If hand sanitisers kill 99.99% of germs, then who are those 0.01% who survive? There are three major kinds of germs which remain active even when you have used your sanitiser.
Among them, is the norovirus that causes diarrhoea and vomiting outbreaks in places like cruise ships and schools. It is superior to many other viruses because it has a protein capsid, which is resistant to the effects of alcohol.
Norovirus is a group of viruses that causes common illnesses and is also very contagious. It is especially active in the colder month and comes back seasonally. The first norovirus outbreak occurred in Norwalk, Ohio, USA, in a school in 1968, this is where it gets it name from.
The next on the list is enterococcus faecium, and it lives in the gut. As per a 2024 study titled Enterococcus faecium: evolution, adaptation, pathogenesis and emerging therapeutics, published in Nature journal, it is a Gram-positive bacterium that is a core member of the intestinal microbiota of humans and animals and an opportunistic pathogen that causes life-threatening infections, particularly among hospitalized patients. It mutates in a way that it absorbs carbohydrates and forms a gooey, slime-like substance called the biofilm, which makes it resistant to alcohol.
Another one is clostridium difficile. This is responsible for causing horrendous diarrhoea and vomiting in hospitalised patients. It also has a remarkable ability to respond to environmental stressors including alcohol gel by going to sleep. It produces spores and allows all metabolic activity.
Clostridium difficile (C. diff) is a type of bacteria that can cause colitis, a serious inflammation of the colon. Infections from C. diff often start after you've been taking antibiotics. It can sometimes be life-threatening.
Apart from the germs and pathogens, another reason why your label reads that it kills 99.99% is to avoid any legal hassles. If someone uses a specific product and falls sick, then the person cannot sue the company as the company did not give a 100% safety guarantee against the germs.
A better way to be healthy is always to clean your hands with soap and water and wear gloves wherever is possible.
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Marketed as a "harmless" alternative to cigarette smoking, vaping is increasingly emerging as a health concern, particularly for lung health, doctors warned ahead of World Lung Cancer Day on August 1.
Traditional cigarettes remain strongly linked to lung cancer, chronic obstructive pulmonary disease (COPD), and several other life-threatening illnesses. However, growing laboratory, animal, and population studies suggest vaping may also damage lung tissue, alter DNA, and potentially increase lung cancer risk—especially among people who both smoke and vape.
A recent study published in the peer-reviewed journal ERJ Open Research found that vaping may offer far less protection than many users believe when it comes to cardiovascular fitness, breathing efficiency, lung function, and blood vessel health in young adults.
"E-cigarettes are often advertised as a safer choice and as a way to help people quit smoking. But the evidence behind these claims is weak. We still don't fully know what long-term damage e-cigarettes can do to the lungs, including whether they can cause lung cancer," Dr. Shiba Kalyan Biswal, Head of Pulmonology at Shalby International Hospital, Gurugram, told HealthandMe.
The vapor produced by e-cigarettes contains several harmful chemicals, including substances that can damage cells and DNA—the genetic material inside the body's cells.
Animal studies have found that mice exposed to e-cigarette vapor for about a year developed a type of lung cancer. Ingredients commonly used in e-cigarette liquids, such as propylene glycol and benzoic acid, may also irritate cells and trigger inflammation in the lungs.
"There have also been outbreaks of a serious vaping-related lung disease that has sent people to hospital with severe breathing problems. This shows that the risks of vaping can be unpredictable, especially when products are poorly regulated or contain unknown ingredients," Dr. Biswal explained.
She urged doctors to routinely ask patients about e-cigarette use, particularly those with breathing problems or those at higher risk of lung cancer.
"Since evidence suggests that e-cigarettes add to the risk for people who used to smoke, it may be worth including vaping history when deciding who needs lung cancer screening," she said.
According to Dr. Biswal, lung cancer risk appears to be even higher among people who use both e-cigarettes and conventional cigarettes, often referred to as "dual users."
