Dr.AMiT JAiSWAL

The Rome V updates to Bowel Disorders are now out! 🏟️🆕 Here is what’s new:

Indians are becoming wildly successful... But metabolically? They’re breaking down faster than any other population. Here’s what’s happening inside your body based on science and years of treating South Asians:

Things feel better in the morning. Get some rest and don't dwell on it.

Thoracic aortic aneurysm and dissection can be silent but high risk. Recognizing patterns and risk factors early is key in guiding timely management. @MayoClinic #MedTwitter #Cardiology #AorticDissection #VascularHealth

What a ‘post-antibiotic era’ could mean for modern medicine theconversation.com/what-a-post-an… via @SteveWKerrigan

Vitamin B12 deficiency is not anemia. It is a slow disconnection of your nervous system. By the time you notice weakness, your nerves may already be suffering. Busy poster but worth giving time #VitaminB12 #Neurology #BrainHealth #PeripheralNeuropathy #MedicalEducation #Neurotwitter #Medtwitter

Clinical Pearl for Physicians & Residents A 40-year-old with Type 2 Diabetes (T2DM). ✅Sugars: Well-controlled on medication. ✅Family History: Negative for early MI/Stroke. ✅BP: 120/80 mmHg. 🔴LDL Cholesterol: 120 mg/dL. Should this patient receive a statin for primary prevention? [Poll Options below] A. No, LDL is "normal" B. No, sugars are controlled C. Yes, moderate-intensity D. Only if a risk factor appears

A structured overview of Autoimmune Central Nervous System (CNS) disorders, categorizing them based on the presence and type of associated antibodies. nature.com/articles/s4158…

The biggest shift in cardiovascular prevention in years just dropped — and almost no one is talking about it. As a medical school professor, I've watched heart disease stay America's #1 killer for decades. New AHA/ACC guidelines finally move the line. What changed (via Harvard Gazette): - Risk assessment now starts at age 30, not 40-50 - Universal lipid screening in children ages 9-11 - Lp(a) screening — elevated in 20% of people, 6x stickier than LDL - Coronary calcium and polygenic risk are now formal tools - Treatment threshold dropped to 3% 10-year risk (was 5%) - Old calculator overpredicted risk by 40-50% Striking line: ~80% of cardiovascular disease is preventable through lifestyle. This is the shift I argue for in "Lies I Taught in Medical School" — treat metabolic disease at the roots, not at the event. Metabolic dysfunction is the root cause of chronic disease. Heart disease is the downstream bill. Full breakdown coming on the Health Longevity Secrets podcast @RobertLufkinMD" target="_blank" rel="nofollow noopener">youtube.com/@RobertLufkinMD Source: news.harvard.edu/gazette/story/… #HeartDisease #Prevention #MetabolicHealth #HealthLongevitySecrets

🩸Warfarin Associated Bleeding Management

Most of the joint and tendon pain I see in the office is atraumatic. No fall, twist, and no activity anyone can point to. The shoulder that's been sore for three weeks or the knee that aches when going downstairs. The hip that hurts after a typical walk. The most common explanation people offer is that they slept wrong. That's not what happened. What happened is quieter and slower. Muscles have lost strength while tendons have been losing capacity for months… well, they finally got asked to do something they no longer had the capacity for. Sure, the pain feels sudden because the moment it started hurting seems sudden. But the process that got the tendon there was a long time coming. Nearly 30 years of this, and the pattern is consistent: atraumatic pain is almost always a capacity problem that finally became visible. It’s also just another downstream consequence of poor metabolic health. These are not two independent variables. The tissue didn't fail. The reserve ran out. The inflammatory mediators affected the tendon’s structure and resilience. Traumatic vs atraumatic tendon issues. Those are different problems with very different solutions, and understanding which one you have should matter. It will affect your recovery. Very often… the answer will not be found on your X-ray or MRI. You’ll find many things on those scans, but you won’t find the answer to why thing started hurting and what needs to be done about them. Most of the time, the proper treatment is… improve your metabolic health, aerobic fitness, and consistently load your tissues to improve capacity. Regardless of most of the MRI findings.

