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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.
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:
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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Through the first quarter of the twenty-first century, it has been clear that the global menace of infectious diseases has become very different in terms of their causal factors and predictability.
A 2022 review in Nature Reviews Microbiology by Princeton professors Rachel Baker and Jessica Metcalf aptly pointed out how climate change, urbanization, and wider travel and trade determine when, where, and how outbreaks of infections happen. Examples of such outbreaks are numerous globally, viz. SARS, H1N1, MERS, Ebola, Zika, and COVID-19 outbreaks. It has also been realized by biomedical scientists that more than half of all known pathogenic diseases have at some point been worsened by climate-change-related events.
As a result, research on climate-disease links has surged since the recent pandemic.
Evidence supporting this climate-disease relationship is also abundant in the Indian context. A major example is our experience with dengue infections, which are clearly losing their seasonal predictability. Contrary to its usual temporal link with the monsoon, India has encountered an unusually early transmission in 2026, with nearly 7,000 cases reported by end-February, as per the National Center for Vector-Borne Diseases Control data. The vector has also expanded its geographical distribution, for example into Himalayan towns such as Darjeeling over the past decade.
Meanwhile, the Integrated Disease Surveillance Program in India also reports bimodal waves of influenza transmission and infections with respiratory syncytial virus (RSV) surge during the monsoon. These provide evidence that overlapping and compressed disease seasons are becoming more common.
Warming temperatures and erratic rainfall alter mosquito breeding cycles and pathogen incubation periods, while floods can create sudden transmission spikes in a population. On the other hand, rapid urbanization increases overlap among human, animal, and vector habitats. India is expected to have an urban population of close to 600 million by 2031. This will further intensify livestock density, land-use change, and human-wildlife contact, raising the risk of zoonotic spillovers.
As is evident globally now, global travel and trade will carry the pathogens across borders way faster than health systems can respond. Thus, reactive outbreak responses, of testing, isolating, and reporting only after cases show a surge, are strategically too slow. However, genomic and wastewater surveillance offer scalable alternatives. For example, such efforts in India could detect SARS-CoV-2 variants in sewage much before case counts rose in a population.
Similar experience has been gathered in cities like Bengaluru, wherein wastewater monitoring could track influenza and RSV circulation independent of individual testing. Artificial intelligence and machine learning models further add to the forecasting capacity. Modelling climate, land-use, and animal-movement data can flag likely zoonotic spillover risks well before an outbreak begins.
India's national zoonotic disease prioritization exercise and state-level One Health pilot studies in Gujarat and Rajasthan show that human, veterinary, and environmental data must be integrated. Such interdisciplinary cohort research, tracking populations across seasons and geolocations, can achieve usable forecasts integrating discrete data. Thus, building such predictive, One Health-oriented research and surveillance infrastructure will be imperative for India to achieve optimal pandemic preparedness.
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It has been long suspected that Western diets could contribute to the risk of colorectal cancer. The theory may finally have a clearer scientific explanation.
A new study suggests that gut bacteria can convert compounds produced by high-fat, low-fibre diets into cancer-causing chemicals. The research sheds light on how unhealthy eating habits may lead to cancerous tumour growth in colon in the long term.
Published in the journal Gut, the research was led by Dr. Annika Osswald (first author) and Dr. Soeren Ocvirk (corresponding author), along with a large team of international scientists.
The collaboration included researchers from Technical University of Munich (TUM), Germany, German Institute of Human Nutrition (DIfE), RWTH Aachen University, Freie Universität Berlin, University Hospital of Regensburg, and other institutions.
Researchers found that a western-style diet, which is commonly high in red and processed meat, saturated fats, refined carbohydrates and ultra-processed foods, significantly changes the composition of the gut microbiome.
These altered bacteria then modify bile acids in ways that promote inflammation and create an environment that accommodates the development of colorectal cancer tumours.
According to the researchers, diet alone is not the only factor. The trillions of microbes living in the intestine determine how food is processed, producing metabolites that can either protect the gut or damage it.
