Cardiovascular And Metabolic Health

Is Body Roundness Index (BRI) the future - or just a companion - to BMI? For decades, Body Mass Index (BMI) - weight ÷ height² - has been the standard gauge of healthy weight. But its limitations are well‑documented: it ignores fat distribution, muscle vs. fat mass, sex, age and ethnicity. A muscular athlete (or Olympic-level rugby star) can end up labeled “overweight” by BMI even if they’re metabolically healthy. Enter: the Body Roundness Index (BRI) Developed in 2013, BRI uses waist circumference and height - modeled geometrically using body shape eccentricity - to estimate total and visceral body fat, not just size. Values typically range from 1 to 16, with higher scores indicating a “rounder,” more centrally obese figure. What scientific data suggests: A major study of ~10,000 Chinese adults showed that those with high stable BRI over six years had a 163% higher risk of cardiovascular disease compared to a low-BRI group; mid-range BRI saw a 61% higher risk. This held even after adjusting for age, smoking, cholesterol, etc. In US data from nearly 33,000 adults (from 1999–2018), both very low (<3.4) and high (>6.9) BRI scores were linked to increased all-cause mortality - up to 49% higher risk at the upper extreme compared to the mid-range. The pros of using BRI: Reflects abdominal (visceral) fat, a key driver of metabolic disease risk, something BMI doesn’t capture. Avoids misclassifying highly muscular individuals or those with different body compositions. Shown to correlate with multiple outcomes - heart disease, all-cause and metabolic mortality, fatty liver, hypertension, bone mineral issues - often outperforming BMI alone. Limitations and context: Calculation is more complex, it requires waist measurement and a formula using eccentricity; less convenient than BMI. Accuracy may vary by ethnicity, sex, age; most validation studies have focused on East Asian or US populations. Measuring waist circumference consistently is error‑prone in clinical or home settings. BMI has broad longitudinal datasets, clear thresholds, and institutional support; BRI is promising, but still early in adoption. So … is BRI the new BMI? Not quite, but it’s a compelling complement or upgrade, especially when fat distribution matters. BRI offers a deeper view into shape and risk by focusing on visceral fat. What we should take away: BMI remains a useful starting point but does not tell the full story. BRI