Many of us may have taken ibuprofen, sometimes two pills at once, especially when we are struggling with menstrual cramps. Well, as good these pills may be in treating the pain, they are not recommended for your health, especially if you are someone who consumes it on a daily basis or frequently. Gastroenterologist Trisha Pasricha, MD, writes in The Washington Post about why should you avoid taking nonsteroidal anti-inflammatory drugs, or NSAIDs, such as ibuprofen, naproxen and aspirin.

What happens when you consume pain killers?

She writes that NSAIDs are great in treating short term pain. They comprise of a group of drugs that inhibit the production of prostaglandins, which serve as a variety of purposes in the body. Some of which also includes contracting the uterus during menses and regulating blood flow in our vessels.

While one to two doses every now and then is okay, following a regular dosage routine, which could range from several times a month, or twice in an hour or so could lead to health risk. NSAIDs are well known to increase intestinal permeability. This means, these painkillers could damage the lining of your gut.

A 2018 review by Ingvar Bjarnason et. al., also writes about how NSAIDs can reduce the blood flow in the tiny vessels that feeds our guts. It can also disrupt the intestinal cells forming a barrier between the outside world and your insides.

What can be done?

While people with conditions like migraines, chronic back pain or bad period cramps can find NSAIDs to be helpful. It is always advisable to have a chat with your physicians to explore NSAID alternatives.

Pasricha suggests acetaminophen.

However, if someone is in dire need of NSAID, her tip is to take the pill right at the start of your symptoms. She says that the drug can do a far better job at stopping things at the source than chasing after all prostaglandins.

Why is it a concern?

NSAIDs are available as over the counter drug, which means people do not need a prescription for it and can make medical decision about them without the guidance of a physician.

A 2018 study published in the Official Journal of the International Society for Pharmacoepidemiology by David W Kaufman, et.al., found that 15% of adult ibuprofen users in the US have exceeded the maximum recommended daily dose. The study also mentions that more than a third of ibuprofen users were taking other NSAIDs, like aspirin and naproxen, while consuming ibuprofen at the same time. Out of these, 61% did not realise that they were using NSAIDs.

Pasricha talks about how it ruptures the gut wall, as she herself has rushed to the hospital in the middle of the night "far more times than" she can count "to perform an emergency endoscopy on someone who was bleeding profusely from an ulcer caused by NSAID".

Another 2009 study published in the American Journal of Gastroenterology states that as many as 1 in 4 chronic NSAID users will get an ulcer and about 4% will bleed or rupture through the gut wall.

An older study from 2005 titled A quantitative analysis of NSAID-induced small bowel pathology by capsule enteroscopy, found that as 75 percent of people regularly using NSAIDs develop low-grade inflammation in their small bowels. NSAIDs can also lead to development of fatty liver disease. This happens because your gut lining becomes more permeable, more toxins and bacteria from the outside world enters your liver and leads to inflammation.

A 2011 study titled Haemoglobin decreases in NSAID users over time: an analysis of two large outcome trials, states that as many as 6% of people taking NSAIDs regularly have found their blood count dropping within a few months of starting the medicines, this suggests that this is due to the small, slow amount of bleeding in the gut overtime.

Climate change caused a 10 per cent global increase in Salmonella antibiotic resistance genes between 1940 and 2023, according to the first-of-its-kind study published in The Lancet Planetary Health journal today.

Antimicrobial resistance (AMR) is mainly driven by the overuse and misuse of antibiotics, which allows resistant bacteria to survive and spread.

However, rising temperatures and changing rainfall patterns can influence how bacteria survive, mutate, and spread, potentially increasing the exchange of antibiotic resistance genes.

“The accumulated evidence suggests that climate change is an accelerating force behind the global spread of antimicrobial resistance,” the study authors wrote in the paper.

What Are The Findings?

