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Imagine this. A young teenager, 17, years old, who is fully developed. Now imagine this, the same teenager has a fully developed extra set of limbs and a pelvis. That extra set of pair is attached with chest artery. But, how can this happen?
While it is extremely rare, and has a chance of less than one case occurring per 100,000 births. Such things do happen. This is called parasitic twin.
It is an extremely rare type of cojoined twin where a baby is born with an underdeveloped twin attached to its body. This condition is also known as vestigial twins. The condition is very closely related to conjoined twins, where babies are connected at birth and share organs. However, the main difference is that in conjoined twins, there are two developed babies, whereas in parasitic twins, only one is fully developed, other one is underdeveloped and non functional.
In such a case, the twin who is developed is medically known as the autositic or the dominant twin. The dominant twin is healthy in most aspect but may have extra tissue, organs, or limbs from the parasitic twin.
The parasitic twin may be attached with the dominant twin through several places. The common joints are at the head, torso, chest, pelvis, buttocks, or back. In these cases, the parasitic twin is not alive and they die either in the womb or during the childbirth.
Now, let's go back to the case we referred to, where a young teenager had an extra pair of limbs attached to chest. The teenager who has not been named is from Uttar Pradesh's Unnao neighbourhood, and was treated in AIIMS, Delhi. The team of doctors successfully removed the extra set of limbs from his body.
Dr Asuri Krishna, who led the team of specialist who surgically removed the extra limbs told the BBC that only 40 to 50 cases of parasitic twins have been documented in world medical literature, and in those cases, the surgery had been attempted on children. The doctor said that without much medical literature to guide them, the team of doctors depended on "intuition, skill and knowledge".
The doctor shared that the child had two fully formed legs, buttocks and external genitalia, which weighed around 15kg "protruding from his abdomen".
The doctor shared that first they identified how interconnected the parasitic and host twins were. The doctors took scans and found that parasitic twin was attached to the teen's breastbone. The blood was being supplied from a vessel in his chest. However, "there wasn't much connection with other main organs like the liver or kidneys," said Dr Krishna. The team also found a large cyst in the teen's abdomen.
Then the surgery was performed in two stages. In the first stage, the parasitic twin was removed. Then the cystic mass was extracted from the surrounded area. The entire surgery was completed in two and a half hours and the team of doctors included radiologists, anaesthetists, and plastic surgeons.
The biggest challenge was when the teen's blood pressure dropped as 30 to 40% of his blood flowed to the parasitic twin, however, the doctors were prepared for it and they stabilized him.
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Obstructive hypertrophic cardiomyopathy (oHCM) remains one of the most misunderstood cardiac conditions, despite being the most common inherited cardiomyopathy. Misconceptions around the disease often lead to fear, delayed diagnosis, and hesitation in seeking appropriate medical care.
While oHCM has historically been associated with sudden cardiac death, particularly in young athletes, advances in diagnosis and treatment have significantly transformed its management. Today, with early diagnosis and appropriate treatment, many patients can lead active and fulfilling lives.
Understanding the facts is essential, not only for patients living with the condition, but also for families, caregivers, and the wider community. Separating myths from medical evidence can help ensure timely diagnosis, informed treatment decisions, and better long-term outcomes.
Obstructive hypertrophic cardiomyopathy (oHCM) is a form of hypertrophic cardiomyopathy (HCM)—an inherited heart muscle disorder caused by genetic mutations that affect heart muscle structure and function. These changes cause the heart muscle to become abnormally thick, most commonly affecting the wall (septum) between the two lower chambers of the heart.
In nearly two-thirds of patients with hypertrophic cardiomyopathy, the thickened heart muscle can block the flow of blood leaving the heart—a condition known as obstructive HCM (oHCM). As a result, the heart must work harder to pump blood throughout the body, often leading to symptoms such as breathlessness, chest pain, fatigue, dizziness, palpitations, or fainting during physical activity.