adds value, particularly in cardiovascular and metabolic risk screening. In practice, a combination of metrics (e.g. BMI + WHtR + BRI), plus clinical biomarkers, offers the best health assessment. In summary: BRI isn’t replacing BMI overnight. But it advances our understanding of the most important risk driver: where fat is stored, not just how much. For professionals and health‑savvy professionals evaluating risk in diverse populations, it’s a tool worth knowing and potentially using.

Diabetes is not only a metabolic disease—it is a cardiovascular disease amplifier. The mechanisms are complex, involving endothelial dysfunction, inflammation, glucotoxicity, lipotoxicity, and maladaptive remodeling of the heart and vessels. Where AI fits in: AI has the potential to transform this space by: • Detecting early signals of cardiometabolic risk from EHRs, imaging, and wearable data • Identifying hidden biomarkers and phenotypes for precision cardiology • Predicting adverse cardiovascular events in diabetic patients before symptoms arise • Guiding tailored interventions that integrate lifestyle, pharmacologic, and digital health solutions The fusion of AI driven predictive modeling with deep biological understanding opens the door to personalized prevention and treatment strategies for millions at risk. The message is clear: tackling the intersection of diabetes and CVD requires not just clinical expertise, but also intelligent systems that can synthesize complex, multi-layered data. Follow Zain Khalpey, MD, PhD, FACS for more on Ai & Healthcare. Image ref : Kalra et al. (Cell, 2024. DOI: 10.1016/j.cell.2024.05.044) #Diabetes #CardiovascularDisease #Atherosclerosis #DiabeticCardiomyopathy #EndothelialDysfunction #Glucotoxicity #Lipotoxicity #HeartHealth #PrecisionMedicine #ArtificialIntelligence #AIinHealthcare #PredictiveAnalytics #Cardiology #DigitalHealth #HealthcareInnovation #MedicalAI #ChronicDisease #PreventiveMedicine #SystemsBiology #FutureOfMedicine

Most people think tea, coffee, berries or olive oil are “good for the heart.” Very few understand why, or the measurable biological changes these foods trigger. A new long-term study caught my attention because it finally gives us something beyond the usual wellness slogans. As a cardiologist, I’m always looking for evidence that translates into real life, not theory, not trends, but measurable impact on how we age. And what this research shows is surprisingly practical. It’s