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Over 1 in 100 people worldwide living with celiac disease, consuming even trace amounts of gluten can trigger debilitating symptoms — from severe abdominal pain to long-term complications like malnutrition and increased cancer risk. But despite decades of research, the exact origin of these immune reactions remained something of a mystery.
Now, scientists may have pinpointed the elusive starting point of gluten-triggered immune attacks. In a landmark study published in Gastroenterology, researchers from McMaster University in Canada, along with international collaborators, have uncovered a pivotal role played by the cells lining the gut — not just as bystanders but as active agents in the cascade that defines celiac disease. This finding could pave the way for more precise, non-dietary therapies.
Celiac disease is a chronic autoimmune condition triggered by gluten — a group of structural proteins found in wheat, barley, and rye. While most people digest gluten without issue, those with celiac disease experience an abnormal immune reaction that damages the small intestine.
The symptoms range from bloating, abdominal pain, and diarrhea to fatigue, skin rashes, and nutrient deficiencies. Over time, untreated celiac disease can lead to serious complications including osteoporosis, infertility, and gastrointestinal cancers.
Currently, the only effective treatment is lifelong strict avoidance of gluten — a tall order, given how ubiquitous gluten is in processed food, sauces, and even medications.
One clue to the mystery lies in genetics. Nearly 90% of people with celiac disease carry a specific protein called HLA-DQ2.5, while most of the rest carry HLA-DQ8. These proteins are part of a group called human leukocyte antigens (HLAs), which present bits of proteins to the immune system — essentially acting like flags that identify threats.
In people with celiac disease, HLA-DQ2.5 or DQ8 mistakenly flags gluten fragments as dangerous, prompting an aggressive immune response. But not everyone who carries these genes gets the disease — suggesting something else is required to flip the switch.
Until now, it wasn’t fully understood how gluten peptides made their way past the gut lining and into the immune system’s crosshairs. The McMaster-led study changes that.
By using transgenic mice — mice genetically engineered to carry human versions of the HLA genes — researchers were able to simulate celiac disease at the cellular level. They grew miniature gut models known as organoids, made from real mouse intestinal cells, to observe what happens when gluten meets the gut lining.
What they found was striking: the epithelial cells lining the gut aren’t passive observers — they actively participate in the immune reaction.
These cells release a transporting enzyme that binds to gluten peptides and modifies them, making them even more visible to the immune system. The cells then present these altered gluten fragments directly to immune cells, triggering inflammation.
In other words, your own gut lining might be the place where celiac disease begins.
Another major insight: inflammation and gut microbes appear to amplify the immune response. When the researchers exposed their organoids to inflammatory triggers and bacteria-processed gluten, the cells ramped up production of immune signaling molecules — effectively supercharging the immune reaction.
This discovery opens new avenues for treatment. Targeting the gut’s microbiome or blocking the epithelial cells’ presentation of gluten peptides could offer alternatives to the gluten-free diet — something patients and clinicians alike have long hoped for.
Lead researcher Dr. Elena Verdu, a gastroenterologist at McMaster, notes that while avoiding gluten is currently the only way to manage celiac disease, it is far from perfect.
“This is difficult to do, and experts agree that a gluten-free diet is insufficient,” Verdu says. “Our findings show that the gut lining plays a much bigger role in initiating the immune reaction than previously believed.”
By identifying the specific tissue types and enzymes involved, scientists now have a roadmap for developing targeted treatments. In the future, medications might block the gut’s gluten-presenting function, regulate inflammation, or even alter how gut bacteria break down gluten — all without having to eliminate gluten entirely.
This breakthrough adds weight to the growing understanding that celiac disease is not just about the immune system being “overreactive,” but about how and where that reaction begins.
Tohid Didar, a biomedical engineer on the team, says, “This allowed us to narrow down the specific cause and effect and prove exactly whether and how the reaction takes place.”
Such clarity has never existed before. Now, with this map in hand, researchers can explore new therapies that go beyond dietary restrictions. Of course, these results — while promising — are still early. Most of the experiments were conducted on mice, though they carry human genes. The next step will be to confirm these findings in human tissue and clinical trials.
But the implications are clear: for the first time, we know where gluten reactions start. And we might soon have a path to stop them.
For people living with celiac disease, even a crumb of gluten can cause days of pain and damage. This research brings us one step closer to a world where bread, pasta, and pastries can be safely enjoyed — without fear and without compromise.
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Autism is often painted as a childhood condition, usually spotted in the school playground when social quirks or communication differences raise eyebrows. But what happens when those children grow up without anyone connecting the dots? According to new research from King’s College London, the answer is unsettling: most autistic adults over 40 are still flying under the diagnostic radar.
