Doctor Waqas Ali Khan

Doctor Waqas Ali Khan MBBS (KMC)
MCPS (SURGERY)
MRCS A ( UK )
FCPS II (UROLOGY)

🧠 Scientists have identified a new sign of Alzheimer's — smell. If you lose your sense of smell, there is a chance it co...
01/10/2025

🧠 Scientists have identified a new sign of Alzheimer's — smell.

If you lose your sense of smell, there is a chance it could be an early sign of Alzheimer’s disease, according to new research.

Scientists have long suspected that a fading sense of smell might be linked to the early stages of Alzheimer’s, but the exact cause wasn’t clear until now. In a new study, researchers used brain scans, human tissue samples, and experiments with mice to uncover what’s going on.

They found that the brain’s own immune cells, called microglia, may be breaking down important nerve connections between two key brain areas: the olfactory bulb, which processes smells, and the locus coeruleus, which helps regulate sensory input like smell. These microglia are meant to clean up damaged or unneeded connections, but in this case, they may be attacking nerve fibers too early, possibly because the affected neurons are firing abnormally, a known symptom in the early phases of Alzheimer’s. A fatty molecule called phosphatidylserine, which usually stays hidden inside nerve cell membranes, starts showing up on the outside of these cells, acting like a distress signal.

When microglia detect this signal, they interpret it as a sign the neuron is damaged and destroy the connection, leading to a reduced sense of smell. This process is normally part of brain maintenance, but in Alzheimer’s, it seems to kick in too soon and in the wrong places.

The damage to smell pathways seems to happen before major memory loss or other cognitive issues, meaning it could serve as an early warning sign. If doctors can catch Alzheimer’s this early, before memory problems begin, they may be able to start treatment sooner, potentially improving the outcome.

source
Meyer, C., Niedermeier, T., Feyen, P.L.C. et al. Early Locus Coeruleus noradrenergic axon loss drives olfactory dysfunction in Alzheimer’s disease. Nat Commun 16, 7338 (2025).

🚨✨ Breaking News – A Miracle in Medical History! ✨🚨For the first time in Pakistan and only the 21st time in world histor...
01/10/2025

🚨✨ Breaking News – A Miracle in Medical History! ✨🚨

For the first time in Pakistan and only the 21st time in world history, a patient has survived the deadly rabies virus.

According to the latest official report from the Armed Forces Institute of Pathology (Rawalpindi), both real-time PCR tests (cerebrospinal fluid & saliva) of Hamid bin Ismail (volunteer, Alkhidmat Foundation & Jamaat-e-Islami) have come back negative for rabies virus RNA.

💉 This is conclusive proof that Hamid has defeated one of the world’s most fatal diseases — a moment of relief, joy, and gratitude for his family, friends, and countless well-wishers.

🌍 His survival is not just personal victory — it is a ray of hope for humanity, proving that miracles still happen.

🙏 May Allah bless him with complete health and make this milestone an inspiration for the world.

A low-sugar diet in the first years of life slashes your child’s risk of chronic disease by 35%.Say it with me now: Suge...
01/10/2025

A low-sugar diet in the first years of life slashes your child’s risk of chronic disease by 35%.

Say it with me now: Suger is bad.

A landmark study has revealed that limiting sugar in the first years of life—especially during pregnancy and infancy—can significantly reduce the risk of chronic disease in adulthood.

Drawing on historical data from the UK Biobank, researchers examined adults born just before and after the 1953 end of wartime sugar rationing in Britain. The findings were striking: those exposed to ration-era sugar restrictions in their first 1,000 days of life had up to a 35% lower risk of developing Type 2 diabetes and a 20% lower risk of hypertension later in life. Surprisingly, even in-utero exposure alone showed protective effects.

The study, published in Science and led by researchers from the University of Southern California, UC Berkeley, and McGill University, offers some of the clearest evidence to date on how early-life nutrition can shape long-term health. During wartime rationing, children under two consumed virtually no added sugar—levels that align closely with current dietary guidelines but are rarely followed today.

