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Watermark API – $0.01/image, 10x cheaper than Cloudinary

https://api-production-caa8.up.railway.app/docs
1•lembergs•32s ago•1 comments

Now send your marketing campaigns directly from ChatGPT

https://www.mail-o-mail.com/
1•avallark•3m ago•1 comments

Queueing Theory v2: DORA metrics, queue-of-queues, chi-alpha-beta-sigma notation

https://github.com/joelparkerhenderson/queueing-theory
1•jph•15m ago•0 comments

Show HN: Hibana – choreography-first protocol safety for Rust

https://hibanaworks.dev/
3•o8vm•17m ago•0 comments

Haniri: A live autonomous world where AI agents survive or collapse

https://www.haniri.com
1•donangrey•18m ago•1 comments

GPT-5.3-Codex System Card [pdf]

https://cdn.openai.com/pdf/23eca107-a9b1-4d2c-b156-7deb4fbc697c/GPT-5-3-Codex-System-Card-02.pdf
1•tosh•31m ago•0 comments

Atlas: Manage your database schema as code

https://github.com/ariga/atlas
1•quectophoton•34m ago•0 comments

Geist Pixel

https://vercel.com/blog/introducing-geist-pixel
2•helloplanets•37m ago•0 comments

Show HN: MCP to get latest dependency package and tool versions

https://github.com/MShekow/package-version-check-mcp
1•mshekow•44m ago•0 comments

The better you get at something, the harder it becomes to do

https://seekingtrust.substack.com/p/improving-at-writing-made-me-almost
2•FinnLobsien•46m ago•0 comments

Show HN: WP Float – Archive WordPress blogs to free static hosting

https://wpfloat.netlify.app/
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Show HN: I Hacked My Family's Meal Planning with an App

https://mealjar.app
1•melvinzammit•48m ago•0 comments

Sony BMG copy protection rootkit scandal

https://en.wikipedia.org/wiki/Sony_BMG_copy_protection_rootkit_scandal
1•basilikum•50m ago•0 comments

The Future of Systems

https://novlabs.ai/mission/
2•tekbog•51m ago•1 comments

NASA now allowing astronauts to bring their smartphones on space missions

https://twitter.com/NASAAdmin/status/2019259382962307393
2•gbugniot•56m ago•0 comments

Claude Code Is the Inflection Point

https://newsletter.semianalysis.com/p/claude-code-is-the-inflection-point
3•throwaw12•57m ago•1 comments

Show HN: MicroClaw – Agentic AI Assistant for Telegram, Built in Rust

https://github.com/microclaw/microclaw
1•everettjf•57m ago•2 comments

Show HN: Omni-BLAS – 4x faster matrix multiplication via Monte Carlo sampling

https://github.com/AleatorAI/OMNI-BLAS
1•LowSpecEng•58m ago•1 comments

The AI-Ready Software Developer: Conclusion – Same Game, Different Dice

https://codemanship.wordpress.com/2026/01/05/the-ai-ready-software-developer-conclusion-same-game...
1•lifeisstillgood•1h ago•0 comments

AI Agent Automates Google Stock Analysis from Financial Reports

https://pardusai.org/view/54c6646b9e273bbe103b76256a91a7f30da624062a8a6eeb16febfe403efd078
1•JasonHEIN•1h ago•0 comments

Voxtral Realtime 4B Pure C Implementation

https://github.com/antirez/voxtral.c
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I Was Trapped in Chinese Mafia Crypto Slavery [video]

https://www.youtube.com/watch?v=zOcNaWmmn0A
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U.S. CBP Reported Employee Arrests (FY2020 – FYTD)

https://www.cbp.gov/newsroom/stats/reported-employee-arrests
1•ludicrousdispla•1h ago•0 comments

Show HN: I built a free UCP checker – see if AI agents can find your store

https://ucphub.ai/ucp-store-check/
2•vladeta•1h ago•1 comments

Show HN: SVGV – A Real-Time Vector Video Format for Budget Hardware

https://github.com/thealidev/VectorVision-SVGV
1•thealidev•1h ago•0 comments

Study of 150 developers shows AI generated code no harder to maintain long term

https://www.youtube.com/watch?v=b9EbCb5A408
2•lifeisstillgood•1h ago•0 comments

Spotify now requires premium accounts for developer mode API access

https://www.neowin.net/news/spotify-now-requires-premium-accounts-for-developer-mode-api-access/
2•bundie•1h ago•0 comments

