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We have all seen movies where right before the hero starts fighting, he cracks his knuckles and makes it look like the coolest thing in the world! But then our parents told us that you should not crack your knuckles because that weakens your grip and hand strength. But is that true? While many people do say that they experience a small loss in strength immediately after they crack their knuckles, but are their long-term effects to it? And what is the sound actually coming from?
The reason why people crack their fingers is because the evident and sharp crack noise causes a sense of relief. Many people also do it when they have done an activity that required them to work with their hands a lot like typing or sewing, giving themselves a sense of satisfaction, similar to stretching after doing hard work. That "crack" sound can make some people cringe, while others find it strangely satisfying. Cracking your knuckles is a pretty common habit, but there are a lot of misunderstandings about it. Some people do it without even thinking, others can't stand the noise, and some can't crack their knuckles at all. You might have been told as a kid that it causes arthritis or makes your fingers swell up. But those are just old wives' tales. There's a real science behind this habit, and it's more interesting than you may think.
The "crack" isn't actually bones breaking or anything bad happening to your joints. It's a normal thing called "crepitus." This just means harmless popping, snapping, or grinding sounds that come from your joints. The main reason you hear this sound is because of gas bubbles in the fluid that cushions your joints. This fluid is called synovial fluid. When you move or stretch, these tiny bubbles form and then pop, making the sound. It's totally normal and doesn't hurt you. Sometimes, especially in bigger joints like your knees, shoulders, or ankles, the sound can also happen when the stretchy tissues that connect your bones (ligaments and tendons) move slightly and then snap back into place.
After you crack your knuckles, you can't usually do it again right away. You have to wait a bit. That's because the gas bubbles in your joint fluid have already popped, and it takes a little while for them to build up again. While cracking your knuckles doesn't give you arthritis, doing it too much might cause some problems. Doctors say that cracking them too often could make your joints a little wobbly and might even make your grip weaker. Also, if the stretchy tissues in your joints keep snapping over your bones, they can get irritated and sore.
Sometimes, a pop in your joint is just like cracking your knuckles, nothing to worry about. But other times, it can be a sign of something else. As we get older, the cushiony stuff in our joints, called cartilage, can start to wear down. This cartilage helps your bones move smoothly. When it gets thin or uneven, the bones can rub together, and that can make a grinding or popping sound. This is different from the pop you get from gas bubbles. If this grinding sound happens along with pain, it could be a sign of osteoarthritis. This is a type of joint problem that's more common in older people, but younger people can get it too, especially after a joint injury. If your joints hurt, especially in the morning or after you've been sitting still for a while, feel wobbly, or are hard to move, it's a good idea to see a doctor.
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Due to rising obesity levels, sedentary lifestyles, and a rapidly aging population, type 2 diabetes has become far more common than it was a few decades ago. While high-income countries saw a decline in diabetes-related deaths between 2000 and 2010, this trend reversed from 2010 to 2016. As a result, there has been an overall 5 percent rise in premature deaths linked to diabetes since 2000.
What is especially concerning is that type 2 diabetes is now increasingly diagnosed in children, largely driven by poor diet, excess weight, and lack of physical activity. Beyond its well-known effects on the heart, kidneys, eyes, and nerves, diabetes is also associated with long-term conditions affecting the brain, including dementia.
This raises an important question: how exactly are diabetes and dementia connected? To understand this better, we spoke to Dr Prabhojit Mohanty, Psychiatrist, Sexologist, and De-addiction Specialist, who shared insights on the link.
Diabetes is a long-term metabolic disorder in which blood sugar levels remain consistently high. This happens either because the pancreas does not produce enough insulin or because the body is unable to use insulin properly. Insulin plays a crucial role in helping glucose enter cells to be used as energy. When this process is disrupted, sugar builds up in the bloodstream, gradually causing damage to vital organs such as the heart, eyes, kidneys, and nerves.
The two main forms are Type 1 diabetes, an autoimmune condition that requires lifelong insulin therapy, and Type 2 diabetes, which is linked to insulin resistance and influenced by lifestyle and genetic factors, according to the Cleveland Clinic.
Dementia refers to a group of symptoms marked by a significant decline in cognitive abilities that interferes with everyday functioning. It affects memory, thinking, reasoning, and decision-making. Dementia is not a single disease but an umbrella term for conditions caused by different underlying disorders, the most common being Alzheimer’s disease.