The review, published in the Annual Review of Developmental Psychology, estimates that a staggering 89 per cent of people over 40 with autism remain undiagnosed. To put that into perspective, while around 23 per cent of autistic children under 19 are missed, nearly 96 per cent of those over 60 have never been recognised as autistic. That’s not just a gap; that’s a canyon.
When the researchers broke it down by age and gender, the numbers looked even more lopsided. Among men aged 40 to 59, more than 91 per cent had never been diagnosed. For women in the same age group, the figure was almost 80 per cent. By the time people reached their sixties, both men and women crossed into the 96 to 97 per cent range of being undiagnosed.
Compare that with the 20 to 39 age group, where roughly half remained undiagnosed, and the generational divide becomes clear. Today’s younger adults are far more likely to be spotted, assessed and supported. Older adults, meanwhile, have often been left to muddle through without a name for their lifelong differences.
Gavin Stewart, lead author of the study, explains that a lack of diagnosis means many autistic adults were never offered the right support, leaving them more vulnerable to age-related problems. These range from social isolation to poor physical and mental health.
The review found that autistic people in middle age and beyond have higher rates of almost every health condition compared to non-autistic peers, like heart disease, neurological issues, autoimmune disorders, gastrointestinal problems, anxiety and depression. Add age-related conditions like osteoporosis, arthritis and Parkinson’s disease, and the picture gets even more complicated.
Even more concerning, autistic older adults were six times more likely to report suicidal thoughts or self-harm and four times more likely to develop early-onset dementia.
The study highlighted another layer of challenge: healthcare itself. Many older autistic adults face obstacles in accessing medical support due to communication differences, sensory sensitivities or simply not knowing how to navigate the system. Combine that with a shortage of healthcare professionals trained in recognising autism in adults, and it’s no wonder so many cases slip through the cracks.
Professor Francesca Happé, co-author of the review, stresses that this is a global public health issue. “Understanding the needs of autistic people as they age is a pressing global public health concern. As autistic people age, the nature of the challenges they face changes. We must adopt a lifespan approach that funds long-term research, integrates tailored healthcare, and expands social supports so that ageing autistic people can live happy and healthy lives,” she says. In other words, autism doesn’t disappear after childhood, so neither should support.
The findings also suggest that research into autism may have been skewed for years. If most older adults remain undiagnosed, then studies have largely overlooked them. That means our current understanding of how autistic people age is incomplete at best. No wonder policies and services have not caught up.
Employment struggles, strained relationships and social isolation were all noted as common experiences for older autistic adults. Without the framework of a diagnosis, many never knew why they felt out of step with the world, and their difficulties were often chalked up to personality flaws or “just how they are”.
If you’re wondering whether getting a diagnosis later in life makes a difference, the answer is yes. Recognition can bring clarity, opening doors to support systems, healthcare adaptations and even financial benefits. It can also reshape how family, friends and colleagues understand a person’s behaviour and needs.
The NHS encourages adults who suspect they might be autistic to speak to their GP and ask about a referral for an assessment. Specialists can help by gathering life history, speaking with people who know you well and observing how you interact with others.
The review ends with a clear message: it’s time to stop treating autism as a childhood-only issue. For too long, older autistic adults have been invisible, their experiences untold and their needs unmet. With diagnosis rates still alarmingly low, researchers are urging more studies, better services and a cultural shift that embraces autism across the lifespan.
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When blockbuster diabetes drugs double as miracle weight-loss injections, it seems like everyone wants in. But now, the same medications are making headlines for possible vision loss.
Originally designed to regulate blood sugar in type 2 diabetes, GLP-1 receptor agonists, which cover Ozempic, Mounjaro, Wegovy, Trulicity, Rybelsus and others, quickly became famous in the weight-loss world. Social media crowned them the “skinny jab”, while pharmaceutical companies rushed out new versions to keep up with demand.
But as prescriptions soared, so did reports of odd side effects. Stomach paralysis (gastroparesis), intestinal blockages and now a rare vision condition are creeping into the conversation. It turns out shedding pounds might come with strings attached, ones that affect more than your waistline.
The latest condition in this story is nonarteritic anterior ischaemic optic neuropathy, or NAION for short. It is a mouthful, but the condition itself is no joke. NAION can blur vision permanently or even lead to blindness by damaging the optic nerve.
Whispers of this link first appeared in mid-2024, when Harvard researchers published a study claiming Ozempic users faced a seven-fold higher risk of NAION compared to non-users. Just weeks later, another paper in JAMA Ophthalmology suggested the concern was not limited to Ozempic; it was likely an issue across the entire GLP-1 family.
