@dunja_lim@verguts@BOVYN@PaulNeirynck@SGeysenbergh Een afspraak bij de gynaecoloog is pas over 3-6maand, ik vrees dat velen het vergeten of het probleem reeds (elders) opgelost werd. Wat niet wegneemt dat ze een gemaakte afspraak kunnen annuleren…
@dunja_lim@verguts@BOVYN@PaulNeirynck@SGeysenbergh Bij ons als huisarts kan je niet langer dan 3d op voorhand een afspraak maken juist omdat er anders veel meer no shows zijn. Nu zijn die beperkt tot te laat komen of af en toe van dag vergissen. Wel vervelend om op iets langere termijn te plannen. Dat doen we via mail.
Response to Rebuttals on: "Seven Years of 700 Cholesterol Without Coronary Atherosclerosis".
It’s been really interesting to watch the first 24-hour response to this new paper. The overwhelming majority has been, if not fully enthusiastic, at least curious. And I sincerely appreciate that.
That said, some of the pushback has also been revealing… even comical. So let me address the most common retorts.
⏳1. “He’s too young.”
Asked and answered. HoFH Children with similar LDL and ApoB levels can develop measurable plaque within the first few years of life and even heart attacks by age 8 or 10. Other people around my age, using similar imaging technology, also show measurable plaque. “He’s young” is not a good explanation.
🙄2. “You have a conflict of interest because you’re the patient.”
LMAO! This one might be my favorite. What exactly did I do? Go into the CT scanner and suck in my plaque like I was sucking in my gut? Ask the AI algorithm, “Hey, I’m the patient — do me a solid?” If you think this is a rebuttal, I suggest you don’t join any debate teams.
🦓3. “He’s an outlier.”
Yes. At a population level, I am an outlier. I don’t have obesity, prediabetes, or metabolic syndrome. But that’s one of the broader points: We have a paucity of data on the risks of elevated LDL in metabolically healthy people without underlying genetic lipid disorders.
Outliers are not reasons to stop thinking. They’re opportunities to learn.
🤷♂️4. “It’s a fluke. He’s a one-off.”
What a remarkably uncurious response. Imagine an oncologist had a patient with stage IV pancreatic cancer (~3% five-year survival rate). And that patient somehow cured himself, then went on to win the 100 meters at the Olympics 12 years later.
Would the oncologist say: “Meh… What’s for lunch?”
Of course not. A good scientist or doctor (or curious human) would ask: what happened here?
🧬5. “Oh, you probably just have protective genetics.”
Oh, really? My father had a 99% occlusion of his left anterior descending artery at age 44. My Lp(a) runs between 100 and 194. And on top of that, I have a history of inflammatory bowel disease, a condition associated with chronic systemic inflammation.
🫀6. “But what about the Keto-CTA paper?”
If you’re trying to beat this drum like it’s a trump card, I’d guarantee you’re stuck in an echo chamber and have incomplete information. It has now been clarified repeatedly that the original CLEERLY dataset published on April 7th was not reliable.
CLEERLY had unblinded scans, anomalously results, and refused to perform a quality-control check. And multiple independent analyses have since shown that the KETO-CTA group do not appear to be a high-progression group. This is why we, the authors, took the initiative to retract the paper (NOT the study). The KETO-CTA Heartflow and QAngio data are available as a pre-print. And I’ve seen nobody legitimately try to defend the CLEERLY dataset.
Also, the data show that LDL and ApoB did not predict plaque progression, and even at high LDL and ApoB levels, confirmed regression was observed.
👇
For supporters, feel free to link this the next time you see someone try to deploy these arguments.
For critics, I suggest taking a read and thinking carefully… either to avoid falling onto the pyramid… or to avoid giving me reason to expand it.
Nick is not too young to show soft plaque after seven years of having a cholesterol of 700 mg/dL.
His n=1 case report DOES tell us something incredibly important.
In 1953, it was shown in 300 autopsies of American soldiers who died in the Korean war with a mean age of 22 that 77% had plaque and 15% had luminal narrowing.
Nick is in his 30s so it is expected for him to have some soft plaque even without extremely elevated cholesterol.
Causation can either be necessary, sufficient, or necessary and sufficient.
Nick’s n=1 case shows all on its own that 700 mg/dL cholesterol and its associated high LDL-C and ApoB is not sufficient to cause atherosclerosis.
It may still be necessary to have high LDL-C or ApoB.
In fact, Nick could be the only person on the entire planet who is missing one other factor that, once combined with high LDL-C or high ApoB, is sufficient to cause plaque.
As such it is possible that Nick’s results do not apply to any other person on the planet, when looking at his case report alone.
But that’s totally different from saying we can’t learn a principle from his case report that we know does translate to everyone else.
The principle is that high cholesterol is not sufficient to cause heart disease.
The reason we don’t know if his report generalizes to other people is not because we don’t know if we can generalize that one principle. It’s because we don’t know how Nick is different from other people and we therefore don’t know if anyone else has the same mix of relevant factors.
In other words, it does matter that his n is 1 because for this reason we can’t make a probability statement about the likelihood that someone else can maintain this high cholesterol for the same period of time without showing plaque.
But that’s separate from the point that it only takes a single cause of A coexisting with lack of B to show that A is not sufficient to cause B.
That’s assuming you measured A and B correctly.
Now if we move beyond his case report we can go back to the research showing LDL requires damage to be taken up into plaque and facilitate disease progression.
Maybe Nick is lacking that damage.
Also, the characterization of the LMHR phenotype is suggestive of a generalizable principle connecting Nick with these other folks. It needs a lot more research.
But the point that 700 mg/dL cholesterol for seven years coexists with no plaque is a major demonstration of the insufficiency of high cholesterol or ApoB to cause plaque.
@KetoCarnivore@MikhailaFuller@CarnalDancer Oh yeah, try reading the sardine challenge - sardine fasting groups :) Also; Egg fasting? Water fasting? Seems as if simple instructions are too complicated...
@gorskon@Matt_Pinner I was a teenager in the 80's in Europe. And it was the same. Could hang and go wherever I wanted. But if curfew was 22:00 and I came home 22:05 all hell would brake loose 🤣
@DavidVergucht Ik vermoed omdat als je die patiënten in je eigen praktijk verderhelpt je weldegelijk hun huisarts wordt en dus ze permanent moet aannemen en opvolgen. Noodpost is wachtpost overdag. Uit de nood helpen maar geen continuïteit.
@RetsefL@US_FDA@CDCgov Does nobody see the current illness: NAS? Clinical manifestations seen in neonates due to withdrawal secondary to intrauterine drug exposure most commonly associated with maternal opioid use and can be complicated by IU exposure to benzodiazepines, alcohol and various other drugs
@DrEenfeldt Well the new guidelines dropped in Belgium.
Max 1 egg/day (more then before) and max 300g red meat/week (not processed). 30 experts decided this after looking at all the recent studies they could finf!
https://t.co/8Y2x7hvmt0
@vrtnws
Waarom melden jullie niet dat Vandenbroucke’s kaderwet de partiële conventionering afschaft, premies exclusief aan geconventioneerde artsen koppelt, en de minister RIZIV-nummers kan intrekken?
Dit is meer dan plafonnering, het is dwang en een machtsgreep.
Volledige context aub!