As dementia progresses, symptoms become more severe, affecting mood, behavior, and the ability to carry out routine activities, often leading to increased dependence on others. Early diagnosis can help slow progression and improve quality of life, as noted by the Alzheimer’s Association.
An expanding body of research points to a clear association between diabetes and dementia. Large-scale studies and meta-analyses indicate that individuals with diabetes face nearly a 59 percent higher risk of developing dementia compared to those without the condition. This increased risk applies to both Alzheimer’s disease and vascular dementia and tends to rise the longer a person lives with diabetes. From a clinical perspective, several mechanisms are involved. Persistently high blood sugar levels and insulin resistance cause damage to both small and large blood vessels. Over time, this harms the brain’s microvasculature, reducing blood supply and raising the likelihood of strokes and vascular dementia.
Dr Prabhojit Mohanty explained, “When diabetes occurs alongside hypertension, the danger becomes even greater. Both conditions speed up damage to blood vessels in the brain. High blood pressure weakens vessel walls and contributes to plaque formation, which further limits blood flow to the brain. From a biological standpoint, insulin has roles beyond regulating sugar. When the brain becomes resistant to insulin, it affects neuron health, communication between brain cells, and how the brain uses glucose, increasing vulnerability to neurodegenerative conditions such as Alzheimer’s disease.”
Scientists have also introduced the idea of “type 3 diabetes” to describe Alzheimer’s disease as a condition driven by insulin resistance within the brain itself. According to this theory, impaired insulin signalling in neural tissue plays a role in the buildup of amyloid plaques and tau tangles, which are defining features of Alzheimer’s disease. People with diabetes often also struggle with high blood pressure and abnormal cholesterol levels. Together, these factors further raise the risk of dementia and significantly affect the quality of life of both patients and their caregivers. Detecting diabetes early, maintaining good control of blood sugar and blood pressure, and adopting healthier lifestyle habits can go a long way in protecting cognitive function with age.
In simple terms, there is strong clinical and biological evidence showing a clear and well-established connection between diabetes and dementia.
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People using injectable weight loss drugs may need long-term medical and lifestyle support, researchers have warned, after a large study found that weight is regained far more quickly than with traditional diet and exercise plans. Scientists at the University of Oxford found that people taking medications such as semaglutide (Wegovy) and tirzepatide (Mounjaro) lose weight while on treatment, but typically regain it within around 20 months after stopping the injections.
The study also showed that improvements in blood sugar control, cholesterol levels, and blood pressure fade once the drugs are discontinued, leaving patients back at their original health markers. By comparison, people who lose weight through structured diet and exercise programmes tend to maintain the loss for longer, close to four years on average, although most eventually regain weight as well.
The findings come alongside separate research from University College London and the University of Cambridge, which suggests that people prescribed newer weight loss drugs could face risks such as nutrient deficiencies and loss of muscle mass. Under current NHS rules, Wegovy can only be prescribed for up to two years, while Mounjaro has no set time limit.
Most people using these medications pay for them privately, due to strict NHS eligibility criteria. Research indicates that around half stop treatment, often because of cost, side effects, or because they feel they have reached their target weight.
The Oxford analysis, published in the British Medical Journal, reviewed 37 studies involving more than 9,000 participants. On average, people stayed on medication for 10 months and were followed up for eight months after treatment ended.
Across all weight loss drugs, participants lost an average of 8.3 kg during treatment, but regained 4.8 kg within a year, returning to their starting weight within about 1.7 years. Those taking Wegovy or Mounjaro lost nearly 15 kg, but regained around 10 kg in the first year after stopping. Based on projections from one year of data, full weight regain occurred within roughly 1.5 years. Measures linked to heart and metabolic health, including blood glucose and cholesterol, also returned to baseline within about 1.4 years.
Professor Susan Jebb, professor of diet and population health at the University of Oxford and an adviser to ministers and the NHS on obesity, said the findings were clear. “What we’ve shown is that weight regain after medication is common and happens quickly. The benefits for blood sugar and cholesterol closely track weight changes, so when weight comes back, those benefits disappear too.”
She noted that weight regained after medication happens almost four times faster than after behaviour-based programmes, regardless of how much weight was initially lost. Professor Jebb said long-term solutions may be necessary, whether through ongoing medication, behavioural support, or a combination of both.
“Obesity is a chronic, relapsing condition,” she said. “It’s reasonable to expect that treatment may need to continue for life, much like medicines for high blood pressure. We should think of this as long-term treatment for a long-term condition.”
