A new study published in The Lancet Digital Health suggests that biological age of different organs could predict a person's risk of diseases such as cancer, dementia, and heart disease than their actual chronological age. The research analyzed long-term data from Whitehall II study, which had been followed by over 10,000 British adults for more than 35 years.

The blood plasma samples were collected between 1997 and 1999 from participants between ages 45 to 69. Researchers have now examined a follow up data from 6,235 participants, who were by then aged 65 to 89. This was done to see how aging of specific organ may correlate with the development of diseases over two decades.

What Organs Were Studied?

The study measured the biological age of nine key organs, including:

• Heart
• Blood vessels
• Liver
• Immune system
• Pancreas
• Kidneys
• Lungs
• Intestines
• Brain

The researchers were able to find that different organs aged at different rates in different people. In many of the cases multiple organs showed signs of faster aging within the same individual. What is important to note is that those with accelerated aging in certain organs had a higher risk of developing 30 out of the 40 age-related diseases the study had tracked.

Organ Aging And Disease Risk

Some organ-disease connections were expected—people with rapidly aging lungs were more likely to develop respiratory diseases, and those with aging kidneys had an increased risk of kidney-related conditions. However, the study also found less obvious associations.

For example, individuals with fast-aging kidneys were more prone to diseases in other organs, such as the liver and pancreas. Additionally, multiple fast-aging organs were linked to an increased risk of kidney disease.

One of the most surprising findings was that dementia risk was not best predicted by an aging brain but rather by the immune system’s biological age. This suggests that factors such as chronic inflammation and immune health may play a critical role in neurodegenerative diseases.

What Is Organ Specific Blood Tests?

The study also highlights the important of the potential of developing blood tests that could assess the biological age of specific organs. Unlike previous complex methods that measured the organ health, this new approach could make things simple to detect early signs of disease.

The leader author of the study Mika Kivimaki, who is also a professor at the University College London's Faculty of Brain sciences pointed out that such tests could be helpful when it comes to guiding personalized healthcare. In a news release, Kivimaki said, "They could advise whether a person needs to take better care of a particular organ and potentially provide an early warning signal that they may be at risk of a particular disease."

The study reinforces the idea that aging does not affect all organs equally and that looking beyond chronological age could offer better insights into disease prevention. By understanding which organs are aging more rapidly, medical professionals may be able to recommend targeted interventions for individuals at higher risk of specific conditions. Future advancements in organ-specific blood testing could revolutionize how we detect and manage age-related diseases, potentially leading to more personalized healthcare strategies.

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.

How Chronic Inflammation Causes Lasting Liver Damage

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.

Also read: Smoking, Diabetes, High Blood Pressure May Fuel the Most Dangerous Type of Artery Plaque, Study Finds

Early Detection Can Prevent Disease Progression

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.

Also read: IIT Delhi, AIIMS Develop First Hindi Music Therapy for Stroke Patients: How Survivors Find Their Voice

Who Should Get Screened And Why It Matters

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

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.

More Risk Factors = More Dangerous Plaques

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.

Also read: ICMR Study Highlights India’s Silent Cholesterol Crisis: 9 In 10 Adults Have At Least One Abnormal Blood Lipid

Why Vulnerable Plaque Is Especially Dangerous?

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.

Also read: Risks Of Plastic Pollution: Study Finds Microplastics In Heart Arteries Can Cause Severe Heart Attacks

Smoking, Diabetes And high Blood Pressure Pose High Risk

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

What Is Atherosclerosis?

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.

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.

Can Sleep Be Restored In Alzheimer’s Patients?

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.

Also read: Captain ‘Sully’ Sullenberger, ‘Miracle On The Hudson’ Pilot, Reveals Early-Stage Alzheimer’s Diagnosis

'Paradigm Shifting' Findings

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

Why Do Alzheimer’s Patients Lose Sleep?

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.