Simon Hill MSc, BSc @theproof

We have spent decades treating the number on the scale as the goal. What if it was never the right target? Dr Mauricio Gonzalez, a triple board-certified physician and endocrinology fellow, joins me to explain why liver fat, not body weight, is becoming the real measure of metabolic health, and what that means for how we think about GLP-1 medications, cholesterol, and longevity. For the full show notes head to: theproof.com/why-liver-fat-…

@ProfTimNoakes Scary carbohydrates 👻

Obesity Doctor: How to Lose Weight and Reverse Metabolic Disease in 2026 | Dr. Mau youtu.be/UF3tse9TG3k ⁦@DrMauinforma⁩

The response-to-injury hypothesis was discussed on page 43-49 and 175-178 in "The Cholesterol Wars: The Skeptics vs the Preponderance of Evidence" by D. Stenberg. amazon.com/Cholesterol-Wa… Countless animal models and autopsy studies over the decades have debunked it. 🧵 1/9

Bret Scher, MD @bschermd

3 months ago

Your veins and arteries carry the same blood. Same LDL. Same ApoB. Same everything. Yet veins almost never get plaque. Arteries constantly do. Maybe you've seen the recent discussions about this. It's an interesting question that provides clues in cardiovascular science, and

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Compelling. AND on top of this still more to learn

Pablo Corral MD @drpablocorral

4 days ago

👉OVER A CENTURY OF SCIENCE. ONE CONSISTENT MESSAGE. ☝️In medicine, few hypotheses have been tested as rigorously as the relationship between LDL cholesterol and atherosclerotic cardiovascular disease. 🐇 1913 – Nikolai Anitschkow demonstrated that cholesterol-rich diets induce

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👉OVER A CENTURY OF SCIENCE. ONE CONSISTENT MESSAGE. ☝️In medicine, few hypotheses have been tested as rigorously as the relationship between LDL cholesterol and atherosclerotic cardiovascular disease. 🐇 1913 – Nikolai Anitschkow demonstrated that cholesterol-rich diets induce atherosclerosis in experimental models. ❤️ 1948 – The Framingham Heart Study established the association between cholesterol levels and cardiovascular risk. 🏆 1964 Nobel Prize – Konrad Bloch and Feodor Lynen elucidated the biosynthesis and metabolism of cholesterol. 🏆 1985 Nobel Prize – Michael Brown and Joseph Goldstein discovered the LDL receptor, transforming our understanding of cholesterol regulation and familial hypercholesterolemia. 💊 1994 (4S Trial) – Lowering LDL-C with statins reduced cardiovascular events and mortality. 💊+ 💊2015 (IMPROVE-IT) – Further LDL-C reduction with ezetimibe translated into additional cardiovascular benefit. 💉2017–2018 (FOURIER & ODYSSEY Outcomes) – PCSK9 inhibitors demonstrated that achieving very low LDL-C levels produces further risk reduction. 🧬👫🏻🔬🩻Today – Genetics, epidemiology, pathology, imaging, Mendelian randomization studies, and randomized clinical trials continue to converge on the same conclusion. More than a century of basic science and clinical research has consistently pointed in one direction: 👉LDL cholesterol is causal. ☝️Lower is better. ☝️Earlier is better. ☝️Longer is better. When a scientific concept is supported by experimental biology, human genetics, epidemiology, randomized clinical trials, and two Nobel Prizes in Medicine, it is no longer merely a hypothesis. 🙌 It is biology. @society_eas @nationallipid

Excellent video. @Drlipid presents a measured, granular discussion of one of the most important emerging areas in preventive cardiology: Lp(a)-lowering therapy. At @niCVRI, we have completed two gene-silencing trials targeting Lp(a). One has now advanced to compassionate use—an exceptionally unusual development for treatment of a cardiovascular risk factor after multicenter trial experience. What remains to be shown, and may soon be revealed, is whether profound Lp(a) lowering leads not only to biomarker reduction, but to plaque regression and reduction in major adverse cardiovascular events. Stand by - soon to be revealed.🫵

@RacecarengTom @raphaels7 Details to come. Results surprising.

@raphaels7 @RacecarengTom However we are talking about measurement in people with low plaque burden where the assessment tools are not validated and likely subject to great noise. I’m releasing one of the results from the other analyses soon - showing I had HUGE regression… We need some humility here

@DrGillespie_GP Interesting question. I hadn’t looked at it this way. I guess that makes me happier I’m sharing this as a teaching and awareness tool rather than just using it for myself.

My position is that there isn’t good validation in people with low plaque levels so I’m not sure this should surprise us. Firstly if we accept the 8 re-scans led to different results (this is unpublished data nobody has shared publically) … I think it raises an interesting question. What’s the scan rescan reproducibility of all 3 analyses in subjects with low plaque volume.

Interesting! Good thing about LP(a) is at least the risk is known and drug trials are underway. PCSK9 inhibitors nudge it down by 25% or so - although we don’t know what that means for outcomes. Hopefully one day genetic profiling is more advanced than today and we can all get a detailed genetic map and then tailor drugs accordingly. Have some episodes planned on polygenic risk scoring as a starting point to explore this field.