As sugar consumption soared post-rationing, so did the health risks. Researchers call this a “natural experiment” that demonstrates how short-term dietary changes early in life can have lasting impacts—potentially informing public policy on sugar regulations for infants and toddlers.

Source: “Exposure to Sugar Rationing in the First 1000 Days of Life Protected Against Chronic Disease” by Tadeja Gracner, Claire Boone and Paul J. Gertler, Science, 31 Oct. 2024.

🍠 Sweet potatoes have 1,000x more vitamin A, twice the fiber, and way less impact on blood sugar than white potatoes.Whi...
01/10/2025

🍠 Sweet potatoes have 1,000x more vitamin A, twice the fiber, and way less impact on blood sugar than white potatoes.

While both white and sweet potatoes can be part of a healthy diet, sweet potatoes come out ahead in several important ways, according to nutrition experts.

They contain dramatically higher levels of vitamin A—over 1,000 times more than white potatoes—as well as roughly double the fiber and vitamin C. Sweet potatoes are also rich in antioxidants, which help protect against cell damage and inflammation.

These nutritional advantages make them a standout choice for those focused on immunity, gut health, and disease prevention.

What’s more, sweet potatoes have a significantly lower glycemic response compared to white potatoes, meaning they won’t spike your blood sugar levels as dramatically. In fact, baked white russet potatoes have one of the highest glycemic responses of any food. This makes sweet potatoes especially beneficial for people managing diabetes or looking to maintain steady energy levels. As an added bonus, they also cook faster—making them a convenient and nutrient-dense option for everyday meals.

Source: “White potatoes vs. sweet potatoes: Nutrition and health experts chime in on which is better,” Fox News, June 20, 2023.

🦷 A natural compound found to help fight gum disease — without the harsh side effects of traditional treatments.A natura...
30/09/2025

🦷 A natural compound found to help fight gum disease — without the harsh side effects of traditional treatments.

A natural compound found in fruits, teas, and nuts may soon become a powerful new tool in the fight against gum disease.

Brazilian researchers have developed a controlled-release powder made from morin, a flavonoid found in guava leaves, apple peels, figs, and almonds. In lab tests, this morin-based powder showed antimicrobial, anti-inflammatory, and antioxidant effects against the bacteria responsible for periodontal disease.

The powder can be incorporated into oral care products and may serve as a gentler, plant-based alternative to antibiotics, especially for people who cannot easily maintain oral hygiene.

Developed by scientists at São Paulo State University, the powder is designed to stick to the mouth’s surfaces and slowly release morin over time, resisting the natural cleansing effects of saliva. Researchers say this delivery system could reduce common side effects of current treatments, such as tooth staining and altered taste, while still fighting gum disease effectively. Early lab tests showed the treated bacterial biofilm was visibly less stained and potentially less disruptive to the natural balance of oral bacteria. Human trials are still ahead, but the researchers are optimistic that morin could offer a safe, scalable, and accessible solution for one of the world’s most common chronic diseases.

Source: Sales, L. S., Brighenti, F. L., et al. (2025). “Anti-inflammatory, antioxidant, and antimicrobial evaluation of morin.” Archives of Oral Biology, 24 June 2025.

30/09/2025
Consciousness Emerges From The Oldest Parts of Our Brain, Study ShowsA new analysis of over 100 years of neuroscience re...
29/09/2025

Consciousness Emerges From The Oldest Parts of Our Brain, Study Shows

A new analysis of over 100 years of neuroscience research suggests that the deep, older structures of the brain, such as the subcortex and the cerebellum, play a bigger role in consciousness than previously thought.

Previous theories of consciousness centered on the neocortex, the large, folded outer layer responsible for high-level thinking, sensory perception, and self-awareness.

Damage to this layer can cause noticeable changes in how people perceive themselves and the world. But this study shows that altering activity in the older subcortical regions can have even more dramatic effects: causing unconsciousness, altering mood, or waking an anesthetized animal. Even the cerebellum, once dismissed as irrelevant to consciousness, can influence perception when stimulated. Yet it's difficult to know whether these changes are due to direct effects or because stimulating one part of the brain indirectly affects another.

