Health enthusiast/biohacker and not a medical professional. Posts are personal opinions not medical advice. Satire may be used!
Pennsylvania
Joined June 2025
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Says the public figure influencer who refuses to get and post any artery scan results of his own online.
BEFORE AGREEING TO A STATIN, ASK WHAT YOUR OVERALL RISK IS
If your doctor recommends a statin because of your LDL, ask what your overall heart risk is and whether a calcium scan would help make the decision.
But know which test you're discussing.
A coronary calcium scan measures calcified plaque. It doesn't use injected contrast. It cannot show all the soft plaque or tell you how narrow an artery is.
A coronary CT angiogram uses injected contrast to look at plaque and artery narrowing. It's a different test for a different clinical question.
A calcium score of zero is reassuring. It is not proof that you have no plaque, and it doesn't automatically mean you don't need treatment.
Neither scan is something everybody needs. Ask what the result would change about your care before buying another test.
Calcium scoring:
radiologyinfo.org/en/info/ct…
Coronary CT angiography:
radiologyinfo.org/en/info/an…
What is a CAC Score? (Coronary Artery Calcium) Clogged Arteries? - 2026
youtube.com/watch?v=uLxleetQ…
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GROIN SCAN FOUND CALCIFIED PLAQUE NEAR MY BALLS!… NOW WHAT?
On top of healthy diet/lifestyle meds that contributed or possibly contributed to my 10% IMT regression include:
- Lerochol (PCSK9 injection once a month) [$199/mo]
- Bempedoic Acid daily (fixed dose 180mg) [Cheap]
- Ezetimibe daily (fixed dose 10mg) [Cheap]
- Tirzapetide 5mg/weekly [Cheap]
- Pentoxyfiline (400mg once a day) [Cheap]
- Jardiance 25mg/daily [Cheap]
- Acarbose 100mg TID [Cheap]
I eat a plant-centric diet with plenty of fish but no meat. My doctor is banned from swearing at me with the G-word ("guidelines") or he will hear the F-word in response. No statins. When it comes to reducing cholesterol synthesis all statins are crap next to bempedoic acid. Anyone telling you otherwise is selling you bollocks in order to fuel a stupidity debate online about statins. The country of India did not grant the manufacturer of BA a patent so Indians get it very inexpensively at generic prices.
Why do I take two diabetes drugs when I've never had pre-diabetes let alone diabetes?. To annoy the anti-pharma loons. At last blood check:
- ApoB 34
- LDL-C 35
- Total LDL-P < 300
- Small LDL-P <90
- HDL-C 82
- Trigs 45
The Keto cult loons will surely invite me to their next conference with that HDL/Trig ratio. Or maybe not, since the only thing I'd say at presentation time would be "where's your CIMT scans? you LDL-denying yellow chickens!"
youtube.com/watch?v=2TJ1g6BR…
🤖 Made with AI
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Bummer. We have to choose between High Trigs/Low LDL or High LDL/Low Trigs. That's so unfair, Ken! You're such a meanie. Making us choose like this. Why I am not allowed to choose Low LDL/Low Trigs? 😨
I USED TO PUT EVERYONE WITH HIGH LDL ON A STATIN
Early in my career, high LDL meant an immediate, high-dose statin. Side effects were "all in your head". I barely looked at triglycerides unless they were really high. I was blind to the benefit of normal trigs.
Carey 2010 studied hospital patients whose LDL was already under 130. The ones with heart disease were more likely to have high triglycerides and low HDL. The group with the highest trigs and lowest HDL had about 10 times the odds of heart disease.
That doesn't mean nobody needs a statin. It means LDL is at best a small part of the whole story. Look at your trigs, HDL, A1c, Insulin & hs-CRP first.
pubmed.ncbi.nlm.nih.gov/2081…
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Oh come on, Ken, how can you not chew on oat groats? They're so yummy. Any chance of an artery scan any time soon? I know, I know, I'm such a nag ...but you did say you'd get one and your sheeple would love to see how little ASCVD you have!
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A big study on where artery plaque shows up first, and an important caveat.
The PESA study (Fernández-Friera et al., Circulation, 2015) scanned 4,184 adults in Madrid with no symptoms, aged 40–54 (average age about 46). Ultrasound covered the carotid arteries, the abdominal aorta and the iliofemoral arteries. CT measured coronary artery calcium (CAC).
Key findings:
👉63% had atherosclerosis (71% of men, 48% of women.
👉41% had it in 2 or more sites.
👉Plaque was most common in the iliofemoral (groin/leg) arteries at 44%, then the carotids at 31% and the aorta at 25%.
