia wasn’t investigated, so they can’t say which types of dementia green tea may reduce. Researchers do note, however, that because it’s estimated that Alzheimer’s disease makes up about two-thirds of dementia cases, green tea may help reduce the risk of Alzheimer’s. 

    How Does This Apply to Real Life?

    All types of true teas—green, black, white and oolong—are loaded with antioxidants. They are, after all, plants, and all plants contain antioxidants. But compared to the others, green tea has been shown to have the highest levels of catechins, a specific type of flavonoid antioxidant, providing about four times more catechins than black tea. One of these catechins is epigallocatechin3-gallate (EGCG), which researchers note in previous studies has been linked to reduced Alzheimer’s risk. Reasons for this may be due to EGCG’s ability to reduce inflammation, including in the brain, plus reduce amyloid-beta and tau-tangle accumulation, both of which are implicated in Alzheimer’s disease. 

    That’s not to say that other teas don’t have their own benefits. For example, black tea may help you live longer, and ginger tea can help ease an upset stomach and reduce arthritis pain. Mint tea has been shown to have digestive, respiratory and mental health benefits, as well as antimicrobial and antiviral properties.

    Besides brain health, green tea has also been associated with lower inflammation, better digestion, less bloating, improved blood sugar and cholesterol levels, and reduced risk of cancer. 

    It’s easy to add green tea to your life. Simply brew up a cup. Ideally, we recommend using loose-leaf tea and steeping it in a tea strainer. The reason for this is that some tea bags have been shown to contain microplastics. These tiny particles may end up steeping from the bag into your cup of tea and ultimately into your body, including your brain. If you’re looking to limit your microplastic exposure, a tea strainer may be the best steeping option. 

    Plain green tea is best, but adding a small amount of honey or sugar or a touch of milk is fine if that’s how you prefer it. Just be mindful of how much you add, since too much added sugar has been associated with worse brain health, including dementia. If you want to get to zero additions in your tea, take your usual amount of sweetener and/or cream and begin reducing that amount each week until you’re at nothing but the tea. Doing this gradually will help your taste buds adjust. It’s also important to point out that the longer you steep your tea, the more bitter it’s likely to become. If you don’t care for the bitterness, go with shorter steeping times.

    If you’re not a tea drinker (and even if you are) and want the benefits of catechins, there are a few options for you. Dark chocolate, cherries and berries, including blackberries, raspberries and strawberries, are rich in these powerful plant compounds. Dark chocolate and walnuts make a great brain-healthy snack. And cherries and berries are amazing in smoothies, including our Cherry-Mocha Smoothie,  Raspberry-Kefir Power Smoothie and our Berry-Green Tea Smoothie, which provides catechins from both berries and green tea. 

    If you’re ready to really dive into eating for brain health, then you’ll want to try our 30-Day MIND Diet Meal Plan for Cognitive Health or our Simple 7-Day Cognitive Health Meal Plan. 

    Our Expert Take

    This study suggests that higher consumption of green tea is associated with reduced risk of dementia, compared to those with little to no green tea intake. Other lifestyle habits also contribute to brain health, including overall diet, physical activity, managing stressors and getting plenty of quality sleep. If this feels overwhelming and you’re not sure where to start, choose an area you’re likely to have success in. Adding a couple of cups of green tea each day could be an easy addition and starting point.

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  • Inflammation in Aging Varies by Human Population

    Inflammation in Aging Varies by Human Population

    Inflammation, long considered a hallmark of aging, may not be a universal human experience, according to a new study from Columbia University Mailman School of Public Health. The research suggests that “inflammaging”-chronic, low-grade inflammation associated with aging-appears to be a byproduct of industrialized lifestyles and varies significantly across global populations. The findings are published in Nature Aging.

    Researchers analyzed data from four populations: two industrialized groups-the Italian InCHIANTI study and the Singapore Longitudinal Aging Study (SLAS)-and two Indigenous, non-industrialized populations-the Tsimane of the Bolivian Amazon and the Orang Asli of Peninsular Malaysia. While the inflammaging signature was similar between the two industrialized populations, it did not hold in the Indigenous groups, where inflammation levels were largely driven by infection rather than age.

    “In industrialized settings, we see clear links between inflammaging and diseases like chronic kidney disease,” said lead author Alan Cohen, PhD, associate professor of Environmental Health Sciences at Columbia Mailman School and faculty member of the Butler Columbia Aging Center. “But in populations with high infection rates, inflammation appears more reflective of infectious disease burden than of aging itself.”