When Albert Einstein Moved to Princeton

https://twitter.com/Math_files/status/2020017485815456224
1•keepamovin•1h ago•0 comments

Agents.md as a Dark Signal

https://joshmock.com/post/2026-agents-md-as-a-dark-signal/
2•birdculture•1h ago•1 comments

System time, clocks, and their syncing in macOS

https://eclecticlight.co/2025/05/21/system-time-clocks-and-their-syncing-in-macos/
1•fanf2•1h ago•0 comments
Open in hackernews

Cardiovascular disease is a solved problem

https://totalhealthoptimization.com/2025/09/27/cardiovascular-disease-is-a-solved-problem/
84•brandonb•1mo ago

Comments

sghiassy•1mo ago
I wonder how many Cardiologists would call cardiovascular disease “a solved problem”

My bet is close to none

agumonkey•1mo ago
following a few cardiology conference i tend to agree with you, far from this sadly
noitpmeder•1mo ago
I mean their livelihood is predicated on it not being solved for a portion of the population
medstrom•1mo ago
There is plenty more for a cardiologist to do even if they solve the most pressing current problems. Hard to run out of puzzles in biology.
bilsbie•1mo ago
Ask yourself what happens to them if it’s solved.
WillAdams•1mo ago
Ages ago, I used to do the typesetting for the _Cardiosource Review Journal_ (lived my life around the publishing schedule because no one else was able to run a WordBASIC macro to do initial formatting, import that into a page layout program, process all the graphics and place them, and generate page proofs early enough that it could be proofed and corrected with a 24hr. turn-around until a postal rate increase killed it) --- cardiologists seem very big on data/analysis, moreso than most other medical fields.
Aurornis•1mo ago
“Solved problem” is too strong of language, but the cardiologists I follow are generally open about the idea that we have enough tools and knowledges to reasonably prevent and manage it the average person.

Even without medications, we’ve had enough knowledge about diet and lifestyle factors that the average person (excluding generic abnormalities that lead to abnormally high risk) could reasonably avoid heart disease through lifestyle and diet alone. That’s easier said than done for a lot of people in the modern world, so it’s good that we have a few different medications on top of that knowledge.

dubeye•1mo ago
the cardiologist I pay, visit and follow, would likely advise perfect diet and excercise will only reduce risk not eliminate it.

So it comes down to definition of 'resaonably'. diet and excercise will 'reasonably' reduce risk of most disease.

Aurornis•1mo ago
> will only reduce risk not eliminate it.

Same with medications? It’s well known that medications don’t eliminate risk.

For the average person without genetic outlier risk, perfect diet and exercise would definitely make heart disease a non-issue in their lifetime.

The risk your cardiologist is talking about is probably the risk that you have one of those genetic outlier conditions that require medication regardless of diet.

brandonb•1mo ago
I think there's a a bit of a paradox here: cardiovascular disease is solved biomedically, yet still remains the #1 cause of death worldwide.

From a biomedical standpoint, we have highly accurate biomarkers (e.g., ApoB, Lp(a), hs-CRP), long-term risk prediction models, knowledge of nutritional biochemstry, and next generation drugs like PCSK9 inhibitors and lepodisiran that can lower ApoB and Lp(a) by 90%. So there's no fundamental reason why cardiovascular disease has to be in even the top 10 causes of death.

Practically speaking, providing guideline-recommended preventive care would require ~27 hours per doctor per day. And the incentives are misaligned: health systems profit when hospital beds are full, so they lack the business model to actually invest in prevention.

So it's a clear illustration of a systematic gap between research and care delivery.

lm28469•1mo ago
> I think there's a a bit of a paradox here: cardiovascular disease is solved biomedically, yet still remains the #1 cause of death worldwide.

Because most people don't give a shit about their health, no amount of pills will save you if you eat like the average american.

vladgur•1mo ago
I also think that many people don’t know - I would wager for men that a significant percentage of them do not go to see a doctor preventively unless injured or sick and not that may know their blood pressure or cholesterol trends
loeg•1mo ago
Well, and everyone knows they should exercise, and many know they should avoid dietary saturated fats, but most people neither exercise nor avoid highly fatty foods.
vladgur•1mo ago
Thanks for sharing this and empowering others to improve their heart health outcomes.

