Christoffer Baustad Nilsen 🐈‍

Eat legumes daily. That's it. That's the Tweet.

Introduction of β-carotene-rich orange sweet potato in rural Uganda resulted in increased vitamin A intakes among children and women and improved vitamin A status among children pubmed.ncbi.nlm.nih.gov/22875553/

"We studied the effect of lipid-lowering therapy on LDL permeability and degradation of LDL particles in atherosclerotic aortas of mice by measuring the accumulation of iodinated LDL particles in the arterial wall." ahajournals.org/doi/10.1161/ci…

@kiwi_in_oz_ @cremieuxrecueil All ApoB-containing lipoproteins are atherogenic. And there are almost no oxidized LDL in circulation. Most of it is is oxidized inside the intima. pubmed.ncbi.nlm.nih.gov/33883728/ pubmed.ncbi.nlm.nih.gov/7749869/

@cremieuxrecueil Which LDL are you referring to? The large bouyant LDL, or the small oxidised LDL?

Lowering LDL will extend lifespans. The trials, the genetic studies, and even the prospective cohort studies all agree that the more you lower LDL, the greater the reduction in your risk of heart disease. This is one of the clearest chronic disease prevention findings there is.

"The use of ALA labelled with radioisotopes suggested that with a background diet high in saturated fat conversion to long-chain metabolites is approximately 6% for EPA and 3.8% for DHA. With a diet rich in n-6 PUFA, conversion is reduced by 40 to 50%." pubmed.ncbi.nlm.nih.gov/9637947/

If mechanistic reasoning was sufficient to understand drugs, medicine, and diet, then drugs would not fail in expensive clinical trials. Yet they do in >90% of cases, despite always having a mountain of mechanistic and preclinical evidence to support them.

@MaritKolby @larsms @nicknorwitz @realDaveFeldman They are planning to retract the paper. It would be rather unusual, to put it that way, to revise our paper in order to address a paper that has itself been retracted. @larsms @MaritKolby x.com/nicknorwitz/st…

@larsms @ChristofferBN @nicknorwitz @realDaveFeldman Looking forward to the correction of this (article in Norwegian) as well. scup.com/doi/full/10.18…

And when the facts change again, what do you do then, sir? 🥸 @ChristofferBN @nicknorwitz @realDaveFeldman

@MaritKolby @larsms @nicknorwitz @realDaveFeldman Anyway, we can't correct the article until they correct theirs. (Although it really should be retracted, imho.) And for now, these "results" are just a post on X/Twitter.

@MaritKolby @larsms @nicknorwitz @realDaveFeldman Afaik there's no compelling reason to favour the Heartflow and/or QAngio analysis over the Cleerly analysis (which was preregistrated) to begin with. To put it bluntly: The results with Cleerly didnt say what they wanted so they went with a different method. Also, selection bias

This is an important signal, but it needs careful framing rather than polemics. Statins do robustly reduce ASCVD risk via LDL lowering - that’s not in dispute. But they are pleiotropic drugs, and pleiotropy cuts both ways. There is now reproducible human data showing certain statins (including atorvastatin) reduce circulating GLP-1 and can worsen glycaemic control in a subset of patients - consistent with the well-described increased diabetes risk seen in large meta-analyses. That doesn’t “invalidate” statins, but it does matter clinically, especially in insulin-resistant or prediabetic patients. In practice, this argues for phenotype-guided therapy, not dogma: • ASCVD risk decrease via LDL reduction • Metabolic risk may increase in some • GLP-1 signalling, insulin sensitivity, muscle symptoms, and gut effects deserve monitoring - not omission Good medicine isn’t pro- or anti-statin. It’s about weighing net benefit for the person in front of you, adjusting dose, drug choice, timing, and co-interventions (diet, exercise, sometimes GLP-1s themselves). Transparency about trade-offs strengthens trust - it doesn’t weaken evidence.

Your regular friendly reminder: These four datasets all have the same mean, median, and variance. Moral of the story: Always visualize your data! [Link below.]

Shared this on Bluesky, too: bsky.app/profile/christ…

Most of us born in the West won by a landslide – we hit life's jackpot. But past a certain level of comfort, a bigger jackpot doesn't add much happiness. A better way to feel happier? Share a bit of that luck with others. gieffektivt.no/innsamling/en-…

