Fasting may reset your body, but can it reset your mind? The new trend of dopamine fasting claims it can. And wait, there's more. This trend also works against dopamine resistance, implying that things that did not make you happier before will now do. You see, dopamine is a part of the brain's reward system and plays an important role in your pleasure reception. While this neurotransmitter is not directly linked to an individual's happiness, it triggers feelings of satisfaction, motivation and pleasure.

However, a person can also reach a stage of dopamine resistance if they continue to indulge in activities that trigger its frequent or constant release. In this case, the individual stops feeling the impact of this neurotransmitter and thus, does feel good or happy.

So does dopamine fasting work?

Dopamine fasting is a practice where individuals limit their exposure to activities or stimuli that typically provide a surge of dopamine. The idea behind dopamine fasting is to reset or recalibrate the brain's reward system. This is usually done by abstaining from gratifying things or experiences like social media, junk food, and even sex. Proponents of dopamine fasting argue that continual overstimulation from digital devices, social media, and easily accessible indulgences has numbed our brain's reward pathways. By regularly denying ourselves these dopamine triggers, the idea claims, we might restore our ability to acquire fulfilment from life's basic pleasures.

How Does Dopamine Imbalance Affect Your Mental Health?

Having low levels of dopamine can make you less motivated and excited about things. In Parkinson's disease, there is not enough dopamine in the areas of the brain important for movement. This leads to problems with muscle stiffness and movements such as walking.

The symptoms of a dopamine imbalance depend on what is causing the problem. They include physical symptoms such as:

• muscle cramps, spasms or stiffness
• digestion problems, such as constipation or reflux
• pneumonia
• trouble sleeping
• moving or speaking more slowly than usual

• feeling tired and unmotivated, or sad and lacking hope
• having low libido (sex drive)
• hallucinations (experiencing something that's not real)

How Can I Adjust My Dopamine Levels?

Adjusting dopamine levels is complicated, as it is involved in many different roles in the brain. Your doctor won't measure your dopamine levels directly, and there is no simple test to measure it. Your symptoms will be the clues that tell your doctor if you have too much or not enough dopamine. They will then prescribe medicines to adjust your dopamine level, based on your symptoms, and make adjustments based on how your body responds and how you feel.

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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.

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.

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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.

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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.

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'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.