Researchers point out that while there is a measurable increase in eye complications, the story isn’t as clear-cut as it sounds.
A recent retrospective study found a slight but significant uptick, about 7 per cent, in new cases of diabetic retinopathy (DR) among GLP-1 users. DR is a common complication of diabetes itself, where blood vessels in the retina become damaged. Interestingly, though, these same patients did not show a higher risk of progressing to severe complications like proliferative retinopathy or diabetic macular oedema.
Reports suggest that patients on GLP-1 drugs should be screened regularly for eye problems, no matter their baseline status. In other words, keep your ophthalmologist on speed dial.
While doctors debate the data, lawyers are already busy. Eli Lilly, maker of Mounjaro and Zepbound, has asked federal judges to consolidate the growing pile of lawsuits into one massive multidistrict litigation (MDL). This would lump together claims of optic nerve damage with the thousands of cases already filed over gastroparesis.
The lawsuits accuse manufacturers of pushing profits over patient safety, alleging that the risks of vision loss were downplayed or overlooked. With more patients joining the legal fray, the story is no longer confined to medical journals; it is unfolding in courtrooms across the US.
For people with type 2 diabetes, GLP-1 drugs remain highly effective. They lower blood sugar, help with weight loss, and even offer some protection against heart disease. For many, the benefits still outweigh the risks.
But the newfound spotlight on NAION is a reminder that no drug is without trade-offs. Those weekly injections may slim waistlines, but they also highlight the need for vigilance. Patients should discuss eye health with their doctors, schedule regular check-ups, and report any sudden changes in vision immediately.
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If modern life had a “pause” button, many women would happily press it on their biological clocks. That is essentially what egg freezing offers: a chance to preserve fertility for the future. But the two questions that inevitably surface are how many eggs should you freeze and how many cycles will it take to get there? The short answer is, it depends.
When it comes to egg freezing, more is not always better, but a certain number is definitely necessary. Dr Navina Singh, fertility specialist at Birla Fertility & IVF, Mumbai, says women in their late twenties or early thirties generally need to freeze around 15 mature eggs to have a fair chance at one live birth. For those beyond the mid-thirties, the number usually goes up to 20 or more. Because as time ticks on, both the number and quality of eggs decline, reducing the likelihood of a healthy embryo developing from each egg.
Dr Swati Mishra, another fertility specialist, says, "On average, women in their early thirties are advised to freeze 10–15 mature eggs to maintain good chances of embryo formation later. For women in their late thirties, the target is higher, often 20 or more.”
Many women walk into clinics hoping a single cycle of ovarian stimulation will do the trick. Sometimes it does. But sometimes, biology has other plans.
“Some women respond strongly to stimulation and can collect the required number in one attempt,” explains Dr Singh. “Others, especially those with lower ovarian reserve, may need two or even three cycles. This is not a failure; it is simply how ovaries differ in their response.”
Dr Mishra adds that this variation is one of the biggest surprises for women: “It is natural biology. We prepare women from the outset that while some will achieve the target in one cycle, others may need more. It all comes down to ovarian reserve and individual response.”
In other words, if your ovaries are playing hard to get, patience and persistence are part of the process.
How do doctors know how many eggs or cycles a woman might need? Tests like AMH (anti-Müllerian hormone) and antral follicle counts help gauge ovarian reserve. These markers, combined with age and reproductive goals, give doctors a clearer picture.
A woman aiming for one child might freeze fewer eggs than someone who hopes for two. And lifestyle factors matter too. As Dr Mishra points out, “Weight, nutrition, and stress all influence ovarian response, which is why we encourage holistic preparation before starting treatment.”
Both experts stress the importance of counselling because egg freezing is about managing expectations as much as it is about collecting eggs.
Dr Singh says, “Counselling ensures women understand not just the approximate egg numbers but also the possibility of multiple cycles, costs, and time commitment. Egg freezing does not offer guarantees. What it really offers is choice.”
Dr Mishra agrees: “We want women to approach the process with realistic expectations and a clear plan. With the right guidance, egg freezing becomes a tool for control, not confusion.”
Egg freezing is not a magic wand that guarantees future babies, but it does offer women greater say over their timelines. The number of eggs you need depends on your age, ovarian reserve, and reproductive goals. The number of cycles it may take depends on how your body responds.
What doctors want women to know is, do not see extra cycles or higher egg targets as setbacks. They are just reflections of biology. With the right preparation, information, and mindset, egg freezing is less about uncertainty and more about empowerment.
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