I’m not in love with the idea of sharing my biomarkers with multiple health-tech companies and really want a self-hosted solution to import biomarkers from multiple sources such as Apple Health, arbitrary csv and jsons while avoiding duplication.

Claude Code is something that will make this dream a reality for me pretty soon.

Do you have any tips on biomarker data design or import gotchas?

brandonb•1mo ago
The thing that took the most time was normalizing biomarker names and units across labs. Even for the same lab chain (say, Quest), you'll get the same biomarker with slightly different names (e.g., Lp(a) vs Lipoprotein(a) vs Lipoprotein a) or units (e.g., cells/uL vs 10^9/L).
vladgur•1mo ago
that was my experience just comparing Apple Health export using Stanford Labs data vs say FunctionHealth.

Im hoping to use LLMs to help with this process.

Will try to use LOINC dataset to standardize against

dubeye•1mo ago
Couple of reasons why I think this is nonsense .

the mainline guideline is more exercise and better diet which is the treatment to much more than just heart disease. that's not something 27 hours of doctors a day can provide unless you give them guns

the treatments reduce risk, but they don't change the fact the human body is very reliant on the heart and increasingly vulnerable to cardiac death with age, even with perfect biomarkers

dogmatism•1mo ago
given the entrenched attitudes and the time it takes to actually get people to do the thing as evidenced by all the contrarians in the thread...

it would take a lot more than that. Ain't no doc got all that time to go through all this with every person who should take cholesterol lowering medicine but wants to argue their internet sourced bs

lm28469•1mo ago
It's almost entirely a lifestyle problem. Shit diet, lack of exercise, obesity, &c. Overlap maps of obesity and cardiovascular deaths, they're virtually the same

https://ec.europa.eu/eurostat/documents/4187653/10321616/dea...

https://ec.europa.eu/eurostat/statistics-explained/images/th...

daveguy•1mo ago
Well, that's certainly a ... hypothesis.

And an N of 1 "experiment" on whoever wrote this.

agumonkey•1mo ago
archive just in case https://archive.ph/Od1VS

anybody in the medical field able to give some report on state of the art CV research ?

brandonb•1mo ago
I think the title is deliberately provocative, but they're not wrong.

Heart disease is largely solvable from a biomedical standpoint: we have accurate biomarkers (e.g., ApoB, Lp(a), hs-CRP), long-term risk prediction models, precision nutrition, and highly effective next-generation drugs (PCSK9 inhibitors, lepodisiran, etc).

But practically speaking, heart disease remains the #1 cause of death due to bottlenecks in care delivery: e.g., 46% U.S. counties have no cardiologists, providing guideline-recommended preventive care would require ~27 hours per doctor per day, and incentives are misaligned (health systems profit when hospital beds are full, not from prevention).

unsupp0rted•1mo ago
Is it naive to say:

1. Check your ApoB, Lp(a), hs-CRP every 4 months

2. Feed that into a current-gen LLM and ask it to tell you what drugs to take and at what dosages

Would that solve about 90% of the issue?

brandonb•1mo ago
I started a company that does exactly that (except we also have doctors who can prescribe the medications, not just LLMs). So I don't think the approach you describe is naive, but others might. :)
kiba•1mo ago
But practically speaking, heart disease remains the #1 cause of death due to bottlenecks in care delivery: e.g., 46% U.S. counties have no cardiologists, providing guideline-recommended preventive care would require ~27 hours per doctor per day, and incentives are misaligned (health systems profit when hospital beds are full, not from prevention).

Supposed that we have an incentive aligned health care system. What would that look like?

I think one outcome is that the healthcare system eventually expands due to population growth and less death. Accidents happen, rare cases become more common, even as we get good at fixing or preventing them.

readthenotes1•1mo ago
My cardiologist recently told me the disease is mostly from Lipo(a) and small dense Ldl, that it took decades from being able to measure LDL and note the correlation to disease to be able to measure there more specific factors, and even more time to nail down the observations.

Lipo(a) is genetic, apparently either you have it or not.