    Interestingly, while the indigenous populations, particularly the Tsimane, had high constitutive levels of inflammation, these did not increase with age and, crucially, did not lead to the chronic diseases that plague industrialized societies. In fact, most chronic diseases- diabetes, heart disease, Alzheimer’s, etc.-are rare or largely absent in the Indigenous populations, meaning that even when young Indigenous people have profiles that look similar on the surface to those of older industrialized adults, these profiles do not lead to pathological consequences.

    “These findings really call into question the idea that inflammation is bad per se,” said Cohen. “Rather, it appears that inflammation-and perhaps other aging mechanisms too-may be highly context dependent. On the one hand, that’s challenging, because there won’t be universal answers to scientific questions. On the other, it’s promising, because it means we can intervene and change things.”

    The study used a panel of 19 cytokines-small immune-signaling proteins-to assess inflammation patterns. While these markers aligned with aging in the Italian and Singaporean datasets, they did not replicate among the Tsimane and Orang Asli, whose immune systems were shaped by persistent infections and distinct environmental exposures.

    Key findings include:

    • Approximately 66 percent of Tsimane had at least one intestinal parasitic infection; over 70 percent of Orang Asli had a prevalent infection.
    • Inflammaging markers were strongly linked to chronic disease in industrialized populations, but not in Indigenous groups.
    • The study challenges the assumption of universal aging biomarkers, suggesting instead that immune-aging processes are population-specific and heavily influenced by the exposome-the totality of environmental, lifestyle, and infectious exposures.

    “These results point to an evolutionary mismatch between our immune systems and the environments we now live in,” Cohen explained. “Inflammaging may not be a direct product of aging, but rather a response to industrialized conditions.”

    The authors call for a reevaluation of how aging and inflammation are measured across populations and emphasize the need for standardized, context-aware tools. “Factors like environment, lifestyle-such as high physical activity or a very low-fat diet-and infection may all influence how the immune system ages,” said Cohen. “Understanding how these elements interact could help develop more effective global health strategies.”

    Co-authors are listed in the manuscript.

    The study was supported by the Impetus program, the French National Research Agency (ANR) under the Investments for the Future (Investissements d’Avenir) program, grant ANR-17-EURE-0010; the Deutsche Forschungsgemeinschaft (DFG, German Research Foundation) under project ID 499552394 (SFB 1597/1) and grant HE9198/1-1, and the Intramural Research Program of the NIH, National Institute on Aging.

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  • How a glucose monitor can help tame blood sugar spikes and crashes

    ARI SHAPIRO, HOST:

    Have you ever noticed a few hours after a meal, you start to feel a bit moody, less alert, maybe anxious or even angry? If so, you’re not alone. Scientists have been studying this phenomenon in a lot of people. As Michaeleen Doucleff explains, the fix involves learning how to tame your blood sugar.

    MICHAELEEN DOUCLEFF, BYLINE: At age 76, Judy Freeman is in great health. She’s a well-known potter in Alpine, Texas. She doesn’t have diabetes or heart disease. She’s not overweight, and she’s super active.

    JUDY FREEMAN: I work maybe 20 hours a week out in the studio, and I try to walk at least four or five times a week.

    DOUCLEFF: But in the past year or so, Freeman hasn’t felt like herself. She’s been more tired, and she’d like to shed a few extra pounds. So today, Freeman decided to try a new strategy. She’s going to wear a continuous glucose monitor for a few weeks.

    FREEMAN: Arrow points up, glucose is rising.

    DOUCLEFF: The monitor estimates your blood sugar every few minutes and sends the value to your phone, so you can keep track of your blood sugar throughout the day and see how various foods affect it.

    FREEMAN: I’m interested in finding out how the glucose levels might affect my ability to lose weight and just how it affects my overall energy level.

    DOUCLEFF: She’s ready to insert the device. It contains a needle that goes into your skin.

    OK, you ready? One, two, three.

    (SOUNDBITE OF GLUCOSE MONITOR CLICKING)

    DOUCLEFF: Did it hurt?

    FREEMAN: I didn’t feel a thing – just a little pressure.

    DOUCLEFF: Today, anyone can go online and buy a continuous glucose monitor. It costs about $50 and lasts a couple of weeks. Studies have shown that these devices really help people with diabetes, but they’re still trying to figure out if they can help people without diabetes, like Freeman.