The study provides supporting evidence that AMR doesn’t just increase steadily as temperatures rise, but that the number of resistance genes changes over time in a more complicated way, depending on both temperature and rainfall. This suggests that environmental changes can speed up how bacteria adapt to antibiotics.

“These findings reinforce the idea that climate change alters microbial ecological stability and accelerates resistance evolution across human, animal, and environmental reservoirs," said the global researchers.

How Was The Study Conducted?

The current study analyzed the genomes of more than 480,000 Salmonella samples from 139 countries, collected between 1940 and 2023, and compared levels of antibiotic resistance genes with changes in average temperature and rainfall over time.

Of the total, 82 per cent of countries saw increases in antibiotic resistance genes in Salmonella, with the strongest climate-associated increases occurring in the Middle East and North Africa, followed by South Asia and Sub-Saharan Africa.

While the study shows a link between climate change and antibiotic resistance genes in Salmonella, it does not prove that climate change directly causes the increase.

The study also used a model to predict the change in antibiotic resistance genes in Salmonella by 2100 under different climate emissions scenarios.

The model suggests that if countries meet low-emission climate targets and strengthen efforts to use antibiotics responsibly, levels of resistance genes could be 24% lower than under the highest-emission scenario. However, they caution that these projections, as with all models, involve uncertainty.

The researchers stressed the need to consider climate change when monitoring and addressing AMR. They add that stronger climate action, alongside responsible antibiotic use and improved disease surveillance across humans, animals, and the environment, will be important in limiting the future spread of AMR.

What Is Salmonella?

As per the US Food and Drug Administration (FDA), Salmonella is a group of bacteria that can cause gastrointestinal illness and fever called salmonellosis. It can be spread by food handlers who do not wash their hands and/or the surfaces and tools they use between food preparation steps. It can also happen when people consume uncooked and raw food. Salmonella can also spread from animals to people.

Common symptoms of Salmonella include

• diarrhea,
• fever,
• stomach cramps 6 hours to 6 days after being exposed to the bacteria.

Children younger than 5, adults 65 and older, and people with weakened immune systems are more likely to have severe illness.

Indian summers are not just uncomfortable; they are becoming increasingly dangerous. With temperatures frequently crossing 45–48°C, heatwaves are putting excess stress on the human body, which hitherto had not experienced this level of heat strain. Now, add smoking to this already hostile environment and, like adding fuel to a fire, two harmful components combine to multiply the damage. Dr Shubham Garg, Director of Surgical Oncology, Dharamshila Narayana Superspeciality Hospital, Delhi, spoke about the risks of stepping out to grab a smoke during extreme heatwaves.

Smoking during heatwaves doesn’t just worsen existing risks; it accelerates dehydration, strains the heart, damages the lungs, and pushes the body closer to heat exhaustion or heatstroke. Here’s why lighting up in extreme heat is far more dangerous than most people realise.

Heatwaves Already Stress the Body—Smoking Adds Fuel to the Fire

When temperatures soar, your body works overtime to cool itself. A host of processes happen to aid in this—your blood vessels dilate, there could be an increase in heart rate, and sweating intensifies in order to regulate body temperature. When you smoke, it interferes with these very natural defense mechanisms of your body.

Nicotine results in vasoconstriction—narrowing of blood vessels—which makes it very difficult for the body to release heat trapped inside. The carbon monoxide from cigarettes reduces oxygen delivery to tissues. The result? Less oxygen reaches your organs, which are, in fact, working harder in the extreme heat. This is a perilous combination that can affect the body in many ways.

Dehydration Happens Faster Than You Think

A heatwave leads to sweating and, consequently, loss of fluids and electrolytes. And when you go for smoking a cigarette, it leads to fluid loss and delayed hydration. Nicotine acts as a mild diuretic, which contributes to increased fluid loss. Smoking also suppresses thirst signals, thus delaying hydration.