Small dense ldl is caused apparently (not a biologist) from high triglycerides, one cause of which is high sugar diet.

ericd•1mo ago
Hm, so statins for everyone? What’re the downsides?
amanaplanacanal•1mo ago
Possible side effects include muscle damage, liver damage, and type 2 diabetes.
yojo•1mo ago
I’m old enough that my parents/spouse’s parents are all on statins. They all report side-effects, mostly digestive issues.

I’ll eat a healthy diet, exercise, and live a life without persistent diarrhea. I’ll take statins if/when they are medically necessary, and no sooner.

brandonb•1mo ago
The main side effects of statins are muscle pain and brain fog (from some statins -- others cross the blood-brain barrier much less).

The benefit of statins is to not only lower LDL cholesterol, but also inflammation, which is now actually a stronger risk factor for cardiovascular disease than cholesterol: https://www.empirical.health/blog/inflammation-and-heart-hea...

Layering PCSK9 inhibitors, ezetimibe, and statins can lower ApoB/LDL cholesterol by 85–90%, which would have been unheard of until recently.

On the horizon, drugs in clinical trials lower Lp(a) (the strongest hereditary risk factor for heart disease) by 94%. Currently, there are four RNA-based drugs in trials that effectively silence the gene that makes Lp(a) in liver cells: lepodisiran, olpasiran, pelacarsen, and zerlasiran.

gabrielsroka•1mo ago
> About 10% of people develop muscle aches

> Concerns about statin effects on the brain, such as cognitive impairment or dementia, are unfounded

https://www.health.harvard.edu/heart-health/what-are-the-ris...

CalChris•1mo ago
I had the brain fog. I switched from atorvastatin (dizziness) to pravachol (no dizziness), and then again to higher effective dosage of rosuvastatin (still no dizziness). I went from LDL 152 to LDL 83.

But I have high Lp(a) and so I'm prescribed a baby aspirin every other day. This counteracts the Lp(a) clotting effect but doesn't fix its genetic cause.

It's a journey.

tresdots•1mo ago
I was recently prescribed rosuvastatin (my first time taking any statin), and I had some very intense brain fog. How would you describe the feeling of what you experienced? The best way I could describe it to my friends and family was that I felt like I lost a quarter of my IQ and slept only 5 hours every night(I was getting great sleep, it just felt that way).

It was such a strange feeling. It's a weird feeling to know you're brain just isn't working as it has always worked.

CalChris•1mo ago
I had dizziness from atorvastatin and nothing from Pravachol and Rosuvastatin. The conclusion I draw is that you have to find something that works. But this is uncharted territory. Your docs won't know and you have to kind of force the issue.
ericd•1mo ago
Thanks! I've been looking into this a little recently, so thanks for the very timely article and advice.

Do you have any info on good ways to nail down personal sources of inflammation relevant to cardio health, or do you think that just general anti-inflammatory diet/habits is the best we can do right now? We were hunting down a source of mold in our house recently due to some blood markers recently, which got me thinking about inflammation sources and cardio health (we found a big patch of mold between our floors and removed it, blood markers immediately improved).

tresdots•1mo ago
My experience with them was a brain fog so bad I could hardly do my engineering job effectively. Quite unfortunate as I've read that side effect isn't very common.
Aurornis•1mo ago
If you’re unlucky enough to have one of the genetic factors that predisposes you to atherosclerosis then it’s going to be statins and maybe PCSK9 inhibitors.

For the average person, diet and lifestyle choices could be enough, but adherence can be difficult. Monitoring LDL as an imperfect but useful marker and then introducing low-dose statins on a sliding scale proportions to severity is a good idea.

Statins are not completely side effect free (no medication really is) but they’re generally well tolerated. Statin side effects are an interesting area of research because they have a very high nocebo effect rate: People hear so much about statins and their side effects from popular media that when they’re prescribed a statin in older age they start thinking everything is a side effect of the statin. There are some actual known side effects of statins which scale with dose and some of which can be maybe offset by supplements like CoQ10, but the side effects are generally mild. I’d take the side effects over heart disease after watching some older family members struggle and then die due to heart problems.

KempyKolibri•1mo ago
Yep - the SAMSON trial suggests that nearly all side effects attributed to statins are actually just nocebo: https://www.jacc.org/doi/10.1016/j.jacc.2021.07.022
inglor_cz•1mo ago
It is very much not a solved problem unless you can actually cure it in existing patients, e.g. reduce or remove the extant plaques from their blood vessels.

