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Weight loss is usually considered a good thing, unexpected and extreme weight loss can be a sign of something in your body going very wrong. There could be some underlying issues that are causing your body to pull weight and nutrition from your muscles and body fat to keep you going. As you grow old, your limbs grow weaker, and same for your muscles, so you do lose some weight as you age, but losing a lot of it too quickly could be a sign of something much worse, Dementia. A recent study published in JAMA Network Open 2025 Cardiometabolic Trajectories Preceding Dementia in Community-Dwelling Older Individuals, has identified potential early indicators of dementia, including significant weight loss and specific digestive changes, appearing years before noticeable cognitive decline.
The study showed that people who later got dementia had their Body Mass Index, or BMI, go down faster than those who stayed healthy. BMI is a way to see if someone's weight is healthy for their height. This drop in BMI started happening many years before they were told they had dementia, sometimes as early as 11 years ago. Also, these people often started with a lower BMI to begin with. So, even though everyone's weight might change a little as they get older, the people who developed dementia had a much bigger and faster weight loss.
Along with their BMI, the size of their waist also changed. People who ended up with dementia had smaller waist sizes, and this difference was noticeable about 10 years before they were diagnosed. This means that their bodies were changing in ways that showed up long before they or their doctors noticed any problems. So, not only was there weight loss, but also a loss of abdominal fat. This measurement is important because fat around the waist can be related to other health issues.
The study also found changes in their blood. Specifically, the "good" cholesterol, called HDL, went up in people who developed dementia. This increase happened about five years before they were diagnosed. It's tricky because HDL is usually seen as a good thing for your heart. But in this case, it seems like it might be a sign of changes happening in the brain. Scientists are still trying to understand why this happens.
When we see that people with dementia lose weight, it's easy to think that the weight loss is what caused dementia. But experts think it's the other way around. They call this "reverse causation." This means that the brain changes that cause dementia also cause people to lose weight. The brain changes can affect things like appetite, how the body uses food, and how people go about their daily lives. For example, people might forget to eat, have trouble making meals, or move around less.
While the study revealed a lot about different indicators of dementia and bodily changes, there are many limitations to the study. Everyone loses some weight as they get older. So, it's hard to know when weight loss is just a normal part of aging and when it's a sign of dementia. The study found that people with dementia lost weight faster, but it's still tricky to tell the difference in everyday life. Doctors need to look at other things, like memory tests, to figure out if someone's weight loss is a cause for concern.
If someone is losing weight without trying, and they're also having problems with their memory or thinking, it's important to talk to a doctor. It's not just about the weight loss; it's about the whole picture.
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Liver disease is unusual among serious conditions in that it can progress significantly without producing symptoms that would prompt most people to seek medical attention. Hepatitis, which is inflammation of the liver, is the most common starting point for that progression.
It may be caused by viral infections including Hepatitis B and Hepatitis C, excessive alcohol consumption, fatty liver disease, certain medications, or autoimmune conditions. In many cases, the person carrying it feels entirely well while damage accumulates over months and years.
The liver does regenerate, but that capacity has limits. When inflammation persists, healthy liver cells are progressively replaced by scar tissue, a process called fibrosis.
Continued scarring eventually produces cirrhosis, where the liver loses its structural integrity and its ability to perform the functions the body depends on it for, such as processing toxins, producing proteins involved in blood clotting, regulating metabolism, and supporting digestion. At this stage, the damage is largely irreversible.
The timeline from hepatitis to cirrhosis typically spans years or even decades, which is precisely what makes delayed diagnosis so consequential. Each year of untreated inflammation is a year of accumulated scarring.
By the time cirrhosis produces obvious symptoms such as jaundice, abdominal swelling from fluid accumulation, internal bleeding from enlarged veins in the oesophagus, cognitive changes from toxin build-up, kidney involvement, the disease has already reached an advanced stage. Cirrhosis also carries a significantly elevated risk of liver cancer.
