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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.
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.
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.
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.
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Every year on July 6, we mark World Zoonoses Day. The date marks the day in 1885 when Louis Pasteur gave the first rabies vaccine. It falls right in the middle of our monsoon, which is exactly when zoonotic diseases claim the most lives. So this year, instead of a routine health advisory, let us go through the questions I get asked most often, by patients, by family, and honestly, by fellow doctors too.
A zoonosis is any disease that spreads from animals to humans. The animal could be a rat, a dog, a bat, or even livestock in your backyard. Sometimes the animal itself looks perfectly healthy while carrying the germ that makes us sick. About six out of every ten infectious diseases known to affect humans started in animals at some point. COVID reminded the whole world of this. We have been living with zoonotic threats for years, quietly, every rainy season.
If I had to list the usual suspects, it would be this:
Leptospirosis is the one that rises sharply and predictably every single monsoon. The bacteria live in the kidneys of rats and other rodents and are released into soil and water through their urine. When the rains come, our fields, drains, and waterlogged roads become the perfect place for the infection to spread. Anyone walking barefoot through flood water, working in paddy fields, or wading through stagnant water near their home is at risk.
Scrub typhus rises a little later, once the rain eases and people go back into overgrown fields and gardens to clear vegetation, exposing themselves to the mite larvae hiding there. Our own data from KIMSHEALTH, based on 241 patients over seven years, shows this pattern clearly. Cases start climbing in September, peak in December, and drop off by January.
This means the disease follows the cool, humid weeks right after the monsoon leaves, not the rainy months themselves. Low temperature and high humidity suit the mites best, which is why the weeks just after the monsoon, not the heavy rain itself, are scrub typhus season. Our data also showed a smaller rise between June and August, so the risk is actually spread across two windows around the monsoon, not just one.
This year, our own health department figures have already shown this pattern. Fever clinics across the state have been seeing well over 10,000 patients a day at the peak, with leptospirosis and Shigella infections climbing sharply. Northern districts of Kerala Kannur, Kozhikode, and Malappuram have reported some of the sharper spikes, and rat fever sadly remains the biggest killer among these in most years.
Nipah is not strictly a monsoon disease. It tends to appear when fruit bats are under stress, often during their breeding season or when their natural food is disrupted. Kerala has had confirmed cases in recent years. The good news is that Kerala now has one of the fastest outbreak response systems in the country for Nipah, with quick contact tracing and isolation.
For leptospirosis:
For scrub typhus:
For rabies:
See a doctor without delay if you have a fever along with any of the following:
Leptospirosis in particular can look just like an ordinary viral fever in its first two or three days, and then get worse quickly, leading to kidney failure or bleeding problems. Starting antibiotics early makes a big difference to the outcome. This is not a disease where it is safe to simply wait and watch.
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With less time and more work, chronic fatigue has become a moniker of modern society. However, this not only reduces the quality of life but also constitutes a social issue that affects work efficiency and leads to accidents. On the surface, the cause of fatigue is often attributed to not getting enough rest, but there may be another underlying issue—the lack of proper nutrition.
The world moves at a hectic pace these days. If you feel like you're constantly running on empty, you're not alone. Many people say that they just don't have the energy they need to accomplish all they need to. Sometimes the cause of fatigue is obvious — for example, getting over the flu or falling short on sleep. Sometimes a vitamin deficiency is part of the problem. It might be worth asking your doctor to check a few vitamin levels, such as the three we've listed below.
Anemia occurs when there aren't enough red blood cells to meet the body's need for oxygen, or when these cells don't carry enough of an important protein called hemoglobin. Fatigue is usually the first sign of anemia. A blood test to measure the number of red blood cells and the amount of hemoglobin can tell if you have anemia. The first step in shoring up your body's iron supply is with iron-rich foods (such as red meat, eggs, rice, and beans) or, with your doctor's okay, over-the-counter supplements.
Your body needs sufficient vitamin B12 in order to produce healthy red blood cells. So a deficiency in this vitamin can also cause anemia. The main sources of B12 are meat and dairy products, so many people get enough through diet alone. However, it becomes harder for the body to absorb B12 as you get older, and some illnesses (for example, inflammatory bowel disease) can also impair absorption. Many vegetarians and vegans become deficient in B12 because they don't eat meat or dairy. When B12 deficiency is diet-related, oral supplements and dietary changes to increase B12 intake usually do the trick. Other causes of B12 deficiency are usually treated with regular injections of vitamin B12.
A deficit of this vitamin can sap bone and muscle strength. This vitamin is unique in that your body can produce it when your skin is exposed to sunlight, but there also aren't many natural food sources of it. You can find it in some types of fish (such as tuna and salmon) and in fortified products such as milk, orange juice, and breakfast cereals. Supplements are another way to ensure you're getting enough vitamin D (note that the D3 form is easier to absorb than other forms of vitamin D).
Taking this into account, a research group led by Professor Hiroaki Kanouchi at Osaka Metropolitan University's Graduate School of Human Life and Ecology focused on nutritional status and water-soluble vitamin deficiencies found in unbalanced diets. The team hypothesized that a lack of folate (B9) and vitamin B12 may be related to fatigue, and centered their research around homocysteine (Hcy), a biomarker known to increase when these deficiencies are present.