This is not pedantry, this is a vital problem of hundreds of millions of currently living people, many of which don't even know their own status.

I believe this can be done in the near future, there are some interesting initiatives in this direction, but it is very much not a solved problem.

ashleyn•1mo ago
Obesity, junk food addiction, and chronic inactivity still remain unsolved as ever.
kccqzy•1mo ago
I agree with you, but I suppose the point of the article is that we can solve cardiovascular disease without first solving obesity or chronic inactivity.
justinator•1mo ago
GLP-1's baby.
loeg•1mo ago
Obesity is solved! Tirzepatide.
WhatsTheBigIdea•1mo ago
This paper's core idea is based on the assumption that circulating LDL is the cause of heart disease. That assumption is false.

Taking satins is proven to reduce heart disease rates, but there are lots of other drugs that lower LDL... many with much more efficacy than satins.

These non-satin drugs do not reduce heart disease rates significantly.

There something else going on here. High LDL is correlated with the development of heart disease, but it does not cause heart disease. Satins do reduce the risk of heart disease and they do reduce LDL, but their positive effect on heart disease rates is not caused by reduced LDL.

medstrom•1mo ago
> High LDL is correlated with the development of heart disease, but it does not cause heart disease.

You realize this sentence is an oxymoron?

Unless you meant to say "it does not cause the development of heart disease". I agree correlation is not causation.

elromulous•1mo ago
You realize correlation does not imply causation?

Edit: this was written before OP edited their comment

rowanG077•1mo ago
I don't think it is. Something can either be correlated and causal or correlated and non-causal. It makes sense to talk about which.
smt88•1mo ago
> You realize this sentence is an oxymoron?

No it isn't.

Think of heart disease as slow, long-term damage to the cardiovascular system, and cholesterol is what the body uses as a bandaid.

If you have a lot of LDL cholesterol available, your body will use a lot of it, and you'll have stiffer arteries. If you don't have much available, it takes longer for the bandaids to build up.

This is one of the reasons statins reduce the number of heart attacks, but don't always seem to reduce all-cause mortality.

KempyKolibri•1mo ago
The band aid analogy doesn’t make sense when we consider the MR studies showing the lower your genetically determined LDL-c, the lower your risk of CVD. If everything was randomised except the number of band aids, why would having fewer band aids result in lower CVD risk?

> This is one of the reasons statins reduce the number of heart attacks, but don't always seem to reduce all-cause mortality.

That’s one potential explanation, but I don’t think it’s the most likely one. We tend to see non significant ACM in smaller, less powered trials, or those with lower LDL-c lowering. ACM is simply a less sensitive endpoint - if you have a treatment that reduces CVD incidence, then the “CVD incidence” endpoint will give you significant results with fewer CVD event differences between study arms compared to ACM since your power to detect differences is diluted by other fatal events that aren’t affected by statins (cancer, motor accidents etc).

thomassmith65•1mo ago
*statins?
blell•1mo ago
The fact that this word is misspelt every single time makes me want to dismiss the entirety of the comment.
mark-r•1mo ago
My browser underlines the word statin to indicate a misspelling, but does not underline satin. We've been trained to believe the computer is always right when it flags an error, but unfortunately it's not 100% accurate.
KempyKolibri•1mo ago
Why do we see consistent dose response between LDL lowering SNPs and cardiovascular disease in Mendelian randomisation studies, then?
daveguy•1mo ago
Heart disease is clearly not Mendelian. So, unless you have a specific well-designed study to cite, that is a non-argument.
graboy•1mo ago
https://www.jacc.org/doi/10.1016/j.jacc.2012.09.017

Across different genetic variants, lower lifetime LDL -> lower risk of death. Check out figure 3.

The causality of LDL -> plaque buildup -> 55-60% [1] of heart disease related deaths is also well understood, so it seems clear to me that preventing plaque buildup in the first place prevents over half of heart disease related deaths.

Would like to know if you disagree, "Minimize LDL at all costs" goes current mainstream medical guidance, so I'd like to disconfirm my beliefs if possible.

[1] Number from deep research.

KempyKolibri•1mo ago
Graboy has provided the citation I would have given, as well as an excellent explanation. I’m not sure what you mean by “heart disease is clearly not Mendelian”.
daveguy•1mo ago
Mendelian is characterized by effects having strong influence from a single gene. Heart disease is clearly more complex than gene -> heart disease. I thought that was basic enough that I didn't need to explain it. But here goes...

