I found plaque in my coronary arteries at 38, after a decade of eating well. Here's what I've done since.

Bone density isn't everything, say 6 experts on @theproof incl. @hjluks. piped.video/watch?v=-SwfgYWN… 15:50 LIFTMOR, 44:17 knees Images courtesy of The Proof with Simon Hill. Not affiliated, we just love the episode. Not medical advice. #longevity #podcast #bonehealth #osteoporosis

In people with a new diagnosis of coronary artery disease, no prior statin Rx (N=104), getting the LDL down to ~40 vs 70 mg/dL (via the 2 regimens, randomized, shown below) led to 20% more regression of atherosclerotic plaque in just 18 months @JAMACardio The lower the LDL, the more regression jamanetwork.com/journals/jam…

👉Can high HDL-C neutralize the risk associated with apoB? ☝️Not so fast 1️⃣ ApoB reflects the number of atherogenic particles, a key driver of atherosclerosis. 2️⃣ This is an observational study. It identifies associations and statistical interactions, but cannot establish causality or demonstrate that high HDL-C protects against apoB-related risk. 3️⃣ A flatter risk curve does not mean atherogenic particles become biologically harmless. 4️⃣ These findings cannot determine whether lowering apoB is less beneficial in individuals with high HDL-C. ☝️Atherosclerosis is driven by cumulative exposure to apoB-containing particles. An observational statistical interaction should not override established causal and interventional evidence. ☝️Association ≠ causation. High HDL-C does not invalidate apoB biology 🔓🔗 doi.org/10.1093/eurjpc/zwag4… @society_eas

Apparently, cause of death was cardiac triggered anaphylactic shock from an overdose of CJC1295 (Ipamorelin). I remember having a conversation with @CoffeeBlackMD a while back about the risk of anaphylactic shock. Be careful out there.

No surprises here - lower us better and the longer it is lower is best. And combo therapies is where is at!

🫀 Can coronary atherosclerosis actually regress? Our new randomized FLOWPROMOTE trial analysis, published TODAY in JAMA Cardiology, shows remarkable coronary plaque regression with intensive LDL-C lowering! Atherosclerosis is not necessarily a one-way process. 📄 JAMA Cardiology: doi.org/10.1001/jamacardio.2… #Atherosclerosis #LDL #Cardiology #CCTA

Millions take fish oil for brain health. A two-year study found no benefit sciencedaily.com/releases/20…

Statins and plaque stability

Important point here that needs to be fully understood/contemplated when someone says "but ApoB is only a problem if your artery wall isn't healthy". "there is little doubt that impaired glycocalyx barrier function can help increase LDL entry and accumulation, but the point is, even under otherwise healthy conditions, there can still be significant regional differences in glycocalyx structure and protection." I would also hypothesise that genetics play a role in glycocalyx function/health (i.e something that's non-modifiable just like bifurcations are)

If I had a lot of liver fat and/or elevated Hba1c, FBG, insulin, Waist:Ht ratio etc this is what I would do with my nutrition: - Focus on getting at least 1.2-1.6g per Kg of protein - Prioritise unsaturated fats - foods like fatty fish, avocado, olive oil, nuts and seeds - Lower carbohydrate intake to a low-moderate intake from whole foods (starchy vegetables, legumes and whole-grains). Legumes would be my go-to here as they come with fibre and protein. The more physical exercise you do the more carbohydrate load you will tolerate. - Broth based soups and salads before meals - Chew my food and eat slowly (not mindlessly watching tv or scrolling on social media) - Minimise the consumption of calorie dense, irresistible packaged foods (cookies, cakes, biscuits) - Some people may find they eat less calories over the day if they slightly shorten their eating window to 8-12 hours. It doesn't work for everyone but it can be a helpful lever to promote weight loss which is a top priority for lowering liver fat and restoring metabolic health. I think this is a pretty simple, uncontroversial plan, that would work for most.