I had my CT Angiography analysed by QAngio, Heartflow and Cleerly at two time points 16 months apart. Both scans were done at the Lundquist Institute using the same machines and protocol. It was interesting to see where these analyses agreed with one another and where they disagreed. Without spoiling what’s to come - the pleasing result was that they all agreed I have very little plaque that most cardiologists have laughed at. And they agreed I don’t have rapid plaque progression. Phew! 🥵 I'll be releasing various data from these analyses over the coming weeks/months. First up is QAngio. Thanks to @BudoffMd for helping me run this analysis. Data summarised in this graph and charted next to Keto-CTA data (given the primary outcome was Qangio measured plaque change) with mean, median and IQR's. According to QAngio my Total Plaque Volume (TPV) is very small at approx. 11 mm3 total plaque and the annualised change was just +0.79 mm3/yr. Dr Budoff described this change as within noise - treat as stable without progression. The Keto-CTA mean TPV on follow up was 70 mm3 with a mean change of +18.7 mm3 and mean change of +6.6 mm3. I will add that 70 mm3 is also considered a small amount of absolute plaque. Note 1: what we’re seeing here in both my case and Keto-CTA could well be affected by measurement noise due to low plaque volumes and insufficient time between scans. Note 2: while I believe elevated ApoB (above physiologic levels) is necessary for atherosclerosis not everyone with same ApoB will have the same plaque burden. There are clearly other established and not yet established risk factors. Humility is needed but as a general rule of thumb getting ApoB to goal as well as optimising other risk factors seems like a sensible approach. I’m a great example of someone who probably wouldn’t have started lipid lowering therapy (commenced after these scans) had I not known I had some plaque (albeit a tiny amount). My ApoB was already at 70-80 mg/dl with lifestyle. But with some soft plaque and strong family history of early CAD why risk it when I can get ApoB to 30-40 mg/dl safely with monotherapy. Note 3: I’m sharing this data because I hope it encourages more people to be proactive with their health and at the very least discuss a basic risk factor assessment with their doctor. Especially if they have a family history of cvd. Note 4: The next scan I’ll do to continue this case study will be at year 5. This will be interesting given my recent commencement of LLT. Note 5: Could we cherry pick one data point from Keto-CTA to compare to me? Perhaps a regressor? Yes! And the point proven would be that n=1 data should be interpreted with absolute caution and humility for what it is and what it is not - I don’t seem to have much plaque or rapid progression - that’s about all I’m prepared to say. Final note: I have a series of episodes coming out with CT imaging experts, cardiologists, lipidologists and other experts for us to learn from. In one of these episodes will spend time on an analysis which showed marked regression of plaque (>40%).

@dvfollowsls @RonKarlsbergMD @RonBlankstein @realDaveFeldman @BudoffMd @Drlipid @NutritionMadeS3 @DrNadolsky Mostly because I should only need monotherapy to get under 40 mg/dl an an injection 1 x month suits my lifestyle. The best medication is the one you adhere to!

@pacifieraka @RonKarlsbergMD @RonBlankstein @realDaveFeldman @BudoffMd @Drlipid @NutritionMadeS3 @DrNadolsky If you think any diet can protect everyone against developing plaque - especially if done for <25% of one’s life - I recomend you read more on the pathophysiology of CAD.

@NOTAINOTSPAM @RonKarlsbergMD @RonBlankstein @realDaveFeldman @BudoffMd @Drlipid @NutritionMadeS3 @DrNadolsky Reduced at age 30 with lifestyle. Before that ldl-c usually at 120-130 mg/dl

Also to put this in perspective. 11mm3 total plaque is about the volume of half a grain of rice. And not in a single spot but distributed along the length of the LAD as a thin, diffuse layer lining the artery wall - over nearly 2 cm of vessel, with the lumen still comfortably open (plaque often remodels outward in early stages).

Ohh it’s a good old PLAQUE-OFF! Who doesn’t love a showdown. I predicted this would follow. You were quicker than I thought. Few things: So we have more in common than not. Very low risk of a cvd event any time soon and we both take lipid lowering drugs. Albeit for different reasons. I take mine to safely lower ApoB < 40 mg/dl and you take yours off label for brain health. I’m secretly rooting for the artery and brain benefits! You have had very high ApoB for approx 7 years and are about a decade younger than me. I had moderate ApoB for 30 years (best estimate from historical bloods) and low for 9. A lifetime ApoB burden analysis would be interesting. I have a strong family history of early CAD (early 40’s). You have an inflammatory auto-immune condition. We both have low LP(a) to my knowledge. Two different people with different genes, health experiences and exposures. Both low risk and both on lipid lowering drugs. And I hope both very healthy for decades to come so we can continue to debate the data and what it means.

@Tellit007 Totally agree

@realDaveFeldman @RonKarlsbergMD @RonBlankstein @BudoffMd @Drlipid @NutritionMadeS3 @DrNadolsky Is the data available to tun a sub analysis on 35-40 year olds?

@duckhunterbits @nicknorwitz @realDaveFeldman @RonKarlsbergMD @RonBlankstein @BudoffMd @Drlipid @NutritionMadeS3 @DrNadolsky Thanks for sharing Joe. Best of luck with the CT 🤞🏼. Sounds like you’re under the care of a cardiologist?

@MurseDarius @realDaveFeldman @RonKarlsbergMD @RonBlankstein @BudoffMd @Drlipid @NutritionMadeS3 @DrNadolsky Haha all good!