The study found that specific bacterial groups transformed bile acids into compounds that stimulated tumour growth in the colon.
This provides one of the strongestt explanations yet for why western dietary patterns have consistently been associated with higher risk of colorectal cancer.
"Our findings highlight the critical interaction between diet, gut microbes and cancer biology," the researchers noted, adding that targeting the microbiome could become a future strategy for preventing colorectal cancer.
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A western diet typically includes:
Previous research has repeatedly linked this eating pattern with obesity, diabetes, heart disease and colorectal cancer, but scientists have long found it challenging to explain the exact cause until now.
The human gut is home to trillions of bacteria that help digest food, regulate immunity and produce beneficial compounds like fatty acids.
A fibre-rich diet supports good bacteria that reduce inflammation, whereas diets high in fat and processed foods can cause microbial imbalance.
The new findings suggest this imbalance changes how bile acids are metabolised, increasing the production of molecules capable of damaging the colon and supporting cancer growth in the long run.
Also read: WHO Cancer Agency Flags 3 Common Medicines As Carcinogenic: What It Means For Millions Of Patients
Earlier research has linked harmful gut bacteria, including toxin-producing E. coli, with DNA damage that may begin early in life and contribute to the rise of colorectal cancer among younger people.
However, the latest findings do not prove diet alone causes cancer. Genetics, obesity, physical inactivity, sedentary life, smoking and alcohol consumption also influence risk.
However, they say maintaining a fibre-rich diet with fruits, vegetables, legumes and whole grains may help preserve a healthier gut microbiome and lower long-term colorectal cancer risk.
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Could air pollution may do more than harm the lungs and heart? A new study has found that exposure to polluted air could trigger painful flare-ups in people living with rheumatoid arthritis (RA).
The study comes when evidence is mounting that environmental factors contribute significantly to autoimmune diseases.
The study, published in the Annals of the Rheumatic Diseases, found that excessive exposure to air pollutants, particularly fine particulate matter (PM2.5), was associated with increased rheumatoid arthritis activity and a greater risk of flare ups.
Researchers say the findings suggest that improving air quality should become an important part of managing the chronic condition, alongside treatment, medications and lifestyle changes.
"Our findings highlight that environmental exposure, especially air pollution, may significantly influence rheumatoid arthritis disease activity and flare risk," the researchers said, noting that patients and clinicians should consider air quality as a modifiable risk factor.
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Rheumatoid arthritis is an autoimmune disease in which the immune system attacks healthy joints, causing pain, swelling, stiffness and, over time, permanent joint damage.
While genetics, smoking and infections have been recognised as risk factors, scientists are investigating how environmental pollutants may worsen the disease.
The latest findings are particularly relevant for countries such as India, where millions are exposed to unhealthy air for large parts of the year. Previous reports have already linked poor air quality in cities like Delhi to rising concerns over autoimmune diseases.
Also read: Severe COVID-19 Can Reactivate Dormant Viruses, May Fuel Long COVID Symptoms: Study
A flare is a period when rheumatoid arthritis symptoms suddenly worsen. During this time, people may experience:
Flares can last from a few days to several weeks and are often triggered by infections, stress, missed medications or other environmental factors.
Researchers believe tiny airborne particles like PM2.5 can enter the lungs and bloodstream, triggering inflammation throughout the body.
This inflammatory response may overstimulate the immune system, making rheumatoid arthritis symptoms worse and increasing the likelihood of painful flare-ups.
Also read:
The researchers emphasised that the study shows an association rather than proving that air pollution directly causes rheumatoid arthritis flares.
However, the consistent link suggests reducing exposure to polluted air may help lower the chances of flare-ups in high-risk individuals.
Experts advise patients to continue prescribed medications, constantly monitor local air quality, avoid outdoor activities during periods of severe pollution when possible, and discuss symptom changes with their rheumatologist.
The findings add to a growing body of research linking air pollution with autoimmune diseases.
Earlier studies have suggested that long-term exposure to pollutants may increase the risk of developing rheumatoid arthritis, while the new research indicates polluted air may also worsen symptoms in people already living with the disease.
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