not about eating “healthy”, it’s about what your body actually does with what you eat. Researchers followed thousands of adults for over a decade. Instead of just asking them what they ate, they checked biomarkers and metabolites in blood and urine. This is the part I love: we can see the footprint of certain foods inside the body, and that footprint predicts things like cholesterol, blood pressure, and inflammation. The big takeaway? A few simple foods create metabolic signatures linked to better cardiovascular ageing. People who regularly consumed polyphenol-rich foods had: → Higher HDL ( good cholesterol) → Better blood pressure → Lower inflammation markers → Overall slower rise in cardiovascular risk with age. And the effect held even when accounting for BMI, alcohol, sodium, calories… So this isn’t just “healthy lifestyle bias.” There’s real biology at play. A detail I wish more people understood: Not all polyphenols are the same. – Berries → flavonoids that support cholesterol. – Coffee & whole grains → phenolic acids linked to better BP. – Nuts & seeds → lower triglycerides and CRP ( inflammation marker) It’s not magic. It’s specific compounds doing specific things. And no, you don’t need a “superfood.” The pattern matters more than perfection: A cup of tea. A handful of nuts. Some berries a few times a week. Olive oil instead of processed fats. Whole grains most days. Small habits, repeated. That’s what influences cardiovascular ageing, not the dramatic 30-day detox. Because this is exactly where functional cardiology shines: connecting everyday choices with measurable biological changes long before symptoms appear. Your body is constantly giving us signals. Our job is to listen early, and act early.

Your gut isn’t just digesting food. It might be aging your blood vessels. A brand-new study in Nature Aging uncovered something wild: Certain gut microbes—specifically a strain of Clostridium—produce metabolites that can accelerate vascular aging. Here’s the breakdown 👇 🧬 Researchers found that two metabolites—phenylacetic acid (PAA) and phenylacetylglutamine (PAGln)—were significantly elevated in older adults and aged mice. 🦠 These are byproducts of protein fermentation by specific gut bacteria. 