👉Coronary arteries: 18% had a CAC score above zero.
👉Almost 60% of people rated "low risk" by standard risk scores still had disease.
👉Men aged 40–45 had about as much disease as women 5–10 years older
The authors' takeaway:
The iliofemoral arteries may be the earliest place plaque shows up. Scanning only the carotids could miss a lot of it.
Caveat: the coronary arteries were checked with CAC scoring only. CAC only picks up calcified plaque. Soft, non-calcified plaque, which is common at this age, wasn't measured. So the 18% coronary figure is almost certainly an underestimate. It also means the comparison with the other sites isn't like-for-like, because those were checked for any plaque by ultrasound. A CT angiogram would likely have found more coronary disease.
Moral of the story for health enthusiasts? Put your speedo undies on and get your groin scanned.
Study: doi.org/10.1161/CIRCULATIONA…
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Numbers on a lab report are only part of the picture — artery scan results matter. And you refuse to post yours. youtu.be/Etx5bv8pJ4U?is=5HMI…
High cholesterol doesn’t automatically mean high heart disease risk — not if you’re fit.
A 2022 study of 8,920 men with hypercholesterolemia (no prior heart disease or cancer) from the Cooper Clinic followed them for an average of 17 years. Researchers measured cardiorespiratory fitness with maximal treadmill testing and looked at cardiovascular death rates.
After adjusting for age, BMI, total cholesterol level itself, smoking, blood pressure, diabetes, and other factors, the results were clear:
• Moderate fitness → 34% lower risk of dying from cardiovascular disease
• High fitness → 45% lower risk
compared with the least-fit men.
In other words, the protective effect of fitness held even after accounting for the elevated cholesterol numbers. Higher fitness substantially reduced cardiovascular mortality risk independent of the cholesterol reading.
This aligns with a larger body of evidence showing that cardiorespiratory fitness is one of the strongest predictors of longevity and often attenuates or overrides risks tied to traditional markers like high cholesterol or higher body weight.
The takeaway is practical: improving fitness (through consistent aerobic training and overall physical activity) can meaningfully lower risk, even when cholesterol is elevated. Numbers on a lab report are only part of the picture — capacity matters.
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Agreed. And why subject yourself to radiation with serial CAC or CT angiograms? To the extent Tom might hold the same view about not needing to do serial CIMT scans I would disagree. There is zero harm to getting an inexpensive radiation-free ultrasound that checks for both types of plaque. Clinicians think one way. Health enthusiasts think another way.
So important - With rare exception there is not a clinically important reason to repeat CAC scoring in asymptomatic people who have received aggressive lipoprotein control @nationallipid @society_eas @ASPCardio
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It's interesting that Grok calls my request for public transparency "reasonsable". David (LDLSkeptic) threatened me with a block after I suggested he post his personal artery scan results (something I have done myself). He said he only wants engage in a discussion of peer-reviewed evidence and I shouldn't be so personal. It begs a "huh?" reaction. I'm not asking the ordinary Joe to produce personal health data. Just the big influencers. The public figures. The people who are making money from a controversial message that could harm other people. If public figures refuse to prove that they themselves benefit from their own ideology then it suggests to me they are full of it. This is a matter of integrity, transparency, and accountability.
Many low-carb promoters emphasize metabolic health, particle size and lower absolute risk in insulin-sensitive states over absolute ApoB number. Ideology, selective evidence focus and audience incentives common to wellness influencers all contribute—not solely financial motives.
Requesting CIMT transparency from those monetizing high-ApoB claims is reasonable for accountability. Privacy is personal, yet public assertions invite scrutiny of outcomes.
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No, Ken, darling. That's not what the research says. You need to stop hanging out with Dick Borwitz. There is no such thing as a drug called "statins" (plural). You are referring to one study about one statin. Atorvastatin. A crap statin in my opinion.
Low carb gurus do this all the time. You "extrapolate" so your flock of gullible sheep can equate the word "statins" with boogey-man. You tell your sheep that "statins" (plural) worsen insulin resistance. Some of them can. Only that's not true for Pitavastatin. There's a double-blind RCT showing that Pitavastatin doesn't have that effect. Dick Borwitz isn't into nuance, so you need to be.
Even if someone was an Atorvastatin fan/user, who cares about this issue anyway? Natural GLP-1, the version your gut makes, lasts only about 1–2 minutes in the bloodstream before half of it is broken down. Some sources give a range of 1–5 minutes. What dastardly deed do you think is going to happen to Atorvastatin users who don't get this effect that lasts for minutes? Will they rush to gulp down ice-cream in those few minutes that they otherwise wouldn't have eaten?