Collectively these factors raise the risk of severe dehydration, which can trigger dizziness, muscle cramps, low blood pressure, and confusion—all of which are early signs of heat exhaustion. Many smokers ignore these signs or dismiss them altogether.

A Deadly Mix for the Heart

Cardiovascular strain can happen independently through either smoking or heat. That in itself is a threat one should keep an eye out for. However, when combined, they pose a compelling risk of:

1. Sudden spikes or drops in blood pressure
2. Irregular heart rhythms
3. Heat-induced cardiac events

During extremely hot weather conditions, especially during a heatwave, the heart has to exert more effort to maintain circulation and cooling in the body. Smoking elevates heart rate and blood pressure further while also thickening the blood and increasing the risk of heart attacks and strokes, especially in people with pre-existing diabetes, hypertension, or heart disease.

Lungs Struggle More in Hot, Polluted Air

Hot weather is bad for air pollution levels too, as it traps smoke, dust, and harmful gases close to the ground. When one smokes in these conditions, it severely compromises lung function:

1. Airways become inflamed and constricted
2. Oxygen exchange efficiency drops
3. Symptoms like breathlessness, coughing, and chest tightness worsen

For people with asthma, COPD, or other respiratory conditions, smoking during a heatwave is likely to trigger severe flare-ups and emergency hospital visits.

Heat + Smoking Accelerates Ageing and Skin Damage

Extreme heat is damaging not just for the heart but for the skin as well. The skin becomes dehydrated, and collagen breaks down. Smoking compounds this damage by reducing blood flow and oxygen supply to the skin.

The result:

1. Faster wrinkles and sagging skin
2. Increased pigmentation and dullness
3. Delayed healing of rashes, infections, and sun damage

In short, smoking during summer doesn’t just harm internal organs; it visibly accelerates the ageing process.

Higher Risk of Heat Exhaustion and Heatstroke

Smoking reduces the body’s ability to regulate temperature effectively. This makes smokers more vulnerable to heat exhaustion (fatigue, nausea, headache, dizziness) and heatstroke (confusion, collapse, organ failure).

Heatstroke is a medical emergency and can be fatal if not treated promptly. Smokers often misread early warning signs as ‘normal summer weakness,' thus delaying care.

Why Cutting Down Isn’t Enough

Many smokers try to “reduce” smoking during summer. While any reduction helps, heatwaves are one of the worst times to smoke at all. Even a few cigarettes can significantly increase physiological stress when temperatures are extreme.

Smoking during heatwaves is not just bad—it’s dangerously synergistic. If there ever is a time to quit, or at least pause, this should be it. Because in peak summer, smoking doesn’t just harm you slowly. It fast-tracks damage, turning heat into a silent but serious health threat. In extreme heat, choosing not to smoke isn’t just a lifestyle choice—it’s a life-saving one.

When the heart stops functioning, time doesn’t stop with it. In cases of cardiac arrest, time serves as one of the most decisive factors between survival and irreversible loss. Within a couple of seconds, the body starts losing its oxygen supply. In a few minutes, the brain starts to suffer damage. And with each passing minute without intervention, the chances of survival reduce significantly.

This severe reality is at the centre of what Dr Ankit Desai, Paediatric Anaesthetist and Founder & Director of Children’s Anaesthesia Services, explains as “a race against biological shutdown — one where the bystander is the only lifeline”.

The silent collapse: what happens in cardiac arrest

Several people have the misconception that cardiac arrest is similar to a heart attack, but they are very different. A heart attack is a circulatory issue where the heart might still be beating. However, in cases of cardiac arrest, there is an electrical failure, and the heart suddenly stops pumping blood effectively.

Whenever this occurs, blood flow to the brain and other vital organs ceases immediately. The oxygen reserves in the brain are extremely limited and typically last for about 4 to 6 minutes before any permanent injury occurs.

This is where the concept of time sensitivity becomes more important. For every passing minute without CPR or defibrillation, the chances of survival drop by approximately 7–10%. By the time 10 minutes have elapsed without intervention, survival is extremely unlikely in most cases.