🧫 When young mice were colonized with this Clostridium strain, they developed signs of endothelial cell senescence—meaning the cells lining their blood vessels aged faster. So what’s actually happening? PAA triggers oxidative stress in the mitochondria → This means more hydrogen peroxide (a reactive oxygen species), which damages the cell from the inside. That stress activates the SASP (Senescence-Associated Secretory Phenotype) → Think of this as a “toxic soup” of inflammatory signals released by senescent cells. → It spreads stress and dysfunction to neighboring cells—amplifying aging across tissues. The result? → Poor blood vessel regeneration. → Stiff, inflamed arteries. → A cellular environment primed for disease. But here’s the part that got me: 🧂Sodium acetate—a short-chain fatty acid and a byproduct of fiber fermentation in the gut—was able to reverse the damage. It lowered oxidative stress, suppressed the SASP, and improved blood vessel function in the mice. Why this matters: Because aging isn’t just about time. It’s about how well your systems communicate, recover, and regenerate. This study connects the dots between: – The gut microbiome – Protein fermentation – Mitochondrial oxidative stress – And the early breakdown of vascular integrity And it reinforces something powerful: The foods you eat—and the microbes they feed—can shape your biological aging in very real, very measurable ways. We often talk about gut health as if it only affects digestion. But the ripple effects extend into your brain, your vessels, your mitochondria—and possibly your healthspan. 🧾 Read the full study summary here: https://lnkd.in/eNf4EceA #GutBrainHeartAxis #EndothelialHealth #MicrobiomeAndAging #MitochondrialResilience #FiberFeedsFunction #BiologicalAging #ScienceOfAging

𝗕𝗠𝗜 𝘃𝘀 𝗪𝗛𝘁𝗥 𝘃𝘀 𝗪𝗛𝗥- 𝗪𝗵𝘆 𝗪𝗮𝗶𝘀𝘁-𝘁𝗼-𝗛𝗲𝗶𝗴𝗵𝘁 𝗥𝗮𝘁𝗶𝗼 𝗪𝗶𝗻𝘀 (𝗘𝘀𝗽𝗲𝗰𝗶𝗮𝗹𝗹𝘆 𝗳𝗼𝗿 𝗜𝗻𝗱𝗶𝗮𝗻𝘀) We’ve relied on 𝗕𝗠𝗜 for decades but what if it’s the 𝗹𝗲𝗮𝘀𝘁 𝘂𝘀𝗲𝗳𝘂𝗹 𝗻𝘂𝗺𝗯𝗲𝗿 𝗳𝗼𝗿 𝗽𝗿𝗲𝗱𝗶𝗰𝘁𝗶𝗻𝗴 𝘆𝗼𝘂𝗿 𝗵𝗲𝗮𝗹𝘁𝗵? When it comes to metabolic health and early disease risk, not all measurements are equal: 𝟭. 𝗕𝗠𝗜 (𝗕𝗼𝗱𝘆 𝗠𝗮𝘀𝘀 𝗜𝗻𝗱𝗲𝘅) Good for population studies but poor for real-life health decisions. It cannot distinguish between: • Fat vs muscle • Visceral fat vs subcutaneous fat • Ethnic differences in fat distribution An Indian with a “𝗻𝗼𝗿𝗺𝗮𝗹 𝗕𝗠𝗜” 𝗰𝗮𝗻 𝘀𝘁𝗶𝗹𝗹 𝗵𝗮𝘃𝗲 𝗵𝗶𝗴𝗵 𝘃𝗶𝘀𝗰𝗲𝗿𝗮𝗹 𝗳𝗮𝘁 𝗮𝗻𝗱 𝗯𝗲 𝗮𝘁 𝗵𝗶𝗴𝗵 𝗿𝗶𝘀𝗸 𝗳𝗼𝗿 𝗱𝗶𝗮𝗯𝗲𝘁𝗲𝘀, 𝗣𝗖𝗢𝗦, 𝗳𝗮𝘁𝘁𝘆 𝗹𝗶𝘃𝗲𝗿, 𝗮𝗻𝗱 𝗵𝗲𝗮𝗿𝘁 𝗱𝗶𝘀𝗲𝗮𝘀𝗲. 2.  𝗪𝗛𝗥 (𝗪𝗮𝗶𝘀𝘁-𝘁𝗼-𝗛𝗶𝗽 𝗥𝗮𝘁𝗶𝗼) Better than BMI because it considers body shape and central fat. But it has limitations: • Varies by gender • Varies by ethnicity • Less predictive of visceral fat than newer metrics Useful, but not perfect. 𝟯. 