Many smokers who turn to e-cigarettes intending to quit end up continuing to use both products rather than switching completely.
"This means they stay addicted to nicotine and may be exposed to even more harmful substances."
Doctors are also reporting more lung cancer cases among young people who have never smoked, particularly women.
Indoor air pollution, biomass fuel exposure, second-hand smoke, occupational hazards, and genetic susceptibility are increasingly contributing to the disease, said Dr. Akshay Budhraja, Senior Consultant and Head of Respiratory and Sleep Medicine at Aakash Healthcare.
"It's no longer just the lifelong smoker in his sixties—we are seeing younger patients, more women, and a growing number who have never touched a cigarette. Air quality, occupational exposure and genetic predisposition are all playing a bigger role than they used to, and that means our screening approach has to widen well beyond the traditional smoker profile," Dr. Budhraja said.
Experts said early detection through low-dose CT screening remains crucial for high-risk individuals. However, symptoms such as a persistent cough or breathlessness are often mistaken for pollution-related irritation or a lingering infection, leading many people to delay getting screened.
They also noted that lung cancer affects more than the lungs, with potential impacts on men's sexual health and women's reproductive health.
According to the World Health Organization (WHO), lung cancer remains one of the world's biggest public health challenges due to its high incidence and mortality. In 2024, it was the leading cause of cancer-related deaths globally, with an estimated 2.6 million new cases and 1.8 million deaths.
Lung cancer develops when abnormal cells grow uncontrollably in the lungs. Treatment depends on a person's medical history and the
stage of the disease.
The doctors stressed that avoiding tobacco remains the most effective way to reduce lung cancer risk.
"Smokers face nearly 20 times the risk of non-smokers, though the rising non-smoker caseload complicates that picture," said Dr. Budhraja. "Second-hand smoke is the third leading cause of lung cancer among non-smokers; radon gas, seeping in from soil, is the leading one, and home testing kits can catch it."
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I've spent over three decades treating heart disease, and in that time, I've seen the same misunderstanding come up again and again, across different patients, different generations, different backgrounds. It's the one that delays diagnosis more than any other. Ask most people what menopause changes, and they'll talk about hot flashes, mood swings, or sleep. Ask me, and I'll tell you it changes something just as important: a woman's heart.
I believe menopause should be treated as a cardiovascular milestone, not just a reproductive one. We talk to women a great deal about bone density, hormonal symptoms, and fertility. We talk far less about what's happening quietly inside their arteries during this same period. That gap in the conversation is costing us early diagnoses. In some cases, it's costing lives.
To understand why, it helps to look at what protects a woman's heart in the first place. For most of her reproductive years, estrogen acts almost like a quiet guardian in the background, keeping the endothelium — the inner lining of blood vessels — working well, and supporting the release of nitric oxide, which helps arteries stay relaxed and open. This is a big reason heart attacks are fairly uncommon in women before menopause, compared to men of a similar age.
Menopause takes that buffer away, slowly, not all at once. The shift usually starts during perimenopause, often well before periods actually stop. LDL, the harmful cholesterol, tends to rise; HDL, the protective kind, often falls. Blood pressure that used to be easy to control starts creeping higher. Arteries stiffen, insulin resistance sets in, and fat tends to shift toward the belly, carrying its own inflammatory effect on blood vessels. None of this feels dramatic on any single day. It just builds, quietly, year after year — enough that by ten to fifteen years past menopause, a woman's heart risk has often caught up to, and sometimes overtaken, a man's of the same age.
Also read: Lifestyle Genetics And Hormones: Understanding The Interplay Of Risk Factors For Ovarian Cancer
Some argue this is simply age catching up, and that menopause gets blamed unfairly. There's truth in that — age alone stiffens arteries in everyone. But in my experience, losing estrogen compresses those changes into a much shorter stretch of time. It isn't one factor or the other; it's ageing, sped up by a hormonal shift arriving right in the middle of life.