Adipose tissue is not merely an inert energy reservoir, but a metabolically active organ whose diverse endocrine, immune, and regulatory functions are summarised in the following chart. Note: I was preparing a post and a table to explain the physiological functions of adipose tissue to complement today’s discussion on metabolic water production from fat oxidation (x.com/ProfSirera/sta…), when I recalled that other communicators, such as @drkeithsiau, had used ChatGPT to create remarkably effective posters—so I set to work.

Researchers focused on deoxycholic acid (#DCA), a compound naturally produced in the gut. They found that it not only improved #bonestrength but also reduced #inflammation and restored balance in #gutbacteria—highlighting a strong gut-bone connection. Lead author Dr. Rupesh K. Srivastava, Department of Biotechnology, AIIMS said, “DCA is a bile acid that is already present in our body and is produced through the action of gut bacteria. Under normal conditions, bile acids are made in the liver, stored in the gallbladder, and released during digestion, with about 95% reabsorbed and a small fraction converted by gut microbes into secondary bile acids like DCA. In our study, we found that levels of these bile acids, including DCA, are reduced in patients with #osteoporosis and bone loss.” #health #bones #inflammation #gutbacteria #aiimsdelhi @timesofindia

D-dimer: What it means, where it helps, and where it misleads 🩸 D-dimer is a cross-linked fibrin degradation product, so it reflects recent or ongoing clot formation followed by fibrinolysis; it is therefore a marker of activated coagulation plus clot breakdown, not a marker of thrombosis location. 🎯 Its most important clinical role is as a rule-out test, not a rule-in test. In suspected DVT or PE, D-dimer is useful only when interpreted with pre-test probability such as Wells score or a similar structured approach. ✅ Negative D-dimer + low or unlikely clinical probability = VTE becomes very unlikely. NICE recommends D-dimer for unlikely DVT and unlikely PE, and if the result is negative, patients generally do not need VTE imaging in that pathway. 🚫 Do not use D-dimer as a stand-alone diagnostic test. A positive D-dimer does not diagnose VTE; it simply means further evaluation is needed, usually imaging such as compression ultrasound for DVT or CTPA/VQ imaging for PE. ⚠️ If clinical suspicion is high, do not wait for D-dimer to “rescue” the case. In likely PE or otherwise high pre-test probability, guidelines recommend proceeding directly to imaging and appropriate interim anticoagulation rather than relying on D-dimer. 👴 Age matters. NICE advises considering an age-adjusted D-dimer threshold in people older than 50 years, because baseline D-dimer rises with age and fixed cutoffs produce many false positives in older adults. A commonly used formula is age × 10 ng/mL when the assay is reported in FEU. 🔬 Know your lab units before interpreting the result. Many labs report D-dimer in FEU while others use DDU; a “normal” cutoff is commonly around 0.5 mg/L FEU or 500 ng/mL FEU, but the numeric cutoff differs when DDU is used. Misreading FEU as DDU is a classic interpretation error. 📈 An elevated D-dimer is nonspecific. It may rise with infection, sepsis, inflammation, recent surgery, trauma, malignancy, pregnancy/postpartum state, liver disease, increasing age, immobilization, heart failure, autoimmune disease, and even sample-related or assay-related issues. 🧠 Clinical pearl: a high D-dimer means “something is activating coagulation/fibrinolysis”, not necessarily PE/DVT. In medical wards and ICUs, it is often elevated for many reasons, so its specificity falls sharply in sick inpatients. 🧮 For DIC, D-dimer is supportive, not isolated proof. In suspected disseminated intravascular coagulation, D-dimer should be interpreted along with platelet count, PT/INR, aPTT, fibrinogen, bleeding/thrombotic phenotype, and the underlying trigger such as sepsis, trauma, malignancy, or obstetric catastrophe. 📊 In DIC, serial trend is often more informative than a single value. Rising D-dimer in the right clinical context supports ongoing consumptive coagulopathy, while response must be read together with platelet count, PT, fibrinogen, and clinical improvement. 💊 Timing matters. D-dimer may be falsely lower after anticoagulation has already started, and interpretation becomes less reliable if testing is delayed or performed after treatment initiation. 🤰 Special settings need caution. Pregnancy, cancer, recent surgery, COVID or severe infection, and hospitalized/critically ill states commonly produce positive D-dimer values even without acute VTE; in these groups, indiscriminate ordering creates noise and unnecessary imaging. 🚑 Best practical use: order D-dimer only when there is a genuine diagnostic question and the patient is in a low or intermediate/“unlikely” probability pathway where a negative result will safely change management. Next....