Myth: A diagnosis of oHCM inevitably leads to sudden death.
Fact: While oHCM was once primarily recognised for its association with sudden cardiac death, advances in medical science have significantly improved patient outcomes.
With timely diagnosis, appropriate medical care, and ongoing monitoring, many people with oHCM can lead active lives with a good quality of life and a near-normal life expectancy. Regular follow-up helps assess disease progression and guides individualized care over time.
Myth: People with oHCM need to avoid physical activities
Fact: Complete avoidance of physical activity is no longer recommended for most patients.
Although high-intensity competitive sports may not be suitable for everyone with oHCM, mild-to-moderate exercise is generally encouraged and offers important cardiovascular benefits. Exercise recommendations should always be individualised after a comprehensive assessment by a cardiologist, taking into account symptoms, severity of obstruction, and overall risk profile.
Myth: Diet and lifestyle are the primary causes of oHCM.
Fact: oHCM is a genetic condition. It is not a lifestyle disease.
Unlike heart conditions caused by high blood pressure, diabetes, or high cholesterol, oHCM develops because of inherited genetic mutations affecting heart muscle proteins. Healthy lifestyle choices remain important for overall cardiovascular health, but they do not cause or prevent the condition itself. Because the disease often runs in families, screening of close relatives may also be recommended.
Myth: Every patient with oHCM will require surgical treatment.
Fact: Surgery is only one of several available treatment options. Care is individualized, and the most appropriate approach depends on each patient's symptoms and clinical condition.
Myth: oHCM cannot go unnoticed.
Fact: The condition can remain silent for years. Some individuals carrying the genetic mutation never develop symptoms, while others experience mild or intermittent symptoms that may be attributed to more common conditions. Typical symptoms include:
Given this variability, individuals with persistent symptoms or a family history of cardiomyopathy or sudden cardiac death should undergo appropriate cardiac evaluation.
Myth: Medication can cure the disease
Fact: Advances in treatment have significantly improved disease management, helping many patients lead healthier and more active lives. While current therapies focus on controlling symptoms and reducing complications, ongoing research continues to expand treatment possibilities.
Treatment aims to reduce symptoms, improve blood flow, minimize obstruction, and lower the risk of complications such as abnormal heart rhythms and heart failure. Long-term follow-up remains an important part of care, allowing treatment to be adjusted as the condition evolves.
Myth: There's no benefit to diagnosing oHCM early
Fact: Early diagnosis can make a significant difference. Because oHCM symptoms often resemble those of other conditions, timely testing is important—especially for those with a family history of the disease. Early detection can help patients access appropriate treatment, manage symptoms effectively, and reduce the risk of complications.
Why Awareness Matters
The understanding and management of obstructive hypertrophic cardiomyopathy have evolved considerably over the past decade. Although it remains a lifelong condition, it is no longer viewed through the lens of fear alone. Advances in medical therapies, improved diagnostic tools, and personalized treatment strategies have changed the outlook for many patients.
By challenging common myths and promoting awareness, more individuals can be diagnosed earlier, receive appropriate treatment, and live healthier, more active lives with confidence.
(Dr. Daljeet Kaur, Cardiac Electrophysiologist at AIG Hospital, Hyderabad)
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It is a common belief that metabolic dysfunction-associated steatotic liver disease (MASLD)—formerly known as non-alcoholic fatty liver disease (NAFLD)—is primarily associated with diet, sedentary lifestyles, and obesity. However, there are other factors as well that affect this aspect. Post-menopausal women experience a significantly higher incidence and faster progression of fatty liver disease, even when maintaining a stable body weight.
In Pre-menopausal women, estrogen plays a central role in metabolism by promoting healthy fat accumulation in subcutaneous tissue (below the skin) rather than around internal organs; it also increases insulin sensitivity and suppresses liver inflammation.