𝗪𝗛𝘁𝗥 (𝗪𝗮𝗶𝘀𝘁-𝘁𝗼-𝗛𝗲𝗶𝗴𝗵𝘁 𝗥𝗮𝘁𝗶𝗼)-𝗖𝗹𝗲𝗮𝗿 𝗪𝗶𝗻𝗻𝗲𝗿  A growing body of evidence shows WHtR is the strongest predictor of: • Diabetes • Fatty liver • Hypertension • Heart disease • All-cause mortality And it works across all ages, genders, and ethnicities. 𝗧𝗵𝗲 𝗿𝘂𝗹𝗲 𝗶𝘀 𝗯𝗲𝗮𝘂𝘁𝗶𝗳𝘂𝗹𝗹𝘆 𝘀𝗶𝗺𝗽𝗹𝗲: “𝗞𝗲𝗲𝗽 𝘆𝗼𝘂𝗿 𝘄𝗮𝗶𝘀𝘁 𝘁𝗼 𝗹𝗲𝘀𝘀 𝘁𝗵𝗮𝗻 𝗵𝗮𝗹𝗳 𝘆𝗼𝘂𝗿 𝗵𝗲𝗶𝗴𝗵𝘁.” Why 𝗪𝗛𝘁𝗥 𝗶𝘀 𝗲𝘀𝗽𝗲𝗰𝗶𝗮𝗹𝗹𝘆 𝗽𝗼𝘄𝗲𝗿𝗳𝘂𝗹 𝗳𝗼𝗿 𝗜𝗻𝗱𝗶𝗮𝗻𝘀 & 𝗦𝗼𝘂𝘁𝗵 𝗔𝘀𝗶𝗮𝗻𝘀, as these populations in particular have: • 𝗠𝗼𝗿𝗲 𝘃𝗶𝘀𝗰𝗲𝗿𝗮𝗹 𝗳𝗮𝘁 𝗮𝘁 𝗹𝗼𝘄𝗲𝗿 𝗯𝗼𝗱𝘆 𝘄𝗲𝗶𝗴𝗵𝘁 • 𝗛𝗶𝗴𝗵𝗲𝗿 𝗶𝗻𝘀𝘂𝗹𝗶𝗻 𝗿𝗲𝘀𝗶𝘀𝘁𝗮𝗻𝗰𝗲 𝗲𝘃𝗲𝗻 𝘄𝗵𝗲𝗻 𝘁𝗵𝗶𝗻 • 𝗛𝗶𝗴𝗵𝗲𝘀𝘁 𝗴𝗹𝗼𝗯𝗮𝗹 𝗿𝗶𝘀𝗸 𝗼𝗳 𝗱𝗶𝗮𝗯𝗲𝘁𝗲𝘀 𝗮𝗻𝗱 𝗵𝗲𝗮𝗿𝘁 𝗱𝗶𝘀𝗲𝗮𝘀𝗲 This means: 𝗠𝗮𝗻𝘆 𝗜𝗻𝗱𝗶𝗮𝗻𝘀 𝘄𝗶𝘁𝗵 𝗮 “𝗻𝗼𝗿𝗺𝗮𝗹 𝗕𝗠𝗜” 𝗮𝗹𝗿𝗲𝗮𝗱𝘆 𝗵𝗮𝘃𝗲 𝗺𝗲𝘁𝗮𝗯𝗼𝗹𝗶𝗰 𝘀𝘆𝗻𝗱𝗿𝗼𝗺𝗲. 𝗪𝗛𝘁𝗥 𝗰𝗮𝘁𝗰𝗵𝗲𝘀 𝘁𝗵𝗶𝘀 𝗲𝗮𝗿𝗹𝘆, 𝘄𝗵𝗶𝗹𝗲 𝗕𝗠𝗜 𝗰𝗼𝗺𝗽𝗹𝗲𝘁𝗲𝗹𝘆 𝗺𝗶𝘀𝘀𝗲𝘀 𝗶𝘁. 𝗦𝘁𝘂𝗱𝗶𝗲𝘀 𝗰𝗼𝗻𝘀𝗶𝘀𝘁𝗲𝗻𝘁𝗹𝘆 𝘀𝗵𝗼𝘄 𝗪𝗛𝘁𝗥 𝗱𝗲𝘁𝗲𝗰𝘁𝘀 𝗿𝗶𝘀𝗸 𝟱–𝟭𝟬 𝘆𝗲𝗮𝗿𝘀 𝗲𝗮𝗿𝗹𝗶𝗲𝗿 𝘁𝗵𝗮𝗻 𝗕𝗠𝗜 𝗶𝗻 𝗦𝗼𝘂𝘁𝗵 𝗔𝘀𝗶𝗮𝗻 𝗽𝗼𝗽𝘂𝗹𝗮𝘁𝗶𝗼𝗻𝘀. WHtR is the most actionable, precise, and predictive metric you can track at home. 𝗢𝗽𝘁𝗶𝗺𝗮𝗹 𝗹𝗼𝗻𝗴𝗲𝘃𝗶𝘁𝘆 𝗪𝗛𝘁𝗥: 📏 𝟬.𝟰𝟮 – 𝟬.𝟰𝟴 (𝗳𝗼𝗿 𝗯𝗼𝘁𝗵 𝗺𝗲𝗻 & 𝘄𝗼𝗺𝗲𝗻) Longevity #MetabolicHealth #PreventiveHealth #IndianHealth #HealthForIndians #WHtR #VisceralFat #BMI #HealthEducation #LifestyleMedicine #FunctionalMedicine

🫀 𝐍𝐞𝐚𝐫𝐥𝐲 𝐡𝐚𝐥𝐟 𝐨𝐟 𝐚𝐥𝐥 𝐡𝐞𝐚𝐫𝐭 𝐚𝐭𝐭𝐚𝐜𝐤𝐬 𝐡𝐚𝐩𝐩𝐞𝐧 𝐢𝐧 𝐩𝐞𝐨𝐩𝐥𝐞 𝐰𝐡𝐨𝐬𝐞 𝐋𝐃𝐋 𝐜𝐡𝐨𝐥𝐞𝐬𝐭𝐞𝐫𝐨𝐥 𝐥𝐨𝐨𝐤𝐬 “𝐧𝐨𝐫𝐦𝐚𝐥,” which immediately tells us LDL isn’t the whole story. Massive studies of hospitalized heart patients show that many had LDL levels below current guideline targets, often without ever taking cholesterol-lowering drugs. In other words, acceptable LDL numbers did not protect them from heart disease. 𝐒𝐨 𝐰𝐡𝐚𝐭 𝐩𝐫𝐞𝐝𝐢𝐜𝐭𝐬 𝐫𝐢𝐬𝐤 𝐛𝐞𝐭𝐭𝐞𝐫? Metabolic health… specifically insulin resistance. Long-term research comparing dozens of biomarkers found that 𝐢𝐧𝐬𝐮𝐥𝐢𝐧-𝐫𝐞𝐬𝐢𝐬𝐭𝐚𝐧𝐜𝐞 𝐦𝐚𝐫𝐤𝐞𝐫𝐬 𝐩𝐫𝐞𝐝𝐢𝐜𝐭𝐞𝐝 𝐩𝐫𝐞𝐦𝐚𝐭𝐮𝐫𝐞 𝐡𝐞𝐚𝐫𝐭 𝐝𝐢𝐬𝐞𝐚𝐬𝐞 𝐮𝐩 𝐭𝐨 𝐬𝐢𝐱 𝐭𝐢𝐦𝐞𝐬 𝐦𝐨𝐫𝐞 𝐬𝐭𝐫𝐨𝐧𝐠𝐥𝐲 𝐭𝐡𝐚𝐧 𝐋𝐃𝐋. Even widely praised lipid markers like ApoB were far weaker predictors by comparison. One simple, powerful indicator stands out: the 𝐭𝐫𝐢𝐠𝐥𝐲𝐜𝐞𝐫𝐢𝐝𝐞-𝐭𝐨-𝐇𝐃𝐋 𝐫𝐚𝐭𝐢𝐨. It can be calculated from a standard lipid panel and acts as a practical proxy for insulin resistance. A ratio above 2 signals metabolic trouble; above 3 is a clear red flag. Across multiple studies, 𝐭𝐡𝐢𝐬 𝐫𝐚𝐭𝐢𝐨 𝐜𝐨𝐧𝐬𝐢𝐬𝐭𝐞𝐧𝐭𝐥𝐲 𝐨𝐮𝐭𝐩𝐞𝐫𝐟𝐨𝐫𝐦𝐞𝐝 𝐋𝐃𝐋 𝐢𝐧 𝐩𝐫𝐞𝐝𝐢𝐜𝐭𝐢𝐧𝐠 𝐡𝐞𝐚𝐫𝐭 𝐚𝐭𝐭𝐚𝐜𝐤𝐬 𝐚𝐧𝐝 𝐝𝐞𝐚𝐭𝐡, even when LDL levels were identical. 𝐂𝐚𝐫𝐝𝐢𝐨𝐯𝐚𝐬𝐜𝐮𝐥𝐚𝐫 𝐫𝐢𝐬𝐤 𝐢𝐬 𝐝𝐫𝐢𝐯𝐞𝐧 𝐟𝐚𝐫 𝐦𝐨𝐫𝐞 𝐛𝐲 𝐦𝐞𝐭𝐚𝐛𝐨𝐥𝐢𝐜 𝐝𝐲𝐬𝐟𝐮𝐧𝐜𝐭𝐢𝐨𝐧 than by cholesterol alone. Improving insulin sensitivity through diet, movement, sleep, and lifestyle addresses the root cause… something no LDL-lowering pill can fully accomplish. 𝘙𝘦𝘧: 𝘉𝘢𝘴𝘦𝘥 𝘰𝘯 𝘢 𝘭𝘦𝘤𝘵𝘶𝘳𝘦 𝘣𝘺 𝘋𝘳 Benjamin Bikman.