    Sarah Berry is one scientist leading this effort. She’s a nutritionist at King’s College London and chief scientist at the company Zoe, which sells nutrition plans that use these monitors. She and her colleagues have analyzed data from thousands of people wearing glucose monitors. What they found is that many people are what she calls…

    SARAH BERRY: Dippers.

    DOUCLEFF: That’s right – dippers. Basically, after eating carbohydrates, their blood sugar rises quickly, and then about two hours later, dips low – way low.

    BERRY: So you’ll have this big increase followed by this big crash.

    DOUCLEFF: In one study, Berry and her colleagues showed that these dips can trigger people to overeat.

    BERRY: If you are a dipper, those people feel more hungry more quickly. They tend to, on average, eat 80 calories more at their next meal and 320 calories more over a whole day.

    DOUCLEFF: Berry and her team published their findings in the journal Nature Metabolism. They also found that dips correlate with moodiness and fatigue, which brings us back to Judy Freeman in Alpine, Texas. The first day she wore the monitor, guess what her blood sugar did a few hours after lunch?

    FREEMAN: Sure enough, it had shot up at some point, and then it plummeted down to the lowest point.

    DOUCLEFF: Freeman had a huge dip, and during it, she felt anxious – even depressed.

    FREEMAN: It’s a sinking feeling, like, if I don’t get up, I’m just going to stop breathing and die. It was so overpowering.

    DOUCLEFF: She says she’s had this feeling from time to time, but she never connected it to what she ate. So how can Freeman keep these dips from occurring? Dalia Perelman is a research dietitian at Stanford University. She says, No. 1 – avoid meals and snacks that consist mostly of carbohydrates.

    DALIA PERELMAN: Don’t eat naked carbs. Eat them with some proteins, some healthy fats.

    DOUCLEFF: And with more fiber. So for example, add beans to breakfast, canned fish and nuts to lunch, lentils and seeds to dinner.

    No. 2 – don’t eat all your carbs for the day at one meal. Sprinkle them across several meals.

    PERELMAN: It doesn’t matter at the end of the day how many carbs you ate. It matters at the end of the meal.

    DOUCLEFF: Finally, nutritionist Karen Kennedy says, at meals, eat the protein and fat first – carbs last.

    KAREN KENNEDY: Let’s say you have a steak and a salad and a baked potato. If you were to eat the salad and the steak first, then you will see that you don’t have as much of a spike or as much of a drop afterwards.

    DOUCLEFF: And here’s the great part. You don’t need to buy a glucose monitor to figure this out. Simply pay attention to how you feel about two hours after a meal. If you get moody, anxious or super hungry, you’re probably a dipper.

    For NPR News, I’m Michaeleen Doucleff.

    (SOUNDBITE OF MUSIC) Transcript provided by NPR, Copyright NPR.

    NPR transcripts are created on a rush deadline by an NPR contractor. This text may not be in its final form and may be updated or revised in the future. Accuracy and availability may vary. The authoritative record of NPR’s programming is the audio record.


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  • Men’s Health Month: Prostate Cancer Q&A with Dr. Dahut – American Cancer Society

    1. Men’s Health Month: Prostate Cancer Q&A with Dr. Dahut  American Cancer Society
    2. Nyberg: Yale professor speaks on importance of prostate health  WTNH.com
    3. A healthy aging guide for prostate health: Risks, prevention and care  Mayo Clinic Press
    4. Health Experts Emphasize Importance of Prostate Cancer Screenings  LakeWalesNews.net
    5. Men warned about the “stealthiness” of prostate cancer  Baku.ws

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  • Scientists Investigating whether Ambroxol Can Slow Parkinson’s-Related Dementia

    Scientists Investigating whether Ambroxol Can Slow Parkinson’s-Related Dementia

    Although a cough medicine called Ambroxol is approved in Europe for treating respiratory conditions and has a long-standing safety record, including use at high doses and during pregnancy, it is not approved for any use in the United States or Canada.

    Ball-and-stick model of ambroxol molecule. Image credit: Marina Vladivostok / ChemSpider.

    Parkinson’s disease dementia causes memory loss, confusion, hallucinations and mood changes.

    About half of those diagnosed with Parkinson’s develop dementia within 10 years, profoundly affecting patients, families and the health care system.