After menopause, when estrogen levels drop, this protective function is lost; there is redistribution of fat leading to more fat accumulation around internal organs, including the liver, thus leading to increased chances of NAFLD and also increasing insulin resistance. Needless to say, with age, our metabolic rate also goes down, which also plays a role in this.
The important part lies not only in understanding the above but in going further in early detection and prevention of menopause associated NAFLD. As we know, fatty liver is a silent disease and often does not cause any signs and symptoms till a very advanced stage.
First and foremost is to change lifestyle with advancing age, changing both the dietary habits and physical activity. Regular screening and monitoring are warranted with blood tests, routine metabolic panels, keeping a tab on weight, sugar, and cholesterol levels, and a basic ultrasound of the abdomen. For someone already diagnosed with second or third stage fatty liver, a simple non-invasive FibroScan can help monitor and assess the response to treatment.
Coming to the treatment part of NAFLD in post-menopausal women, being primarily a lifestyle disease, the core of management also lies in managing lifestyle. Medicines are available for treating and controlling NAFLD in conjunction with lifestyle management. Hormone replacement therapy (HRT), when initiated early in post-menopausal women for symptomatic relief, may offer secondary benefits by maintaining metabolic health. However, HRT should always be initiated after proper evaluation and expert guidance.
NAFLD is a silent epidemic and primarily a lifestyle disease; knowing about it and knowing the triggering and precipitating factors helps with understanding and prevention better. Menopause, being a natural biological phenomenon in every female’s life, makes it essential for us to know how it affects our liver health and overall health as well.
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Eating healthy is often associated with loading your plate with salads, fruits, whole grains, legumes, smoothies and sugar-free products. However, a diet that is considered healthy for one person may trigger digestive discomfort in another. Bloating, excessive gas, abdominal cramps, constipation or loose stools after eating “healthy” foods may indicate that your gut is struggling with the quantity or type of foods you are consuming.
One common reason is a sudden increase in dietary fibre. Fibre is essential for bowel health and can support regular bowel movements, but increasing it too quickly can cause fermentation in the large intestine, resulting in gas and bloating. Adults generally need around 22–34 grams of fibre daily, depending on age and sex, but it is better to increase intake gradually rather than making a sudden dietary shift.
Certain nutritious foods can also contain FODMAPs—short-chain carbohydrates that are poorly absorbed in the small intestine. Foods such as onions, garlic, beans, lentils, cauliflower, certain fruits and some dairy products can trigger bloating, abdominal discomfort, diarrhoea or constipation in susceptible individuals, particularly those with irritable bowel syndrome (IBS). A low-FODMAP diet may help selected IBS patients, but it should ideally be undertaken with medical or dietetic guidance and followed by gradual reintroduction of foods.
“Sugar-free” does not necessarily mean gut-friendly either. Sugar alcohols such as sorbitol, mannitol, xylitol and maltitol can be incompletely absorbed and may cause gas, bloating or diarrhoea in some people. Similarly, large quantities of fruit, fruit juices or certain whole grains may aggravate symptoms in people with specific carbohydrate intolerances.
Another overlooked factor is how we eat. Eating very quickly, consuming large meals, drinking fizzy beverages, chewing gum or using straws can increase swallowed air and contribute to belching and bloating. Smaller meals, slower eating and adequate hydration can often make a meaningful difference.
The solution is not to abandon healthy foods, but to personalise your diet. Maintain a food-and-symptom diary, introduce fibre gradually, identify individual triggers and avoid unnecessarily restrictive diets. Persistent symptoms should not simply be attributed to “food intolerance.” Recurrent abdominal pain, unexplained weight loss, anaemia, blood in the stool or black stools require medical evaluation because these may indicate an underlying gastrointestinal condition rather than simple dietary sensitivity.
A healthy diet should nourish your body without consistently making your gut uncomfortable. The goal is not to follow every trending diet, but to understand what works for your individual digestive system.
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