🌟 New observational evidence that “metabolically healthy” obesity may not be benign 🌟 In data from over 150k UK Biobank participants followed for 13 years, the investigators examined how obesity & metabolic health jointly relate to various cardiometabolic outcomes. Metabolic health was defined as no hypertension, diabetes, or dyslipidemia. Compared with folks with “normal” BMI & no metabolic abnormalities, people with obesity but “normal” metabolic profiles had higher risk of: 🔹 Atherosclerotic cardiovascular disease (ASCVD): HR 1.46 (men), 1.34 (women) 🔹 Heart failure: HR 1.63 (men), 1.69 (women) 🔹 MASLD: HR 2.37 (men), 4.44 (women) 🔹 All-cause mortality: HR 1.36 (men), 1.27 (women) If any metabolic dysfunction coexisted w/ obesity, risks ⬆️ further and extended to end stage renal disease (≈5–8× higher risk). Risk increased with: 🔹 Higher BMI class (I → II → III) 🔹 Central obesity 🔹 # of metabolic abnormalities present These data reinforce that “metabolically healthy obesity” or “preclinical obesity” may represent transitional states, not stable low‑risk phenotypes. Clinical implications: 🔹 Treat obesity first. Even with normal blood pressure, glucose, & lipids, excess adiposity was linked to higher long‑term ASCVD, HF, MASLD, and mortality. Waiting for development of hypertension, diabetes, and/or dyslipidemia before intervening may ⬆️ risk for adverse outcomes. 🔹 Presenting clinically with “metabolic healthy obesity” is likely a window for early prevention, not a reason to defer or delay care. 🔹 Lifestyle intervention (nutrition, physical activity, sleep, stress management, and weight loss for patients who seek it) should be prioritized early. Obesity medications may also have a role before complications develop. 🔹 Make adiposity (especially central adiposity) part of routine risk assessment, considering BMI class, waist circumference (or WHR), % body fat, ect in CVD & liver risk discussions. Things to consider: 🔹 Generalizability-UK Biobank is a volunteer, mostly White UK cohort that is healthier than the general population 🔹 Metabolic status was measured only once and adiposity was assessed by BMI and waist circumference. Hypertension, diabetes, and dyslipidemia were treated as binary. Subclinical dysfunction may be missed, meaning some “healthy” participants already had early metabolic stress. 🔹 Observational design and residual confounding remains possible. The study cannot determine whether intentional weight loss or early pharmacologic treatment in "metabolic healthy obesity" will ⬇️events as this requires randomized trials. Taken together, this study suggests that excess adiposity itself could carry measurable long‑term cardiometabolic risk, even before traditional risk factors cross diagnostic thresholds, but RCTs are needed for confirmation. Note: authors did not use patient-first language. See here for why you should: https://lnkd.in/eVkPC8X2

High blood pressure: what if we’re managing numbers instead of biology? “I’m on medication for high blood pressure.” “My doctor prescribed tablets for it.” “I’ve been taking them for years.” These statements are so normal they rarely invite a second question. Yes—high blood pressure is a major risk factor for heart attack, stroke, heart failure, and kidney disease. Managing it matters. But an uncomfortable question remains: What actually drives high blood pressure in most people? Beyond the diagnosis While genetics, salt sensitivity, environmental exposure, and pollutants all play a role, a growing body of metabolic research points to insulin resistance as a primary upstream driver for many adults. In practical terms: Central (belly) fat is metabolically active and contributes to vascular dysfunction Insulin resistance alters sodium handling, vascular tone, and sympathetic activity Chronic inflammation keeps blood vessels in a constant state of constriction Treating pressure without addressing metabolism