To explore this further, researchers looked at clinical cases. People with cortex damage can still appear alert and even functional. Meanwhile some children born without most of their cortex, who, according to textbooks, shouldn’t be conscious at all, can laugh, cry, recognize people, and respond emotionally. Likewise, animals with their neocortex removed often continue to behave in clearly purposeful, emotional, and social ways. These findings suggest the brain’s ancient structures may not just support consciousness, but may actually be enough for basic conscious experience.

source
Peter Coppola . "A review of the sufficient conditions for consciousness." 2025. Neuroscience

🚨 Scientists created a gene therapy that *restores* bone density, not just maintains it.And experts now say they are on ...
29/09/2025

🚨 Scientists created a gene therapy that *restores* bone density, not just maintains it.

And experts now say they are on the brink of reversing osteoporosis.

In a groundbreaking study, researchers from Germany and China identified a key gene, GPR133, that acts as a cellular switch in bone-building cells called osteoblasts.

When this gene was activated in mice using a compound called AP503, it triggered remarkable results: even mice with advanced osteoporosis began growing stronger, denser bones. The effect wasn’t just preventive—it was regenerative.

AP503 works like a molecular "on" button, enhancing the activity of osteoblasts and accelerating bone formation. When paired with physical activity, the results improved even further. This approach is radically different from current osteoporosis treatments, which mainly aim to slow bone loss and often come with diminishing results or significant side effects.

While the research is still in its early stages and based on animal models, scientists believe the underlying biology is likely similar in humans—opening the door to therapies that restore skeletal strength and transform treatment for millions at risk of brittle bones.

Source: "The mechanosensitive adhesion G protein-coupled receptor 133 (GPR133/ADGRD1) enhances bone formation." Signal Transduction and Targeted Therapy, 30 June 2025.

🚫 More protein ≠ more muscle. In fact, too much can stress your kidneys and increase health risks.Protein is essential t...
29/09/2025

🚫 More protein ≠ more muscle. In fact, too much can stress your kidneys and increase health risks.

Protein is essential to human health—it builds muscle, supports immunity, and helps create enzymes and hormones. But when it comes to protein, more isn’t always better.

Most adults already get more than enough through regular meals.

While athletes and strength trainers may benefit from slightly higher intakes—up to 1.6 grams per kilogram of body weight—consuming more than that doesn’t build extra muscle. Instead, the excess is either burned for energy or stored as fat if you’re in a calorie surplus. And in some cases, overconsumption can carry risks.

Too much protein can strain the kidneys in people with existing issues and, in rare cases, lead to protein poisoning if the diet lacks enough fat and carbohydrates. Historically, this was seen in explorers who ate mostly lean meats like rabbit.

The source of your protein also matters: diets heavy in fatty animal proteins are linked to increased risks of heart disease, type 2 diabetes, and some cancers, while plant-based proteins from beans, lentils, and whole grains offer added benefits like fiber and cholesterol reduction. The bottom line? Your body needs protein—but it thrives on balance. A varied diet with a mix of plant and animal sources is far healthier than loading up on powders and high-protein snacks.

source
A. Achrekar M.D.,. "Protein is an important part of a diet — up to a point" KOAT. 2025

🚨 Scientists just discovered that alpha cells in your pancreas can make GLP-1 — just like the popular drug Ozempic. Here...
28/09/2025

🚨 Scientists just discovered that alpha cells in your pancreas can make GLP-1 — just like the popular drug Ozempic.

Here's what it means👇

A stunning new discovery from Duke University suggests your pancreas might already be producing a hormone similar to Ozempic—naturally.

Researchers found that pancreatic alpha cells, long believed to only release glucagon (a hormone that raises blood sugar), can also produce GLP-1, the same hormone targeted by blockbuster diabetes drugs like Ozempic. Even more intriguing, these cells appear to increase GLP-1 production during metabolic stress, acting as a natural backup system to support insulin release and stabilize blood sugar.