    “Our goal was to change the course of Parkinson’s dementia,” said Dr. Stephen Pasternak, a cognitive neurologist at Parkwood Institute, St Joseph’s Health Care London and Robarts Research Institute.

    “This early trial offers hope and provides a strong foundation for larger studies.”

    The 12-month clinical trial involved 55 participants with Parkinson’s disease dementia.

    The authors gave one group daily Ambroxol while the other group received a placebo.

    They monitored memory, psychiatric symptoms and GFAP, a blood marker linked to brain damage.

    According to the team, Ambroxol was safe, well-tolerated and reached therapeutic levels in the brain.

    Psychiatric symptoms worsened in the placebo group but remained stable in those taking Ambroxol.

    Participants with high-risk GBA1 gene variants showed improved cognitive performance on Ambroxol.

    GFAP increased in the placebo group but stayed stable with Ambroxol, suggesting potential brain protection.

    “Current therapies for Parkinson’s disease and dementia address symptoms but do not stop the underlying disease,” Dr. Pasternak said.

    “These findings suggest Ambroxol may protect brain function, especially in those genetically at risk. It offers a promising new treatment avenue where few currently exist.”

    Ambroxol supports a key enzyme called glucocerebrosidase (GCase), which is produced by the GBA1 gene.

    In people with Parkinson’s disease, GCase levels are often low. When this enzyme doesn’t work properly, waste builds up in brain cells, leading to damage.

    “This research is vital because Parkinson’s dementia profoundly affects patients and families,” Dr. Pasternak said.

    “If a drug like Ambroxol can help, it could offer real hope and improve lives.”

    The results appear in the journal JAMA Neurology.

    _____

    Carolina R. A. Silveira et al. Ambroxol as a Treatment for Parkinson Disease Dementia: A Randomized Clinical Trial. JAMA Neurol, published online June 30, 2025; doi: 10.1001/jamaneurol.2025.1687

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  • This Survey Asked Neuroscientists If Memories Can Be Extracted From the Dead. Here’s What They Said

    This Survey Asked Neuroscientists If Memories Can Be Extracted From the Dead. Here’s What They Said

    The allure and terror of transferring your consciousness to a computer has long been fodder for cyberpunk novels and billionaire-backed immortality startups. But a substantial chunk of neuroscientists think it might be possible to extract memories from a preserved brain and store those memories inside a computer, according to a new study.

    The study, published in the journal PLOS One, suggests that most neuroscientists believe that memory has a physical basis and, on average, give a 40% probability that we might one day be able to emulate a human brain. But there was little consensus as to what exactly that physical basis is, highlighting just how little we know about what memories are made of.

    The authors surveyed 312 neuroscientists—both memory experts and general neuroscientists—to get their thoughts on the feasibility of preserving a human brain and later extracting its memories. It was led by Ariel Zeleznikow-Johnston, a neuroscientist at Monash University in Australia and the author of The Future Loves You: How and Why We Should Abolish Death. 

    While the researchers wrote that the questions of memory extraction from preserved brains are “strange and speculative,” they provide insight into how neuroscientists think about memory formation.

    Results of the survey show that neuroscientists largely agree that memories have a physical substrate rather than relying on a dynamic process that ceases at preservation; they’re likely stored in the synaptic connections between neurons, which strengthen and weaken with experience. The survey showed that 70% of neuroscientists agree that a physical, molecular record of a memory exists—stored in stable changes to neural connectivity and interactions between proteins and other cellular components—of which you could theoretically take a snapshot.

    However, “there was no clear consensus on exactly which neurophysiological feature or scale is critical for memory storage,” the authors wrote in the study. The surveyed scientists didn’t agree on what resolution—from the atomic-level composition of biomolecules to nanometer-level resolution of subcellular structures—would be required to extract a memory from a preserved brain. This is largely due to the fact that, while most neuroscientists agree that memory has a physical basis, it’s still up for debate exactly what that basis is.

    The survey also asked whether existing tools could theoretically preserve the structure of a brain well enough to extract memories. Preserving a brain in such a way that the proteins and cells remain intact is tricky, since freezing can damage neural tissue. But one way neuroscientists could do this is through aldehyde-stabilized cryopreservation, a technique that combines chemical fixation with vitrification—the process of turning a substance into a glass-like solid by cooling it down rapidly. The study asked neuroscientists to assign a probability that memories could be extracted from a cryopreserved brain. The participants gave a wide range of estimates, but the median answer was around a 40% probability.