She added that combining diet and exercise programmes with drug treatment helps people lose more weight initially. However, once medication stops and appetite returns, those strategies alone often fail to prevent regain. In contrast, people in behavioural programmes without drugs may practice these habits more consistently, which could explain why weight regain is slower.
Professor Jebb said it is clear that some form of ongoing intervention is needed if the benefits of weight loss drugs are to last. Some patients try tapering doses or using medication intermittently, while others rely on lifestyle support alone, but she said evidence on what works best remains limited.
Sam West, a postdoctoral researcher at the University of Oxford and co-author of the study, said: “People on medication lose more weight than those in behavioural programmes, but they regain it about four times faster.”
The researchers also questioned whether long-term drug treatment is cost-effective for the NHS. They concluded that since obesity is a long-term, relapsing condition, extended use of weight management medications may be needed to maintain health benefits.
Separate findings published in Obesity Reviews highlighted gaps in nutritional guidance for people taking semaglutide and tirzepatide. Dr Marie Spreckley from the University of Cambridge said many patients receive little structured advice on diet quality, protein intake, or micronutrient needs, despite significant appetite suppression.
“If nutritional care isn’t built into treatment,” she said, “there’s a real risk of trading one health problem for another, through avoidable nutrient deficiencies and unnecessary muscle loss.”
An NHS spokesperson said that while these drugs are a valuable addition to weight loss treatment, they are not a quick fix. “They must be combined with lifestyle and behavioural support, including advice on healthy eating and physical activity, to help people maintain weight loss over time,” the spokesperson said.
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Long COVID should be viewed as a web of overlapping symptoms rather than a single, uniform condition, according to a new systematic review published in eClinicalMedicine and reported by the Center for Infectious Disease Research and Policy (CIDRAP). The review highlights several recurring symptom patterns linked to long COVID, including neurological, respiratory, smell and taste-related, cardiopulmonary, and fatigue-driven clusters.
Researchers led by a team from Lanzhou University in Gansu, China, examined data from 64 studies conducted across 20 countries, covering nearly 2.4 million people. They grouped long COVID patients into subtypes using different approaches: symptom overlap in 30 studies, affected organ systems in 16 studies, symptom severity in nine, clinical markers in three, and other classification methods in the remaining research.
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Among studies that focused on how symptoms appear together, fatigue stood out as the most consistently reported issue. It often occurred alone or alongside problems such as muscle and joint pain, brain fog, or breathlessness. Other symptom pairings that appeared frequently included loss of smell and taste, anxiety with depression, and various forms of musculoskeletal pain.
When researchers classified patients based on affected organ systems, respiratory problems were the most widespread, seen in about 47% of long COVID patients. Neurological symptoms followed at 31%, while gastrointestinal issues were reported by 28%. The authors stressed that these percentages reflect how often these clusters appeared within long COVID cases studied, not how common they are in the general population.
A smaller number of studies sorted patients by how severe their symptoms were, dividing them into mild, moderate, or severe categories using symptom scores, symptom counts, or quality-of-life measures. Three studies used clinical indicators for classification, including abnormal triglyceride levels and signs of restricted lung function on imaging.
The review also found that long COVID subtypes vary based on demographic, socioeconomic, and medical factors. Women were more likely to report fatigue and neuropsychiatric symptoms, while men more commonly experienced respiratory issues. Older adults tended to show higher rates of respiratory, cardio-renal, and ear, nose, and throat symptoms.
Racial and ethnic differences also emerged. Black and Hispanic individuals were more likely to experience respiratory, cardiac, and neuropsychiatric symptoms, whereas White patients showed higher rates of fatigue and musculoskeletal complaints.
COVID-19 variants appeared to influence symptom patterns as well. The researchers noted that the Alpha variant was closely linked to smell-related and respiratory symptoms, while the Delta variant raised the risk of ENT-related problems. In addition, higher body mass index, socioeconomic disadvantage, and existing conditions such as chronic obstructive pulmonary disease were strongly associated with cardiopulmonary symptom clusters and a heavier overall long COVID burden.
Overall, the findings reinforce that long COVID rarely affects just one system in the body. Instead, it tends to involve multiple overlapping symptom groups, pointing to the need for more tailored, patient-specific care.
The authors call for future studies to focus on creating standardized ways to classify long COVID, identifying the biological mechanisms behind different symptom clusters, and testing targeted treatments for specific subtypes. They note that this approach will be essential for moving toward precision medicine and improving outcomes for people living with long COVID.
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