Stop relying on BMI. It can’t tell the difference between muscle and fat. Two people can have the same BMI but completely different health profiles. ​What to track instead: ​1. Waist-to-Hip Ratio (WHR) : Tracks visceral fat risk. WHR > 0.90 for men and > 0.85 for women indicates increased health risks.

Is your sleep causing you pain? 🛌 "Overnight strain" from poor posture can lead to chronic neck & back pain. For a healthy spine, keep your head, shoulders, and hips aligned. 1. Best: Side or back sleeping 2. Avoid: Stomach sleeping 3. Use: Medium-firm mattress & supportive pillows Don’t ignore persistent numbness or stiffness lasting >30 mins. Early correction prevents long-term injury.

ICMR is raising concern about increasing obesity in India - calling it a “belly alarm.” Around 1 in 4 Indian adults (25%+) are overweight or obese, and the number is rising. This is driving lifestyle diseases like: Type 2 diabetes Hypertension Heart disease Fatty liver The problem is widespread - both urban and rural India, with rural areas now also seeing rising obesity alongside undernutrition. Despite years of: various diets fitness programs awareness campaigns there is no clear consensus on what works best. So, ICMR has launched a national initiative to: study what actually works for weight loss compare diet, exercise, and behavioral interventions understand why some people respond and others don’t generate India-specific evidence Important shift: Weight alone is no longer a reliable marker Some normal-weight people have metabolic issues Some overweight people may not show immediate complications My Take. Here is the elephant in the room: Insulin resistance We are still looking at: weight calories activity But ignoring the central driver of most metabolic diseases. You can be: normal weight → and still insulin resistant overweight → but metabolically improving Until we measure and address: fasting insulin HOMA-IR postprandial glucose & insulin response we will keep chasing symptoms, not the root cause. My simple, practical solution: Fix the food environment first - not just carbs, but Ultra-Processed Foods (UPFs) Eliminate or drastically reduce UPFs:packaged snacks biscuits, namkeens, bakery items sugary beverages ready-to-eat foods foods made with refined flours + industrial seed oils + additives These are the real drivers of:chronic overeating insulin resistance inflammation India doesn’t just have a “weight problem.” India has a metabolic health problem driven by insulin resistance. Fix the root - and weight, diabetes, BP, fatty liver will follow. Image credit: Soumen Das from Linkedin

Original Names of Places in Kashmir❌ Original Names of Places in Kashyapmar💔

BREAKING NEWS: Top U.S. Nuclear Chief Caught LEAKING Sensitive National Security Information to Stranger, Reveals Army Chemist Was Exposed to U.S. Chemical Nerve Agent, Confirms U.S. Strike Killed Children in Iran, Discloses U.S. Plans to ‘Kill Iran’s New Supreme Leader’ “If he [Mojtaba Khamenei] doesn't change his ways, yeah, they're [United States] going to kill him.” “The easiest way to get intelligence…send a pretty girl, talk to the guy…I have to resist your eyes.” “Your eyes have mesmerized me so much…Almost like you're an intelligence.” Andrew Hugg, a U.S. Chief of Chemical Nuclear Surety, was caught on hidden camera casually revealing sensitive information to a stranger in a public restaurant. Andrew Hugg, Chief of Chemical Nuclear Surety, in charge of nuclear and chemical safety was caught on hidden camera releasing information regarding the U.S. Nuclear Information. He claims the U.S. still possesses nerve agents and says a U.S. Army chemist recently died from exposure. He also acknowledges U.S. airstrikes have killed children in Iran, calling it “collateral damage,” and revealed to the journalist how nuclear launch decisions are made in real time. Hugg described how the United States could assassinate Iran’s next leader if he “doesn’t change,” while admitting the U.S. has no plans to use nuclear weapons: “We’re not going to nuke anybody.” All of this was casually revealed to an undercover journalist in a restaurant. This raises serious questions about this official's judgment, security, and what’s really happening behind closed doors. We have reached out to the Pentagon and U.S. Army for comment and they are working on a response. @USArmy @DeptofWar

What people believe about their sleep shapes how they perform. Students hooked up to sham EEG and told their REM was above average outperformed those told it was below average on memory and attention tests. Never underestimate the power of the placebo effect.