Tellit Likeitis

14.8K posts

Tellit Likeitis

Tellit Likeitis

@Tellit007

Systematic challenger of metabolic & cardiovascular misinformation. Bradford Hill criteria over cherry-picked studies. RCTs over testimonials.

Katılım Ağustos 2022
555 Takip Edilen874 Takipçiler
Tellit Likeitis
Tellit Likeitis@Tellit007·
@trikomes Not all keto diets are identical, fine. That still leaves the number from your own co-author's paper: mean LDL-C 272 mg/dL in this exact cohort. That is the part Quartz was actually gesturing at, and four paragraphs about soybean oil never touch it.
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Nick Jikomes
Nick Jikomes@trikomes·
Posts like this are certifiably retarded, as they implicitly take "ketogenic diets" to be one singular thing. Two individuals can eat very high-fat, low-carb ketogenic diets with distinct fatty acid profiles. Why does that matter? Individual fatty acids modulate gene expression, and other fatty acids drive DISTINCT gene expression changes. Two ketogenic diets with distinct fatty acid profiles will drive distinct changes in gene expression (not to mention other differences). There is no singular "ketogenic diet" that will always drive the same set of changes observed in the study Quartz is referring to, which used a high-PUFA, high-fat diet comprised largely of soybean oil and lard, both of which contain substantial Ω-6 PUFA content (linoleic acid). Linoleic acid itself modulates gene expression, and does so differently than any number of other fatty acids we could mention.
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Steven Quartz PhD@StevenQuartz

Norwitz's criticism aren't valid - and they ignore the massive red flag this study raises: a ketogenic diet induces lipid-driven metabolic reprogramming in part through a PPAR-delta linked transcriptional program. The long-term consequences of that remain poorly explored, and this study adds to the concern that it's not benign in some tissues. PPAR-delta is a master switch with a substantial and troubling cancer literature behind it. For example, episodic PPAR-delta activation is adaptive, as seen with exercise. That led to a search for exercise mimetics - exercise in a pill. GW1516 (aka cardarine) was identified as a powerful PPAR-delta agonist with endurance-enhancing benefits. But trials were halted due to rapid rapid cancer development. That's not to say that a ketogenic diet is equivalent to cardarine. But a long-term ketogenic diet may convert that intermittent response into a sustained transcriptional program. Should the chronic dietary activation of the same pathway be presumed safe? That's an open question this study addresses. My interpretation is that this fits ketosis better as a temporary metabolic state supporting metabolic flexibility than as a program to be driven long-term. To be clear, this study doesn't show that long-term ketogenic diets cause cancer in humans. But it does provide a biologically specific reason not to presume that chronic activation of this pathway is benign. And contrary to Norwitz's claims, these results are due to lipid overload, not something unique to the mouse diet, and is an unavoidable feature of a ketogenic diet. While ketones didn't drive the effect they also weren't protective.

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Tellit Likeitis
Tellit Likeitis@Tellit007·
@trikomes opens by calling Quartz's post "certifiably retarded," then spends four paragraphs arguing about which vegetable oil a mouse study used. He runs a podcast and a Substack off exactly this kind of fight. Precious. The fatty acid point is fine on its own terms. Ketogenic diets are not one thing, and Quartz's cited paper is about linoleic acid signaling in gut cells, not a diet trial on people. That mismatch is his to answer for. None of it touches the number that actually decides this. Norwitz co-authored the paper that defines this exact cohort: Budoff et al 2024, JACC Advances, 80 people with carbohydrate-restriction-induced LDL-C, mean 272 mg/dL, max 591. His own earlier case report shows the same hyper-responder pattern on a low-saturated-fat version of the diet, so this was never a seed-oil-versus-lard question. It is what carbohydrate restriction itself does to ApoB particle count in a meaningful share of the people who stay on it, whatever fat they are eating. Years of people running numbers like that, and still no randomized trial on hard cardiovascular outcomes, only a one-year plaque study that got retracted and reanalyzed. That gap is the actual red flag. Arguing about soybean oil in mice is how you avoid looking at it. Never a boring moment.
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Nick Jikomes@trikomes

Posts like this are certifiably retarded, as they implicitly take "ketogenic diets" to be one singular thing. Two individuals can eat very high-fat, low-carb ketogenic diets with distinct fatty acid profiles. Why does that matter? Individual fatty acids modulate gene expression, and other fatty acids drive DISTINCT gene expression changes. Two ketogenic diets with distinct fatty acid profiles will drive distinct changes in gene expression (not to mention other differences). There is no singular "ketogenic diet" that will always drive the same set of changes observed in the study Quartz is referring to, which used a high-PUFA, high-fat diet comprised largely of soybean oil and lard, both of which contain substantial Ω-6 PUFA content (linoleic acid). Linoleic acid itself modulates gene expression, and does so differently than any number of other fatty acids we could mention.