    The authors asked the neuroscientists how probable it might be to emulate a whole brain—like, uploading and digitizing a person’s brain onto a computer—from preserved neural tissue. That could open up the possibility of uploading your full self and consciousness into a machine. In this case, the median answer was again around 40%, though the authors note that the responses again varied widely.

    “Admittedly, that’s not 100 percent,” Zeleznikow-Johnston told IFLScience. “That means that there’s not full consensus in the community that yeah, definitely this will work, but it’s not 0.1 percent, or 0.01 percent. That’s a substantial chunk of neuroscientists who think there’s a very real chance that it will work, and my guess is that actually that number will creep up over time as we get better at doing these brain implants, emulations, all these other things.”

    Neuroscientists believe we’re still a long way off from being able to emulate an entire human brain, according to the study. When asked when we might be able to emulate a human brain, the respondents gave a median answer of 2125.

    Still, it’s something to think about.

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  • Many forget the damage done by diseases like whooping cough, measles and rubella. Not these families

    Many forget the damage done by diseases like whooping cough, measles and rubella. Not these families

    SIOUX FALLS, S.D. | In the time before widespread vaccination, death often came early.

    Devastating infectious diseases ran rampant in America, killing millions of children and leaving others with lifelong health problems. These illnesses were the main reason why nearly one in five children in 1900 never made it to their fifth birthday.

    Over the next century, vaccines virtually wiped out long-feared scourges like polio and measles and drastically reduced the toll of many others. Today, however, some preventable, contagious diseases are making a comeback as vaccine hesitancy pushes immunization rates down. And well-established vaccines are facing suspicion even from public officials, with Robert F. Kennedy Jr., a longtime anti-vaccine activist, running the federal health department.

    “This concern, this hesitancy, these questions about vaccines are a consequence of the great success of the vaccines – because they eliminated the diseases,” said Dr. William Schaffner, an infectious disease expert at Vanderbilt University Medical Center. “If you’re not familiar with the disease, you don’t respect or even fear it. And therefore you don’t value the vaccine.”

    Anti-vaccine activists even portray the shots as a threat, focusing on the rare risk of side effects while ignoring the far larger risks posed by the diseases themselves — and years of real-world data that experts say proves the vaccines are safe.

    Some Americans know the reality of these preventable diseases all too well. For them, news of measles outbreaks and rising whooping cough cases brings back terrible memories of lives forever changed – and a longing to spare others from similar pain.

    Getting rubella while pregnant shaped two lives

    With a mother’s practiced, guiding hand, 80-year-old Janith Farnham helped steer her 60-year-old daughter’s walker through a Sioux Falls art center. They stopped at a painting of a cow wearing a hat.

    Janith pointed to the hat, then to her daughter Jacque’s Minnesota Twins cap. Jacque did the same.

    “That’s so funny!” Janith said, leaning in close to say the words in sign language too.

    Jacque was born with congenital rubella syndrome, which can cause a host of issues including hearing impairment, eye problems, heart defects and intellectual disabilities. There was no vaccine against rubella back then, and Janith contracted the viral illness very early in the pregnancy, when she had up to a 90% chance of giving birth to a baby with the syndrome.

    Janith recalled knowing “things weren’t right” almost immediately. The baby wouldn’t respond to sounds or look at anything but lights. She didn’t like to be held close. Her tiny heart sounded like it purred – evidence of a problem that required surgery at four months old.

    Janith did all she could to help Jacque thrive, sending her to the Colorado School for the Deaf and the Blind and using skills she honed as a special education teacher. She and other parents of children with the syndrome shared insights in a support group.

    Meanwhile, the condition kept taking its toll. As a young adult, Jacque developed diabetes, glaucoma and autistic behaviors. Eventually, arthritis set in.

    Today, Jacque lives in an adult residential home a short drive from Janith’s place. Above her bed is a net overflowing with stuffed animals. On a headboard shelf are photo books Janith created, filled with memories like birthday parties and trips to Mount Rushmore.

    Jacque’s days typically begin with an insulin shot and breakfast before she heads off to a day program. She gets together with her mom four or five days a week. They often hang out at Janith’s townhome, where Jacque has another bedroom decorated with her own artwork and quilts Janith sewed for her. Jacque loves playing with Janith’s dog, watching sports on television and looking up things on her iPad.