@EANorway @EffectvAltruism @gieffektivt @EASweden

Why does ApoB outperform LDL-C, triglycerides & TG:HDL-C ratio with regards to predicting future risk of heart attack and stroke? 1. ApoB directly counts atherogenic particles ▪️Each atherogenic lipoprotein particle (LDL, VLDL, IDL, Lp(a)) carries exactly one ApoB molecule. ▪️ApoB therefore reflects the number of artery penetrating particles, not just the cholesterol content. ▪️Atherosclerosis is particle-driven, not cholesterol-mass driven. 2. LDL-C measures cholesterol, not particle number ▪️LDL-C quantifies how much cholesterol is inside LDL particles. ▪️Two individuals can have the same LDL-C but very different numbers of LDL particles. ▪️Higher particle number → more arterial wall entry → higher risk. ▪️ApoB captures this risk; LDL-C often misses it. 3. Small, dense LDL is fully captured by ApoB ▪️Small, dense LDL particles carry less cholesterol per particle. ▪️LDL-C underestimates risk when LDL particles are small and numerous. ▪️ApoB counts them accurately, regardless of size. 4. Triglycerides are an indirect and unstable marker ▪️Triglyceride levels fluctuate with: Recent meals, Alcohol intake, Exercise, and Insulin sensitivity ▪️ApoB is biologically stable and reflects long-term atherogenic burden. 5. TG:HDL-C ratio is a surrogate, not a causal measure ▪️TG:HDL-C ratio estimates insulin resistance and metabolic risk. ▪️It does not directly measure atherogenic particle burden. ▪️ApoB directly quantifies the particles that cause plaque formation. 6. ApoB integrates all atherogenic lipoproteins Unlike LDL-C, ApoB includes LDL, VLDL remnants, IDL, and Lipoprotein(a). These particles all enter the arterial wall and drive plaque growth. 7. ApoB predicts risk even when LDL-C is “normal” ▪️Many cardiovascular events occur in people with “acceptable” LDL-C. ▪️Discordance scenarios: Normal LDL-C + high ApoB → high residual risk ▪️ApoB consistently predicts events in these individuals. 8. Superior risk prediction across populations ApoB outperforms LDL-C and non-HDL-C in: Diabetes, Obesity, Metabolic syndrome, Chronic kidney disease, and South Asians (high particle number at lower LDL-C) 9. Treatment response tracks better with ApoB ▪️Statins, ezetimibe, and PCSK9 inhibitors reduce events in proportion to ApoB reduction, not LDL reduction. ▪️Residual risk correlates with residual ApoB. 10. Atherosclerosis is a particle-retention disease ▪️The initiating event in plaque formation is retention of ApoB-containing particles in the arterial wall. ▪️ApoB is therefore mechanistically causal, not just associative. ✅Summary ApoB measures the number of atherogenic particles, the true drivers of atherosclerosis, making it the most accurate single predictor of future heart attack and stroke. Dr Sudhir Kumar @hyderabaddoctor

🤔 Why Is Hypercholesterolaemia So Prevalent? 🧬An Evolutionary Perspective 🔍 Key Points 👉 LDL is an evolutionary by-product, not a purposeful cholesterol-delivery system. It arises from VLDL—our ancestral engine for energy transport and survival during famine. 👉 Our genes were shaped for scarcity, not abundance. Traits that once promoted energy efficiency now drive hypercholesterolaemia, obesity, and ASCVD in high-calorie, low-activity societies. 👉 Ancestral LDL-C levels were ~50–70 mg/dL, far below today’s “normal” values (~120 mg/dL), and much closer to the levels associated with minimal atherosclerosis. 👉 APOE4 is the quintessential thrifty allele—adaptive for energy retention in harsh environments, maladaptive in modern lifestyles. 👉 Natural selection won’t correct this problem. Hypercholesterolaemia causes disease after reproductive years, so evolution has no incentive to eliminate it. 👉 Infants’ LDL-C levels (20–40 mg/dL) reflect our physiological baseline, supporting the safety—and evolutionary coherence—of aggressive LDL-lowering today. 👆Takeaway Hypercholesterolaemia isn’t a coincidence—it’s a mismatch. Our Stone-Age biology meets a modern environment it wasn’t built for. Only prevention, lifestyle, and targeted lipid-lowering therapy can bridge that evolutionary gap. 🔗academic.oup.com/eurheartj/arti… @society_eas @ehj_ed

1. If you & your friend (same size, age, weight) ate the same 1,000-calorie surplus every day for 3 months, will you gain the same amount of weight? A landmark experiment on identical twins helps us answer this question and that our 🧬 direct the body's response to overeating 🧵

Perhaps the greatest failure of the economics profession has been our inability to sell the idea that we should tax "bads" like congestion and pollution. One reason building is so expensive is that we have so many regulations instead of just prices.

@cremieuxrecueil Spicy dude

Decker is going down the route of America's most controversial philosopher, Stephen Kershnar. Let's look through some of Dr. Kershnar's incredible intellectual and philosophical contributions!🧵 Firstly: Why Americans shouldn't be grateful to veterans.

@MaritKolby No multiple comparisons correction (Bonferroni etc)

"Higher intake of high-fat cheese and high-fat cream was associated with a lower risk of all-cause dementia, whereas low-fat cheese, low-fat cream, and other dairy products showed no significant association" pubmed.ncbi.nlm.nih.gov/41406402/

@alojoh @cremieuxrecueil No, there isn't. There's esterified ('stored') and unesterified ('free') cholesterol.

@cremieuxrecueil You realise there is good and bad cholesterol?

The fact that your baseline dietary cholesterol intake affects the effects of dietary cholesterol intake has confused so many people into thinking nonsense things like "eggs don't raise your cholesterol". This even fools many researchers, despite this being known for decades!