In mouse studies, when glucagon was blocked, alpha cells responded by ramping up GLP-1 output, improving insulin secretion and glucose control. This built-in flexibility could lead to therapies that boost the body's own GLP-1 production, offering a more natural alternative to synthetic drugs. If future research confirms these findings in humans, it could pave the way for diabetes treatments that work with the body’s hormonal system—reducing reliance on medications and potentially lowering side effects. The pancreas, it turns out, may be more self-regulating than we ever imagined.

Source: "α cells use both PC1/3 and PC2 to process proglucagon peptides and control insulin secretion." Science Advances, 2025.

🦴Scientists may have found a way to strengthen bones for life!In so doing, they discovered a potential treatment for the...
27/09/2025

🦴Scientists may have found a way to strengthen bones for life!

In so doing, they discovered a potential treatment for the bone-weakening disease, osteoporosis, and it involves a specific cell receptor called GPR133.

In a study led by researchers from the University of Leipzig and Shandong University, activating this receptor in mice triggered a boost in bone-building activity, strengthening both healthy and osteoporotic bones. The team focused on osteoblasts, the cells responsible for bone formation, and found that when the GPR133 gene was missing, the mice developed brittle bones that mimicked human osteoporosis. But when GPR133 was activated using a compound called AP503, bone strength improved sharply. The substance acts like a switch, dialing up osteoblast activity.

The compound AP503 was identified through computer modeling and worked even better when combined with physical activity.

This suggests the treatment could one day be paired with lifestyle changes for enhanced effects. Although the study was conducted on mice, researchers say the mechanism is likely similar in humans, and especially relevant for postmenopausal women, who face a heightened risk of bone loss. Unlike current treatments for osteoporosis, which often come with side effects or lose effectiveness over time, this approach shows promise not just for slowing bone loss, but for actually rebuilding bone. The discovery also hints at broader uses: potentially enhancing bone health before any damage occurs, not just reversing deterioration.

source
Juliane Lehmann, Hui Lin, Zihao Zhang, Maren Wiermann, Albert M. Ricken, Franziska Brinkmann, Jana Brendler, Christian Ullmann, Luisa Bayer, Sandra Berndt, Anja Penk, Nadine Winkler, Franz Wolfgang Hirsch, Thomas Fuhs, Josef Käs, Peng Xiao, Torsten Schöneberg, Martina Rauner, Jin-Peng Sun, Ines Liebscher. The mechanosensitive adhesion G protein-coupled receptor 133 (GPR133/ADGRD1) enhances bone formation. Signal Transduction and Targeted Therapy, 2025;

Microplastics are making Alzheimer’s even worse, study shows. Researchers from the University of Rhode Island looked at ...
27/09/2025

Microplastics are making Alzheimer’s even worse, study shows.

Researchers from the University of Rhode Island looked at how tiny plastic particles, like the ones found in bottled water, food, and the air, might affect brain health when combined with a gene called APOE4, which is known to increase the chance of developing Alzheimer’s disease.

They used two groups of mice: one with the high-risk APOE4 gene, and one with a more neutral APOE3 version. Some mice in each group were given water containing microplastics, while others weren’t. The result? Only the APOE4 mice that consumed microplastics showed signs of cognitive problems.

The mice with the same gene but no microplastics behaved normally, as did the APOE3 group. This suggests that the combination of plastic exposure and genetic risk, not either one alone, may be driving early brain changes. The study also found s*x differences: male mice became more apathetic, while female mice had memory issues, which mirrors how Alzheimer’s tends to affect men and women differently in humans. Inflammation was also observed in the brains of the exposed mice, a sign commonly linked with Alzheimer’s disease. While the mice didn’t develop full-blown Alzheimer’s, the brain changes were enough to raise concern. Many people with the APOE4 gene never go on to develop Alzheimer’s, which means other factors, like diet, stress, or environmental toxins, must play a role. This study adds microplastics to the list of possible contributors.

source
Short-term exposure to polystyrene microplastics alters cognition, immune, and metabolic markers in an apolipoprotein E (APOE) genotype and s*x-dependent manner
Lauren Gaspar, 2025

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