The clinical picture is meaningfully better when liver disease is identified early. Effective antiviral medications can control chronic Hepatitis B and cure most cases of Hepatitis C, substantially reducing the risk of progression.
Fatty liver disease, when caught before significant fibrosis has occurred, can often be reversed through weight management, blood sugar control, reduced alcohol intake, and consistent physical activity. These interventions are accessible, evidence-based changes that work when applied before the disease has advanced.
Screening is where early identification happens. Blood tests measuring liver enzymes and imaging studies can detect liver inflammation and early fibrosis well before symptoms appear.
For individuals with diabetes, obesity, a family history of liver disease, a history of blood transfusions, or other known risk factors, periodic liver assessment is a practical and important part of routine care rather than an optional precaution.
The pattern that gastroenterologists consistently encounter is patients presenting with advanced liver disease who had risk factors identifiable years earlier. Hepatitis B and C are both detectable through simple blood tests.
Fatty liver shows up clearly on ultrasound. The window for effective intervention exists, and it is considerably wider earlier in the disease than most people assume when they have never been tested.
This draws attention to a disease that carries a substantial global burden but remains widely undertreated because it does not announce itself. For anyone with known risk factors, or who has never had their liver function assessed, the appropriate response to that is a conversation with a physician, before symptoms, rather than after.
By Dr. Saswata Chatterjee, Senior Consultant – Gastroenterology, CMRI Hospital
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Smoking, diabetes, high blood pressure, high cholesterol, and obesity have always been recognized as major risk factors for heart disease.
New research has emerged saying these preventable conditions may do more harm than simply contribute to plaque buildup in the arteries. They may also encourage the formation of the most dangerous type of plaque, the kind that is most likely to rupture and trigger a massive heart attack.
The findings, presented at the European Society of Cardiology (ESC) Congress 2026, show that people with a greater number of modifiable cardiovascular risk factors were more likely to have widespread coronary plaque.
They may also have unstable and vulnerable plaques that can suddenly rupture, disrupting blood flow to the heart.
Researchers analyzed coronary artery imaging data to understand how both modifiable and non-modifiable cardiovascular risk factors affect the characteristics of plaque.
The study found that patients with a higher burden of modifiable risk factors had plaques distributed across all three major coronary arteries.
More importantly, these individuals were more likely to develop lipid-rich plaques with thin fibrous caps, a trait of vulnerable plaques that are more likely to rupture.
On the other hand, people whose risk profile was dominated by non-modifiable factors, such as age or genetics, tended to have more stable plaque types.
"Our findings suggest that modifiable cardiovascular risk factors are associated not only with a greater amount of coronary plaque but also with more vulnerable plaque characteristics that are linked to future heart attacks," the researchers said.
Some plaques gradually harden and remain relatively stable for years, causing slow narrowing of the arteries. Others contain large amounts of fat covered by a very thin protective layer known as a fibrous cap.
These unstable plaques can rupture unexpectedly, prompting blood clots to form and suddenly block an artery, leading to a heart attack or stroke.
According to the researchers, individuals with multiple preventable cardiovascular risk factors were significantly more likely to have these high-risk plaques.
Smoking chronically damages the inner lining of blood vessels, making it easier for cholesterol deposits to accumulate while also promoting inflammation and blood clot formation.
High blood pressure places constant stress on artery walls, accelerating plaque development and increasing the likelihood of rupture.
When several of these risk factors occur together, their harmful effects can compound, increasing both the quantity of plaque and likelihood to rupture.
Also read: Vapers & Smokers Have Equally Poor Physical Fitness & Blood Vessel Health, Study Finds
Atherosclerosis is a chronic condition in which fatty deposits made up of cholesterol, inflammatory cells, calcium, and other substances accumulate inside artery walls.
Over time, these deposits narrow the arteries and reduce blood flow to vital organs. The condition often develops silently over decades before causing symptoms.