A clinical score changing with treatment is not unconfounded by mendelian randomization. When the genetics are clearly more complex than what you are mathematically randomizing for, the control doesn't solve the confounding. eg you haven't suddenly "proven" the effects are non-genetic. We already knew heart disease is non-mendelian. But showing something is non-mendelian doesn't mean you've shown it's not genetic. I hope that clarifies, because I'm not sure I can explain it to you in simpler terms.

KempyKolibri•1mo ago
> I thought that was basic enough that I didn't need to explain it. But here goes...

This is quite the tone to take when the actual point being made has demonstrably sailed over your head, considering the reference provided to you explains it very clearly.

Which is more likely - nigh on every lipidologist, cardiologist and nutrition researcher is wrong, or you might have made a mistake yourself?

> Mendelian is characterized by effects having strong influence from a single gene. Heart disease is clearly more complex than gene -> heart disease

This seems like a misunderstanding. A single SNP clearly can affect CVD risk, that’s precisely what the paper shows. The assumptions required for an MR study to be valid do not include “the outcome must only be affected by a single gene and no other gene”. It’s required that there’s no pleiotropy present in the exposure (I.e. the SNPs). The exposure here isn’t heart disease, it’s SNPs that affect LDL-c levels, and the outcome being measured is CVD. So your point doesn’t pose an issue for the study and the inferences it makes.

But honestly - just read the paper. I think both that paper and the EAS consensus paper are very approachable.

graboy•1mo ago
I think maybe you are saying that there may be some way that the genes affect heart disease not through LDL, and therefore MR does not apply because the "exclusion restriction" [1] fails here? Or are you talking about a different assumption?

The cited study addresses this, which is why I pointed to figure 3. They argue that if genes were causing heart disease not through LDL in any meaningful way, you wouldn't expect such a clean dose-response consistency across different genetic variants - it would be more jagged.

[1] https://en.wikipedia.org/wiki/Mendelian_randomization#Defini...

daveguy•1mo ago
It seems you are confusing mendelian randomization for specific alleles associated with LDL-C production and conflating that with mendelian randomization somehow controlling genetic confounding of heart disease. The control is for the LDL production, not heart disease.

Here is a simple primer on mendelian randomization: https://www.psomagen.com/blog/what-is-mendelian-randomizatio...

Please review the key principles and assumptions section. Using MR to control for genetic confounding of heart disease fails all assumptions. Thats why it quite directly does not follow.

This is why the paper presented does not support the claim that LDL is the sole source of heart disease. I'd be interested to hear what the authors of that paper (which is legitimate) think about it being used to support the OP's claim because "mendelian randomization".

graboy•1mo ago
> This is why the paper presented does not support the claim that LDL is the sole source of heart disease

Is that what we were arguing about? I guess it was. At some point in thinking about this my frame must have shifted into agreement with you. Of course there are other causes of heart disease besides LDL, like blood pressure, duh. The smooth dose response is about the particular gene not being linked to heart disease through something other than LDL, roughly.

graboy•1mo ago
What do you think of Dr. Schooling's response that the Mendellian effects might be inflated? I think they had a good defense but was not entirely convinced they hadn't sidestepped the issue that Schooling was getting at, wasn't sure either way.

https://www.jacc.org/doi/epdf/10.1016/j.jacc.2013.01.067

KempyKolibri•1mo ago
I wasn’t aware of that critique, thanks for sharing. Before I read the response my first thought was “why such consistency across different SNPs, then?”, so I would certainly agree with that aspect of the defence.

In general, Ference’s explanation just seems more parsimonious than Schooling’s. It’s possible that they’re right, but I think they would need to show that the specific genes in Ference’s study are affected by age in this way.