There is a remarkable difference between finding evidence that challenges your assumptions and finding evidence that conveniently reassures you that you are the exception. This is an interesting paper by Sniderman and colleagues, examining nearly 294,000 UK Biobank participants and finding that higher HDL cholesterol modifies the association between ApoB and cardiovascular events. The interaction is real, statistically significant, and worthy of further investigation. But the leap from an observational association to suggesting that an individual with an LDL of 574 mg/dL and ApoB above 350 might be immune to atherosclerosis is quite another matter. In fact, the authors specifically caution that the observed interaction should not be taken as firm clinical evidence that ApoB ceases to be atherogenic or doesn't require treatment when HDL is high. That's a rather important sentence to leave out when you're discussing immunity. A statistical model showing attenuation of risk at high HDL is not a clinical trial. Nor does it establish that raising HDL is protective, or that someone with extraordinarily elevated ApoB can safely ignore decades of exposure. We've spent years discovering that increasing HDL cholesterol pharmacologically doesn't reliably reduce cardiovascular events. HDL is an interesting biomarker, but biomarkers and causal mechanisms aren't interchangeable. And then there is the problem of extrapolation. The ordinary distribution of ApoB in UK Biobank is not populated by large numbers of otherwise healthy individuals walking around with an LDL approaching 600. A modeled relationship at the extremes of HDL doesn't validate a personal experiment at the extremes of ApoB. Which brings me to my friend Simon Hill, @theproof, who recently published something I found considerably more rigorous and intellectually open. Simon had coronary CT angiograms suggesting a remarkable 48% reduction in plaque volume over 16.5 months. He could have celebrated, announced that his diet had reversed atherosclerosis, and made an excellent marketing campaign out of it. Instead, he examined the scans using three different analysis platforms. One suggested substantial regression, another progression, and the third essentially no change. Rather than promoting the most flattering result, he openly discussed the uncertainty. That's what scientific curiosity looks like when the evidence doesn't cooperate with your expectations. Simon also has something that makes this discussion more than academic. His father had a myocardial infarction at 41 and his grandfather at 49. Simon is now 40. He has lived with the consequences of cardiovascular disease in his family, and it's understandable that he wants to reduce his risk as much as reasonably possible. He has even started a PCSK9 inhibitor despite having an ApoB around 70–80 without medication. We can debate whether targeting an ApoB below 40 with Repatha offers sufficient additional clinical benefit in someone with his particular risk profile. That's a legitimate discussion. But I applaud his desire to live longer and his willingness to question his own most favorable findings. I understand the emotional component of this better than most. My own coronary calcium score is 90. I take rosuvastatin and ezetimibe, achieved an LDL around 60, and have seen it fall further since starting tirzepatide. I have no particular desire to measure every cubic millimeter of plaque in my coronary arteries. I know there is atherosclerosis, I know what the evidence supports, and I am treating the risk factors I can change. Simon wants more information and more aggressive prevention. I am comfortable treating what I already know. Neither approach requires pretending that uncertainty has disappeared. We physicians spend our lives talking about hazard ratios, plaque volumes, confidence intervals, and relative risk reductions. Yet one disrupted coronary plaque with a superimposed thrombus can turn all those abstractions into a very final event. That's why I care more about preventing myocardial infarctions than winning a competition over whose scan looks better. The remarkable thing about the comparison is that both Simon and Norwitz have favorable personal findings. Simon asks whether his are reliable. Norwitz highlights an observational study that might explain why his own findings are reassuring. There is a lesson there about confirmation bias, and it applies to all of us, physicians included. The Sniderman paper deserves attention. It may teach us something important about HDL biology and cardiovascular risk. But it does not establish immunity from ApoB, and it certainly doesn't overturn the causal evidence supporting LDL lowering. Science progresses when we investigate the observations that don't fit our models, not when we promote the observations that make us feel invulnerable. After all, the goal isn't to prove that your arteries are special. It's to live long enough that they never become the reason you aren't.

Sad news

Nope! Just did some genetic profiling with Robert Green