“The tragedy is not just the cardiac arrest itself,” explains Dr Desai, “but the silence that follows — when no one knows what to do or hesitates too long to act.”

The brain’s narrow window of survival

The brain is the first organ to be affected during cardiac arrest. Neurons are highly sensitive to oxygen deprivation. Brain cells start to malfunction within 3 minutes. By 5 minutes, the damage starts becoming increasingly severe. Beyond 10 minutes, the chances of meaningful recovery drastically reduce. This is why immediate CPR is not just a supportive measure but a bridge that keeps oxygen flowing artificially until a normal rhythm can be restored.

Chest compressions manually pump blood to the brain and heart, delaying cell death.

Why bystander action matters more than ambulance time

Emergency medical services, even in well-equipped systems, often take several minutes to reach a patient. In urban areas, response times may be shorter, but they are rarely instantaneous. In cardiac arrest, those minutes matter more than any hospital intervention.

Dr Desai emphasises that “the first responder is almost always not a doctor — it is a family member, a colleague, or a nearby stranger”.

This makes bystander CPR the most critical determinant of survival. Studies consistently show that when CPR is initiated immediately, survival rates can double or even triple compared to cases where no bystander action is taken.

Yet fear, hesitation, and lack of training remain major barriers. Many people worry about performing CPR incorrectly, causing harm, or being held legally responsible. In reality, doing nothing is far more dangerous than taking imperfect action.

The Chain of Survival: breaking down the timeline

Medical professionals often refer to this situation as the “Chain of Survival”, which includes early detection of cardiac arrest, immediate CPR, rapid defibrillation (AED use), advanced medical care, and post-resuscitation support. Every link in this chain is highly time-sensitive. Any delay in one step weakens the entire outcome. The strongest determinant, however, remains the second step — early CPR.

Automated External Defibrillators (AEDs), if available, can help restore a normal heart rhythm if used quickly. But again, their effectiveness decreases sharply with delay. The combination of CPR and early defibrillation within the first few minutes offers the best chance of survival.

Why awareness changes everything

The key difference between life and death is less about complexity and more about readiness.

Awareness training helps transform bystanders into responders. A person who knows how to identify cardiac arrest — unresponsiveness, absence of breathing, sudden collapse — is far more likely to act immediately rather than wait.

Dr Desai highlights a critical cultural gap: “We often associate medical emergencies with hospitals. But cardiac arrest begins in living rooms, offices, gyms, and streets. The response must begin there, too.”

Basic CPR training takes less than an hour to learn, but can influence outcomes for decades. Schools, workplaces, and community programmes play a vital role in normalising this skill.

Overcoming hesitation: the psychological barrier

One aspect of cardiac arrest that often gets overlooked is human hesitation. Bystanders often freeze due to shock and uncertainty. Some assume that someone else will step in. Others underestimate the severity of the situation.

Public awareness campaigns help highlight the simplicity of CPR, which helps overcome this barrier. Hands-only CPR focuses on continuous chest compressions without mouth-to-mouth breathing, making intervention much easier and more accessible. The message is simple: push hard, push fast, and don’t stop until help arrives.

A shift from reaction to preparedness

Cardiac arrest survival is not just a medical issue, but also one of public preparedness. The Chain of Survival starts long before the emergency happens. It starts with education, confidence, and awareness.

Dr Desai states that “if more people understood how little time they truly have, more lives would be saved not by hospitals, but by ordinary people doing extraordinary things in the first five minutes”.

Conclusion: time is the real patient

In cardiac arrest, the patient is not just the person who collapses — it is time itself. Every second lost reduces the chance of recovery. Every trained bystander becomes a potential lifesaver. The science is clear, the timeline is unforgiving, and the solution is remarkably simple: act immediately, compress the chest, and keep blood flowing until professional help arrives.