    Janith marvels at Jacque’s sense of humor, gratefulness, curiosity and affectionate nature despite all she’s endured. Jacque is generous with kisses and often signs “double I love yous” to family, friends and new people she meets.

    “When you live through so much pain and so much difficulty and so much challenge, sometimes I think: Well, she doesn’t know any different,” Janith said.

    Given what her family has been through, Janith believes younger people are being selfish if they choose not to get their children the MMR shot against measles, mumps and rubella.

    “It’s more than frustrating. I mean, I get angry inside,” she said. “I know what can happen, and I just don’t want anybody else to go through this.”

    Delaying the measles vaccine can be deadly

    More than half a century has passed, but Patricia Tobin still vividly recalls getting home from work, opening the car door and hearing her mother scream. Inside the house, her little sister Karen lay unconscious on the bathroom floor.

    It was 1970, and Karen was 6. She’d contracted measles shortly after Easter. While an early vaccine was available, it wasn’t required for school in Miami where they lived. Karen’s doctor discussed immunizing the first grader, but their mother didn’t share his sense of urgency.

    “It’s not that she was against it,” Tobin said. “She just thought there was time.”

    Then came a measles outbreak. Karen – who Tobin described as a “very endearing, sweet child” who would walk around the house singing – quickly became very sick. The afternoon she collapsed in the bathroom, Tobin, then 19, called the ambulance. Karen never regained consciousness.

    “She immediately went into a coma and she died of encephalitis,” said Tobin, who stayed at her bedside in the hospital. “We never did get to speak to her again.”

    Today, all states require that children get certain vaccines to attend school. But a growing number of people are making use of exemptions allowed for medical, religious or philosophical reasons. Vanderbilt’s Schaffner said fading memories of measles outbreaks were exacerbated by a fraudulent, retracted study claiming a link between the MMR shot and autism.

    The result? Most states are below the 95% vaccination threshold for kindergartners — the level needed to protect communities against measles outbreaks.

    “I’m very upset by how cavalier people are being about the measles,” Tobin said. “I don’t think that they realize how destructive this is.”

    Polio changed a life twice

    One of Lora Duguay’s earliest memories is lying in a hospital isolation ward with her feverish, paralyzed body packed in ice. She was three years old.

    “I could only see my parents through a glass window. They were crying and I was screaming my head off,” said Duguay, 68. “They told my parents I would never walk or move again.”

    It was 1959 and Duguay, of Clearwater, Florida, had polio. It mostly preyed on children and was one of the most feared diseases in the U.S., experts say, causing some terrified parents to keep children inside and avoid crowds during epidemics.

    Given polio’s visibility, the vaccine against it was widely and enthusiastically welcomed. But the early vaccine that Duguay got was only about 80% to 90% effective. Not enough people were vaccinated or protected yet to stop the virus from spreading.

    Duguay initially defied her doctors. After intensive treatment and physical therapy, she walked and even ran – albeit with a limp. She got married, raised a son and worked as a medical transcriptionist.

    But in her early 40s, she noticed she couldn’t walk as far as she used to. A doctor confirmed she was in the early stages of post-polio syndrome, a neuromuscular disorder that worsens over time.

    One morning, she tried to stand up and couldn’t move her left leg.

    After two weeks in a rehab facility, she started painting to stay busy. Eventually, she joined arts organizations and began showing and selling her work. Art “gives me a sense of purpose,” she said.

    These days, she can’t hold up her arms long enough to create big oil paintings at an easel. So she pulls her wheelchair up to an electric desk to paint on smaller surfaces like stones and petrified wood.

    The disease that changed her life twice is no longer a problem in the U.S. So many children get the vaccine — which is far more effective than earlier versions — that it doesn’t just protect individuals but it prevents occasional cases that arrive in the U.S. from spreading further. ” Herd immunity ” keeps everyone safe by preventing outbreaks that can sicken the vulnerable.

    After whooping cough struck, ‘she was gone’

    Every night, Katie Van Tornhout rubs a plaster cast of a tiny foot, a vestige of the daughter she lost to whooping cough at just 37 days old.

    Callie Grace was born on Christmas Eve 2009 after Van Tornhout and her husband tried five years for a baby. She was six weeks early but healthy.

    “She loved to have her feet rubbed,” said the 40-year-old Lakeville, Indiana mom. “She was this perfect baby.”