If a plaque ruptures, a blood clot can rapidly block blood flow, resulting in a heart attack or stroke. Smoking, diabetes, high blood pressure, obesity, and elevated LDL ("bad") cholesterol are among its leading preventable causes.
The researchers said the study highlights the importance of early identification and management of modifiable cardiovascular risk factors through smoking cessation, blood pressure control, diabetes management, cholesterol-lowering treatment, regular physical activity, a healthy diet, and maintaining a healthy weight.
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Sleep disturbances are among the most debilitating symptoms of Alzheimer’s disease. It often appears years before significant memory decline and other symptoms.
A new study from researchers at the University of Kentucky suggests that this sleep loss may not be permanent.
Instead, it could be driven by an immune response in the brain that may be reversible, sparking hope for new treatments.
Published in the journal Alzheimer’s & Dementia, the study found that brain immune cells called microglia, rather than amyloid plaques themselves, are the primary cause of sleep disruption in Alzheimer’s disease.
In mouse-based trials, researchers were able to restore more than two hours of sleep per day by temporarily removing these immune cells, without reducing amyloid plaques.
For years, scientists believed that sleep problems in Alzheimer’s were caused by the accumulation of amyloid plaques or the gradual death of brain cells. However, this study points in a different direction.
Researchers discovered that when amyloid plaques begin forming in the brain, they activate microglia, the brain’s resident immune cells.
Instead of protecting the brain, these cells cause inflammation that keeps brain circuits active, preventing sleep.
Using a drug called pexidartinib (PLX3397), the researchers temporarily depleted around 87% of microglia in Alzheimer’s mouse models.
This restored over two hours of daily sleep, particularly non-rapid eye movement (NREM) sleep, which is essential for tissue repair, memory strengthening, and clearing waste products from the brain.
Notably, the improvement occurred without changing amyloid plaque levels, suggesting that inflammation is manageable.
Lead researcher Dr. Shannon L. Macauley, associate professor of physiology at the University of Kentucky College of Medicine, said, “Basically, we showed that it is not the plaques themselves, or solely dysfunctional neurons, that cause sleep loss but actually microglia.
Microglia are immune cells that, when they respond to plaques, kick off this elaborate cascade of inflammation, as if the microglia are partying all night, and keeping the brain awake.”
She also highlighted why losing restorative sleep can accelerate disease progression.
“That restorative sleep is super important for physical repair, learning and memory and washing out the toxins of the day. When Alzheimer’s patients lose this stage, they lose their brain’s primary cleaning cycle, creating a feed-forward loop that may drive further damage,” she explained.
First author Dr. Nicholas J. Constantino said one of the biggest surprises was that sleep problems did not worsen as amyloid plaques increased.
“I expected that as plaque burden became more severe, sleep disruption would also worsen. The disruptions in sleep… did not worsen by 18 months, despite more than double the amount of plaque burden,” Constantino said.
Also read: What Is Type 3 Diabetes? Insulin Resistance In The Brain That Could Trigger Alzheimer’s
Poor sleep and Alzheimer’s create a vicious cycle. Sleep deprivation reduces the brain’s ability to clear amyloid-beta and tau proteins, which can accelerate disease progression, while worsening sleep.
Sleep disturbances affect up to half of people living with Alzheimer’s disease. The disease disrupts sleep due to various reasons:
Overactive microglia: As shown in the new study, immune cells become chronically activated by amyloid plaques, releasing inflammatory signals that keep the brain in a heightened state of activity.
Damage to sleep-regulating brain regions: Alzheimer’s progressively affects areas like the hypothalamus and brainstem that regulate the sleep-wake cycle.
Loss of NREM sleep: Due to lack of deep sleep, the brain’s ability to clear metabolic waste, including amyloid plagues weakens.
Circadian rhythm disruption: Degeneration of the brain’s internal clock leads to broken sleep and daytime drowsiness. This fuels confusion and agitation associated with the disease.
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