That said, menopause alone doesn't determine a woman's future with heart disease. It sets the stage, but daily habits decide how the story plays out. Smoking, inactivity, weight around the middle, a diet heavy in processed food, unchecked blood pressure and blood sugar, chronic stress, poor sleep, and skipped check-ups all add their share. The reassuring part is that nearly everything on that list can be changed. I've watched patients shift their own trajectory with fairly ordinary steps — walking regularly, eating simply, sleeping better, getting basic tests done once a year.
Also read: Mood Swings, Anxiety & Brain Fog During Menopause? Expert Recommends Looking Beyond Hot Flashes
What troubles me most in practice is how often real cardiac symptoms get mistaken for "just menopause." Chest pressure rather than sharp pain. New breathlessness during simple activity. Fatigue that doesn't lift with rest. Pain in the jaw, upper back, or between the shoulder blades instead of the classic left-arm pain. Palpitations that don't settle. A few months ago, a woman in her early fifties came to me convinced she had acidity — tightness in the chest, breathlessness on stairs, an occasional fluttering heartbeat. An angiogram showed a significant coronary blockage. "I thought heart problems were a man's disease," she told me. I hear some version of that sentence often, and it worries me every time.
My advice to patients is simple: perimenopause is the right time for an honest conversation with a doctor about the heart, not after something has gone wrong. That means a blood pressure check, a proper lipid profile, blood sugar and HbA1c testing, and a baseline ECG — with an echocardiogram, stress test, or coronary calcium score for those with added risk factors.
Menopause changes a great deal about a woman's body. Her heart is one of those things, whether she's thinking about it or not. Don't wait for a scare to start the conversation. Start it now, while there's still so much you can do.
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For decades, many cancer patients in India have lived with a frightening belief — that a biopsy can make cancer spread. This misconception continues to delay diagnosis, often costing patients the opportunity for timely treatment. This is one of the most common fears I encounter in clinic.
Almost every week, someone tells me, 'Doctor, if you cut it, it will spread.' Families repeat it, neighbors reinforce it, and patients postpone the test. Actually, this concern is linked to a genuine scientific phenomenon known as needle-tract seeding. These phenomena suggest that a few tumor cells may be displaced along the path of the biopsy needle.
However, this event is extremely uncommon and should not be confused with cancer spreading. Seeding is not the same as spreading. A few displaced cells sitting in a needle track are not a metastasis.
Published studies estimate the risk of needle-tract seeding to be extremely low. A 2015 systematic review reported the overall incidence to be below one percent, while more recent reviews, including a 2024 analysis of breast needle biopsy, found no evidence that diagnostic biopsies increase cancer recurrence or reduce long-term survival.
If tumor cells are displaced during a biopsy, they are usually removed when the tumor is surgically excised. In many cases, radiotherapy, systemic treatment and the body's own immune system also eliminate these cells.
In many tier-two and tier-three cities, it takes two to three weeks to reach final report to the treating doctor. During that period, the untreated cancer continues to grow naturally. The patient does not see natural history. He sees cause and effect. The biopsy happened; the lesion grew. The conclusion writes itself — and it is wrong. This delay unintentionally reinforces the misconception that the biopsy triggered the growth, when in reality the cancer was progressing on its own.
At the same time, every tissue injury, including a biopsy, activates the body's wound-healing response, leading to inflammation and new blood vessel formation. Laboratory and animal studies suggest that this temporary inflammatory environment may favor tumor cells. However, these findings have not translated into poorer outcomes for patients. So, the fear is not irrational. It is simply misdirected, and it is mis proportioned.
The diagnosis is not the danger. The delay is. Biopsy helps precision oncology. It helps deciding the treatment approach. Without this we would be treating in the dark.
The consequences of delaying diagnosis are serious. Patients of oral cancer diagnosed while the disease is still localized have a five-year survival rate of nearly 79 per cent. Once the cancer spreads to distant organs, survival drops to around 19 per cent. Unfortunately, nearly two-thirds of oral cancer patients in India are still diagnosed at an advanced stage.
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