    When Callie turned a month old, she began to cough, prompting a visit to the doctor, who didn’t suspect anything serious. By the following night, Callie was doing worse. They went back.

    In the waiting room, she became blue and limp in Van Tornhout’s arms. The medical team whisked her away and beat lightly on her back. She took a deep breath and giggled.

    Though the giggle was reassuring, the Van Tornhouts went to the ER, where Callie’s skin turned blue again. For a while, medical treatment helped. But at one point she started squirming, and medical staff frantically tried to save her.

    “Within minutes,” Van Tornhout said, “she was gone.”

    Van Tornhout recalled sitting with her husband and their lifeless baby for four hours, “just talking to her, thinking about what could have been.”

    Callie’s viewing was held on her original due date – the same day the Centers for Disease Control and Prevention called to confirm she had pertussis, or whooping cough. She was too young for the Tdap vaccine against it and was exposed to someone who hadn’t gotten their booster shot.

    Today, next to the cast of Callie’s foot is an urn with her ashes and a glass curio cabinet filled with mementos like baby shoes.

    “My kids to this day will still look up and say, ‘Hey Callie, how are you?’” said Van Tornhout, who has four children and a stepson. “She’s part of all of us every day.”

    Van Tornhout now advocates for childhood immunization through the nonprofit Vaccinate Your Family. She also shares her story with people she meets, like a pregnant customer who came into the restaurant her family ran saying she didn’t want to immunize her baby. She later returned with her vaccinated four-month-old.

    “It’s up to us as adults to protect our children – like, that’s what a parent’s job is,” Van Tornhout said. “I watched my daughter die from something that was preventable … You don’t want to walk in my shoes.”


    The Associated Press Health and Science Department receives support from the Howard Hughes Medical Institute’s Department of Science Education and the Robert Wood Johnson Foundation. The AP is solely responsible for all content.

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  • No Evidence that Medications Trigger Microscopic Colitis in Older Adults

    Study from Mass General Brigham and Karolinska Institutet researchers suggests that patients with the condition do not need to stop taking important medications.


    Microscopic colitis (MC) is a chronic inflammatory bowel disease that severely reduces quality of life. MC is responsible for over 30% of all chronic diarrhea cases in people over 65 years of age, and its prevalence is rising worldwide. Although little is known about what causes MC, previous studies have suggested that a range of common medications could trigger the condition, including non-steroidal anti-inflammatory drugs (NSAIDs), blood pressure medications, and selective serotonin reuptake inhibitors (SSRIs).

    However, according to a new large-scale, longitudinal study of older adults in Sweden from Mass General Brigham, Broad Institute of MIT and Harvard, and Karolinska Institutet researchers, most of these medications are not associated with increased risk of MC. Results are published in Annals of Internal Medicine.

    “Our study demonstrated that, contrary to the previous belief, it’s unlikely that medications are the primary triggers for microscopic colitis,” said corresponding author Hamed Khalili, MD MPH, associate director of the Clinical and Translational Epidemiology Unit and director of Clinical Research at the Crohn’s and Colitis Center at Massachusetts General Hospital, a founding member of the Mass General Brigham health care system. “Clinicians should carefully balance the intended benefits of these medications against the very low likelihood that they cause microscopic colitis.”

    To look for associations between medication use and MC diagnosis, the researchers analyzed data for over 2.8 million individuals aged 65 years and older in Sweden. The data included information on prescribed medications, hospitalizations, medical diagnoses, and gastrointestinal biopsy results.

    Overall, they found that the risk of developing MC was less than 0.5%. There was no association between NSAIDs, angiotensin converting enzyme (ACE-I) inhibitors, angiotensin II receptor blockers (ARBs), proton pump inhibitors (PPIs), or statins and the risk of developing MC, but individuals prescribed SSRIs had a 0.04% higher risk of developing MC. However, the researchers also showed that individuals prescribed SSRIs were also more likely to receive a colonoscopy, which is necessary to diagnose MC.

    “Our analyses suggest that surveillance bias is a likely explanation for earlier findings that implicated medications in the pathogenesis of microscopic colitis and may also explain the continued association with SSRIs,” said senior author Jonas F. Ludvigsson, MD PhD, pediatrician at Örebro University Hospital and Professor at the Department of Medical Epidemiology and Biostatistics, Karolinska Institutet in Sweden.

    The study did not include data on primary care visits, which could impact the likelihood of colonoscopy, or lifestyle factors such as diet and smoking status.

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