is often symptom control, not resolution. The overlooked role of magnesium An estimated large proportion of adults in the UK, Australia, and the US consume sub-optimal magnesium levels. Magnesium matters because: • It helps relax vascular smooth muscle • It supports blood pressure regulation • It is required for vitamin D activation • Stress, alcohol, caffeine, and sugar increase magnesium loss Low magnesium status has been associated with: – Hypertension – Metabolic syndrome – Cardiovascular risk Yet it is rarely assessed in routine care. A systems question worth asking A medical practitioner will often:  Prescribe antihypertensive medication  Write repeat prescriptions  Schedule a follow-up in 3–6 months That approach can be necessary and lifesaving. But the question we rarely ask is: Where do natural, nutritional, lifestyle, and metabolic therapies sit in this pathway—especially for prevention and reversal? Medication can lower numbers. But biology still needs addressing. A reframing for the future What if high blood pressure was treated not just as a cardiovascular condition—but as a metabolic signal? One pointing to: • Insulin sensitivity • Mineral balance • Stress load • Sleep quality • Inflammation Root-cause work doesn’t replace medicine. It completes it. How will your health look and feel in 2026— if today’s strategy stays the same?

He rewrote the definition of obesity — for a billion people. ↓ Prof. Anoop Misra is Chairman of Fortis C-Doc Centre of Excellence for Diabetes, Metabolic Diseases and Endocrinology, New Delhi. He is also Chairman of the National Diabetes, Obesity and Cholesterol Foundation (N-DOC). Why his work matters to every clinician in South Asia: → He proved that Asian Indians develop metabolic disease at far lower BMIs than Caucasians — leading to India-specific obesity and waist circumference cutoffs now used nationwide → 375+ publications, h-index of 111, and ranked #1 among Indian diabetes researchers in Stanford University's Top 2% Scientists list (2024) → Created Project MARG — Asia's largest school health programme covering 500,000 children across 10 cities for prevention of childhood obesity and diabetes He received the Dr. B.C. Roy Award (India's highest medical honour) and the Padma Shri — both for his work on metabolic disorders in Indians. My takeaway: Before his research, we were using Western BMI cutoffs for Indian patients and missing metabolic risk in "normal weight" individuals. Today, when I flag a patient with a BMI of 24 and a waist of 90 cm as high-risk, I'm applying Misra's framework. His work is the reason we don't wait for BMI 30 to act. What's one clinical guideline you follow that was shaped by Indian research? Tell me below 👇 🔖 Diabesity Changemakers #Diabesity #DiabetologyChangemakers #ObesityMedicine #AsianIndianPhenotype #DoctorsOfLinkedIn

⚖️It’s Time to Rethink BMI as a Health Metric In 2024, we’re still using BMI—a metric created in the 1830s by Adolphe Quetelet, a Belgian mathematician, to measure population averages, not individual health. BMI was never intended to assess personal health, yet it’s still widely used, even though it ignores critical factors like bone structure, muscle mass, and body composition. As a registered dietitian specializing in metabolic health, I believe it’s time to shift our focus to more accurate, insightful indicators. Markers like fasting insulin, triglyceride-to-HDL ratio, Hemoglobin A1c, and C-reactive protein offer a far clearer picture of metabolic function and disease risk than BMI ever could. BMI’s simplicity has kept it in place, but as science evolves, so should our health metrics. These advanced markers help us truly understand an individual’s health at a cellular level—enabling better prevention, targeted interventions, and a stronger foundation for long-term well-being. Let’s move beyond BMI and prioritize deeper, more informative measures of health.