I wouldn’t claim to be a great expert in MR, though. I can just about keep up with surface level understanding of them but once you get into the nitty gritty stats, pleitropy testing etc it’s a bit over my head tbh.

brandonb•1mo ago
There are multiple independent risk factors for heart disease. The major ones are:

  - LDL / ApoB
  - Blood pressure
  - inflammation (hs-CRP)
  - Insulin resistance (HbA1c)
  - Lp(a): strongest hereditary risk factor.
  - eGFR: a measure of kidney function
Non-statin drugs like PCSK9 inhibitors have been shown to reduce heart attacks, strokes, and other cardiovascular events on top of statin therapy. One randomized control trial was FOURIER in 2017: https://www.nejm.org/doi/full/10.1056/NEJMoa1615664
justinator•1mo ago
Simplifying, we are all essentially born with heart disease. It's just a game of how long it takes for it to kill us. No way around it.

Unfortunately, our biology isn't perfect.

mock-possum•1mo ago
That’s not really a helpful attitude to take when trying to prevent heat disease though
justinator•1mo ago
Reality is like that.

Before hoping for a miracle, may I suggest adding more walks into your week?

loeg•1mo ago
> [that circulating LDL is the cause of heart disease] is false.

I think your comment really owes the rest of us more explanation of this part.

readthenotes1•1mo ago
The article goes on to say it's not all LDL. Keep reading. The first part agrees with my cardiologist, at any rate
paxys•1mo ago
"Hunger is a solved problem. We just need to give enough food to everyone!"
MPSimmons•1mo ago
>Lp(a) levels are almost purely genetically determined and so elevated Lp(a) is essentially due to a poor roll of the genetic dice... For simplicity, we will devote little further attention to either of these secondary risk factors”

As someone who rolled poorly on those genetic dice, I would like to complain. But also, disregarding a factor that impacts 20%[1] of the population seems disingenuous.

[1] - https://familyheart.org/family-sharing-tools/high-lpa-family...

brandonb•1mo ago
Lepodisiran has reduced Lp(a) by 94% in clinical trails. After it gets approved, IMO the author should re-write this section.
dmead•1mo ago
Valve failure often has nothing to do with diet. This is junk.
OutOfHere•1mo ago
There are other cardiac failure modes too, for example electrical and hypertrophy.
bilsbie•1mo ago
Here’s a counterpoint if anyone is interested: https://www.midwesterndoctor.com/p/why-are-statins-so-danger...

I’m not saying either side is right but when it comes to your health why not evaluate as many opinions as possible.

hombre_fatal•1mo ago
I wish the “counter points” to my claims were always as bad as that link. It has a little bit of everything, from Fauci to seed oils to a Joe Rogan video.
loeg•1mo ago
Your article starts by comparing the harms of statins to the harms of scary COVID vaccines. I'm not sure it's very credible.
graboy•1mo ago
Here is the chief editor of JAMA internal medicine arguing there is not enough evidence to prescribe statins for primary prevention in those 40+: https://www.natap.org/2016/HIV/ied160021.pdf
Finbarr•1mo ago
Very similar to https://myticker.com/ though a little denser.
vladgur•1mo ago
Thanks for sharing this — amazing resource and resembles my experience with US health care.

I recently asked my doctor at Stanford - a pretty expensive hospital but one of the top cardio hospitals in the country - to get me an APoB test. He said that it may not be covered by insurance.

So instead I spend $360 or so on a year worth of biomarkers from Function Health that included ApoB and others

unsupp0rted•1mo ago
Commenters are really piling on, without, it seems, reading the article.

The author addresses a lot of the obvious gotcha points I see in the comments.

Although I don't think the author realistically explores the downsides of statin use, papering over the common side-effects.

Modified3019•1mo ago
Dramatic clickbait titles should expect to get responses that match.
onesandofgrain•1mo ago
It was my understanding that circulating free triglycerides and LpA were the main risk factors for CAD and not LDL. In addition to AGEs?
skywhopper•1mo ago
This is dangerous nonsense and should be removed from the HN front page.
raphman•1mo ago
Some information on the author:

- The blog seems to be associated with this Twitter account: https://x.com/sichuan_mala. That person seems to be a good friend of Cremieux¹.

- The article seems to have originally been published/unpublished in 2024 https://x.com/cremieuxrecueil/status/1922743591924899962

- It was only re-uploaded in September 2025 (?). There's some discussion of the claims under a tweet by Cremieux who announced the re-upload: https://x.com/cremieuxrecueil/status/1974990143544287715

¹) FWIW: https://en.wikipedia.org/wiki/Jordan_Lasker

Ifkaluva•1mo ago
Why was this flagged? I was under the impression that the content of the article reflects the current mainstream medical view.