Blood concentrations of Hcy, folate, and vitamin B12 in approximately 600 healthy Japanese participants were measured. Participants' fatigue and motivation were assessed using the Chalder Fatigue Scale questionnaire and the Visual Analog Scale. The initial results showed that individuals with higher blood Hcy levels had lower levels of vitamin B12 and folate, regardless of sex.
The researchers then examined the relationship between homocysteine levels and fatigue separately for men and women. In their analysis, factors that may influence fatigue, such as age, sleep duration, workload, and dietary habits, were simultaneously accounted for.
The results revealed that higher Hcy levels were associated with greater physical fatigue in men, while higher levels were associated with decreased motivation in women.
(Dr Alex Mathew, Senior Consultant – Internal Medicine, Max Super Speciality Hospital, Patparganj)
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A casual match still feels like exercise. For a heart that has not been conditioned to meet sudden, competitive demand, it can briefly become something closer to a stress test it never agreed to take. The risk lies less in the sport itself than in how unprepared the body is for it.
For Sunday mornings across recreational pitches host a familiar ritual: amateur footballers, most with desk jobs and six quiet days since their last real exertion, sprinting straight into competitive play. From the sideline, the scene reads as a picture of health, a weekly act of discipline squeezed into a busy schedule. Beneath that surface, the cardiovascular system experiences something closer to an ambush than a workout.
This is the territory of the so-called weekend warrior, an individual whose physical activity arrives in concentrated, high-intensity bursts rather than a steady weekly rhythm, with a heart and coronary arteries rarely tested anywhere near as hard as they are about to be for the next ninety minutes.
Working skeletal muscle during competitive football consumes oxygen at a rate many times its resting baseline, since contraction and sustained movement depend on aerobic metabolism and a steady oxygen supply.
To meet that demand, the heart itself must work harder: heart rate and contractile force both rise, meaning the heart muscle, the myocardium, needs more oxygen simply to keep pumping blood to the rest of the body.
Under normal circumstances, the coronary arteries that feed the heart respond by dilating, widening to allow greater blood flow exactly when it is needed most. That system performs well when demand rises gradually. Sudden maximal exertion, the kind that defines an unplanned sprint for a loose ball, can push myocardial oxygen demand upward by as much as fivefold almost instantly, leaving far less margin for the coronary circulation to compensate, particularly if the vessels are not entirely healthy to begin with.
Roughly one in five sudden cardiac deaths overall occur during or immediately after physical exertion, underscoring exercise's specific role as a trigger rather than simply a background risk. That role intensifies when vigorous activity follows a long stretch of inactivity, which describes the typical week of a recreational footballer far more than a trained athlete's training calendar.
The sequence generally begins with sympathetic nervous system activation: a surge of stress hormones, principally adrenaline, released the moment competitive exertion begins. This catecholamine surge raises heart rate and blood pressure almost immediately, driving myocardial oxygen demand upward at the moment the heart is least prepared for it.
The same surge can act on the coronary arteries directly, provoking constriction or spasm rather than the dilation exercise normally calls for, a paradox that includes rare stress-related conditions such as Takotsubo syndrome. For someone carrying an often undiagnosed plaque burden, a narrowing in the range of 25 to 50 percent of the vessel, this combination can convert a previously silent lesion into one that becomes hemodynamically significant under load. What follows is demand ischemia: a mismatch between the oxygen the heart needs and what the coronary circulation can deliver, arising not because a vessel has abruptly blocked but because demand has outrun supply.
In some cases, this transient oxygen deprivation is severe enough to qualify as a Type 2 myocardial infarction, distinct from the more familiar plaque-rupture heart attack but no less serious.
Risk concentrates most heavily among adults who are otherwise sedentary, since their cardiovascular systems have had no recent opportunity to adapt to exertion, and among those carrying undiagnosed coronary artery disease that produces no symptoms until it is tested by genuine physical stress. Diabetes, hypertension, a history of smoking, obesity, and elevated cholesterol all raise the likelihood that some degree of coronary plaque exists before a single whistle blows. This is a meaningfully different population from trained athletes.
Notably, even habitually active masters-level endurance athletes can show a higher prevalence of coronary atherosclerosis than sedentary peers with similar risk profiles, though their plaques tend to be more stable, which may blunt rupture risk. The weekend warrior, by contrast, often brings unmanaged risk factors and an unconditioned cardiovascular system to the same ninety minutes.
Clinical guidance translates into a handful of concrete principles. Progressive conditioning, building tolerance gradually rather than asking an unconditioned heart to meet maximal demand in a single afternoon, is foundational, alongside regular weekly activity rather than sporadic, all-or-nothing bursts. Easing into intensity rather than launching directly into competitive sprinting gives the cardiovascular system time to adjust.
For adults with elevated risk, particularly relevant family history, multiple risk factors, or symptoms during past exertion, screening, a physical examination, a resting ECG, and, in some cases, formal exercise testing, can surface disease before it is exposed on the pitch. Equally important is recognizing warning signs that should end a match rather than be played through: chest discomfort, disproportionate breathlessness, an unexplained drop in pace, palpitations, or impaired consciousness.
With those precautions, a safe return to recreational sport remains achievable for most adults, including many with treated cardiovascular risk.
None of this indicates football, or recreational sport more broadly. The danger lies not in the game itself but in asking an unconditioned cardiovascular system to absorb sudden, maximal physiological stress without preparation. The heart adapts well to demands placed on it steadily and repeatedly. It adapts far less gracefully to demands sprung on it once a week, after six days of stillness. Consistency, not occasional intensity, is what ultimately protects it.
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