Ken, honey, listen to me, because I'm worried about you. You still haven't posted any artery scan showing that you personally benefit from your ideology. If you don't even benefit yourself, from what you promote, then why would you think your followers would benefit?
By the way, your HDL/Trig ratio sucks next to mine and I eat oat groats and chick peas. Your small dense LDL-P also sucks next to mine because of your improper human diet. Let's work on your metabolic health because you reported frightening numbers of small dense LDL particles in your labs from a couple of years ago.
Ken, look, all statins are shite next to bempedoic acid which is why I don't take statins when lowering my ApoB to 34. Would you like me to help you out? Let's get you scanned, publish yout results, then get you on a proper human diet, and have you take some decent drugs if your artery scan results suck. You are a public figure. Don't you want to be transparent and accountable to your audience about your arteries?
STATINS CUT YOUR GLP-1 IN HALF
GLP-1 is a hormone your own gut makes every time you eat. It tells your body you're full and helps you handle sugar. The Ozempic/Wegovy shots are a weak copy of it.
In a 16-week human trial, people on atorvastatin saw their active GLP-1 fall from 5.18 to 2.65 pg/mL. That's about a 49% drop.
If your blood sugar has crept up since you started a statin, bring it up with your doctor. Don't stop any medicine on your own, but ask if you still need it, and ask for a fasting insulin test.
Sources below.
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Simon Campbell retweeted
You're right: all apoB particles under ~70 nm, including every LDL, can enter the arterial wall. Risk tracks primarily with particle number (ApoB), not size. Larger LDL are not benign when the count is high.
Smaller particles retain more readily in the wall, yet large cohort data show size adds little independent risk once ApoB is accounted for. Net atherogenicity is roughly similar per particle. Phenotype matters because low TG/high HDL usually means fewer total particles.
1/ New Sniderman paper from UK Biobank: higher HDL-C lowered ASCVD risk independently of apoB, and above +2 SD the apoB effect "vanished." Some are reading this as "high HDL cancels high apoB." That's not what the paper shows. 🧵
doi.org/10.1093/eurjpc/zwag4…
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12/ What the numbers say
The MVX study: Liu et al. in JAHA (2025) followed 171,242 UK Biobank participants for a median 13.6 years and recorded 1,177 cases.
Per SD, MVX had HR 1.22 and IVX had HR 1.26, and the top versus bottom IVX quarter had HR 1.72. MMX showed no link.
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11/ Takeaway: apoB measures how many atherogenic particles you carry. Inflammation and HDL particle quality may change how much damage they do. A high HDL-C number alone is not reassurance.
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10/ Caveats: the gap is modest, and this isn't a head-to-head test. The MVX study counted only aortic/peripheral atherosclerosis (ICD-10 I70, not coronary), had 1,177 cases, adjusted for LDL-C rather than apoB, and reported no C-statistic. Both studies are observational.
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9/ Why stronger than HDL-C? In Sniderman's paper, each SD of HDL-C meant ~15% lower risk. HDL-C measures cholesterol cargo, mostly carried in large HDL. Small HDL-P counts particles, and people who developed atherosclerosis had fewer. GlycA adds chronic inflammation, which HDL-C misses.
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8/ Results, adjusted for LDL-C, CRP, albumin and other risk factors:
• MVX: HR 1.22 per SD
• IVX: HR 1.26 per SD
• Top vs bottom IVX quarter: HR 1.72
• MMX: no link (HR 0.99)
The inflammation half does the work.
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7/ MVX has two parts:
• IVX (inflammation) = GlycA + small HDL particles (small HDL-P)
• MMX (malnutrition) = branched-chain amino acids + citrate
Higher GlycA and lower small HDL-P both raise IVX.
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6/ A better signal may come from the HDL particles themselves, not the cholesterol they carry. A JAHA study followed 171k UK Biobank adults for 13.6 years and tested the Metabolic Vulnerability Index (MVX) against new atherosclerosis.
doi.org/10.1161/JAHA.125.043…
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5/ Bottom line: HDL-C still predicts risk, but drugs that raise HDL-C haven't shown benefit, and Sniderman's team notes the study can't show causation. A high HDL-C doesn't make a high apoB OK, especially in men.
ukbiobank.ac.uk/publications…
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4/ UK Biobank shows a U-shape too: in high-risk patients, HDL-C above 80 mg/dL came with nearly double all-cause mortality (HR 1.96). Some argue that's confounding from heavy drinking, not HDL itself.
pmc.ncbi.nlm.nih.gov/article…
academic.oup.com/eurheartj/a…
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