Lp(a) has emerged as a relatively potent driver of residual cardiovascular risk! We are told it is genetic and that a healthy diet cannot effect it! The reality is that several studies show that replacing carbs with saturated fat can and does lower it, sometimes fairly significantly! pmc.ncbi.nlm.nih.gov/article…

Plasma metabolomic signatures in children with autism spectrum disorder and their modulation following a gluten-free modified ketogenic diet Attn: ⁦@ChrisPalmerMD⁩ ⁦@Metabolic_Mind⁩ link.springer.com/article/10…

🚨 Just Released: 10 Years of T2D Remission! 🚨 It is now part of the scientific record. The study documents medication-free remission over a decade, achieved using a low-carbohydrate, lacto-ovo vegetarian diet, with systematic long-term safety evaluation. To our knowledge, this is the first such study conducted globally. What makes this work unique is not just remission, but rigour and duration. For most of this period (approximately 70-75%), I followed a ketogenic diet; during the remaining time, I followed a low-carbohydrate diet with carbohydrate intake below 100 g/day. This is a prospective N-of-1 longitudinal study, followed for a full decade, with repeated assessments across multiple domains: •Glycaemic control (HbA1c, fasting glucose, CGM) 🩸 •Insulin dynamics 🧬 •Advanced lipids including ApoB and Lipoprotein(a) •Inflammatory markers 🔥 •Liver and renal function (including cystatin-C) •Serial coronary artery calcium scans 🫀 •CT coronary angiography 🫀 •Carotid imaging (CIMT) •Bone mineral density (DEXA) 🦴 •Detailed ophthalmic imaging 👁️ Starting Hba1c was 7.2%. FBS 152 & PPBS 253 mg/dl. Achieved remission in the 4th month with Hba1c of 5.2% Over 10 years: •HbA1c, FBS & PPBS remained consistently in the non-diabetic range •Average Hba1c was 5 in 10 years. (4.7 to 5.3) •Average LDL and ApoB remained higher than recommended, but stable •No microvascular complications •No macrovascular disease •No deterioration in renal, skeletal, or ophthalmic health This was achieved without diabetes medication. Importantly, this is an Indian study. The dietary pattern was: •Low carbohydrate •Lacto-ovo vegetarian •Culturally adapted •Sustained for 10 years in a South Asian individual with the MONW (Metabolically Obese Normal Weight) phenotype This directly addresses a major gap in the literature: the absence of long-term, real-world safety data for low-carbohydrate approaches in South Asian, predominantly vegetarian populations. It demonstrates that: •Long-term remission is possible •Sustainability over a decade is possible •Comprehensive safety monitoring is feasible •Replication at larger scale is testable The intent of this work is not to prescribe, but to inform, challenge existing assumptions, and invite replication. As an N-of-1 longitudinal study, these findings are not generalizable by design. They are hypothesis-generating and intended to inform larger, prospective cohorts. India carries one of the highest diabetes burdens globally. Evidence addressing sustainability must emerge from within this context. This study is now part of the scientific record. Big thanks to Dr Jasmeet Phd @jasmeet481, whose relentless effort and scientific rigour made this study possible. She invested enormous time and care in shaping the manuscript and strengthening it to publication standard. Grateful to my guru, Anup Singh, who introduced me to low-carb nutrition in 2015 at the time of my Type 2 diabetes diagnosis. His guidance laid the foundation for my 10-year low-carb journey. Thank you to Arun Kumar who helped me when I was newly diagnosed. Big Thanks to the 3 doctors who were part of my 10 years journey & are the co-authors also. Dr Sharat Kolke MD (Med) - Physician - Criticare Asia Hosp. - Mumbai Dr Mihir Raut - MD - Diabetologist - Nanavati Max Hosp - Mumbai Dr R K Singh MD DM (Interventional Cardiologist) - Gandhi Medical College - Bhopal frontiersin.org/journals/nut…

If insulin resistance is not the same in everyone, can the treatment really be the same for all? Insulin resistance does not arise from a single tissue, a single pathway, or a single cause. It can originate in the liver, muscle, or adipose tissue. It can be driven by inactivity, stress hormones, illness, sleep loss, aging, or excess fuel. Yet it is often approached as one uniform condition with one uniform protocol. Calling all of this “one disease” oversimplifies human physiology. Insulin resistance is tissue-specific, stage-specific, and context-dependent. Two people can have the same HbA1c and completely different underlying biology. This is why lab numbers alone don’t tell the full story. And why blanket explanations often miss the mark. When biology is heterogeneous, standardization has limits. Personalization isn’t a trend or something fancy, it’s actually a physiological necessity.

🚨 Slimming down isn't always a win for your brain. A new study suggests rapid weight loss in mid-life can spike inflammation in the brain's appetite center. The brain interprets sudden calorie deficit as a stress signal, potentially damaging neural connections. Lose weight slowly. Crash diets are crashing more than your metabolism. Source: ScienceDaily (December 28, 2025)