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Tellit Likeitis
Tellit Likeitis@Tellit007·
@DatboyOmar @SamaHoole Haaland also not a great example. He collapsed when his team needed him most. Looks like this raw milk carnivore nonsense is just marketing hype for Sama to sell his unproven coaching business, while down playing cardiovascular risk. Choose wisely.
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Omar Dadabhoy
Omar Dadabhoy@DatboyOmar·
@SamaHoole Love that you’re highlighting athletes drinking raw milk. Besides haaland these are all bad examples. Bryce Mitchell and Marlon Vera have never been title holders in their weight classes. I’d rather know what the 🐐s are doing
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Sama Hoole
Sama Hoole@SamaHoole·
When Erling Haaland wanted milk that made him feel unstoppable, he drove to a farm in Cheshire and bought it raw, a glass every morning and another after training. When Colt McCoy, the NFL quarterback, was asked about the raw milk he has drunk since milking his family's cows as a boy, he waved the fuss away: it's just milk, bro. When Bryce Mitchell won inside the octagon this summer and a reporter asked him the secret, he shrugged and said he thought it was mostly the raw milk. When Marlon Vera fights, he does it on raw milk and will not touch the plant based stuff, keeping it in the house for the whole family, kids and all. The baseball star Bryce Harper is another, pouring it into a coffee in a video that went round the internet. And none of this is new. Paul Anderson, billed as the strongest man alive in the 1950s, is said to have put away fourteen pints of milk in a single day, long before anyone thought to be frightened of it. Different sports, different countries, different eras, the same instinct arrived at independently: that the milk which built strong humans for ten thousand years might be worth more than the version boiled until it survives a month on a shelf. The old authorities spent a century warning everyone off it. The man now running American health drinks his raw. And the ones ignoring the warning keep on winning.
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Tellit Likeitis
Tellit Likeitis@Tellit007·
@SamaHoole Cool. I am interested in trying this. But before I do, could you point me to the hard cardiovascular outcome data for your proposed way of eating that shows this is the way to go? Thanks!
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Sama Hoole
Sama Hoole@SamaHoole·
Here's a handy swap list that will make your next shop much healthier. Breakfast cereal? Swap it for beef. Porridge oats, the wholegrain heart-healthy sludge? Swap it for beef. Chicken breast, dry and apologising for itself? Swap it for beef. The salmon flown in from a Norwegian pen? Swap it for beef. Protein powder, thirty scoops of factory dust? Swap it for beef. The protein bar that costs three quid and tastes of chalk? Swap it for beef. Tofu? Swap it for beef. The plant based burger bleeding beetroot in the pan? Swap it for beef, which is where it was trying to get to the whole time. Your five a day? Swap it for beef. The multivitamin rattling in the cupboard? Swap it for beef, it was a worse copy of it anyway. Kale, massaged, whatever that means? Swap it for beef. The lean turkey mince that needs three sauces to be food? Swap it for beef. Hopefully you're getting the idea here.
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Tellit Likeitis
Tellit Likeitis@Tellit007·
@SamaHoole How did that work out for Haaland in his last WC game? Completely collapsed. Maybe issues with the raw milk? Not enough carbs?
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Sama Hoole
Sama Hoole@SamaHoole·
In October, Erling Haaland pulled up at a tiny Cheshire dairy on his way to training and filmed himself buying raw milk, beef and honey. The farm, a micro dairy called Greenoaks that sells unpasteurised milk straight from the gate, could not keep up with the orders once the video reached his millions of subscribers. But Haaland was never really the story. He calls raw milk his magic potion and swears it is good for the stomach, skin, bones and muscles, yet he is only the loudest voice in something that had been building for years before he picked up a bottle. Look at the numbers. Raw milk sales in America jumped more than twenty percent in a single year, and in the peak weeks as much as sixty five percent. In that same year, sales of the plant based milks fell. Roughly eleven million Americans now drink it raw, states from Oklahoma to Arkansas have torn up the rules that held it back, and the biggest raw dairy farmer in the country says that whatever the FDA tells his customers not to do, they go and do the opposite. Here is the tell. In the middle of all this warning, the agencies sounding the alarm quietly cut their main food safety network from tracking eight germs to two, and two of the ones they stopped counting are the exact bugs they say make raw milk dangerous. Understand what you are watching, because it is bigger than milk. This is the generation switched from butter to margarine by experts who later shrugged, told eggs would stop its heart and then told they were fine, frightened of the fat on a steak for forty years. It has done the arithmetic on how often the warning was the actual mistake, and stopped waiting for permission. The man now in charge of American health drinks his milk raw. The public looked at the men still standing after every other warning collapsed, and started buying it by the gallon. One video sold out a Cheshire dairy. The warnings stopped working the day the people issuing them ran out of credibility.
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Tellit Likeitis
Tellit Likeitis@Tellit007·
@Sjmbtwq @SamaHoole Yeah the French beat you to that for millenia or so. Also part of the Mediterranean diet which, unlike carnivore has excellent cardiovascular hard outcome data.
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Sama Hoole
Sama Hoole@SamaHoole·
I have completed the heretic's fat loss checklist: - I do not count a single calorie - I do not track a single step - I do not weigh my food like a pharmacist - I eat until I am full, then eat some cheese - I do not ration calories for the weekend - I eat the most calorie dense food I can find - I eat as much of it as I can manage - I eat the fat on the meat, then butter on top - I drink raw milk - I do not drink protein shakes - I have not seen a stick of celery in years I will be excommunicated from the weight loss industry, which needs me anxious, hungry and weighing broccoli at 9pm. The fat is coming off anyway.
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Sama Hoole@SamaHoole·
@Gixxer1143 "Balanced diet" sounds reassuring, but it's never been scientifically defined. The body needs nutrients, not a slogan. Balance between what, exactly?
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Sama Hoole
Sama Hoole@SamaHoole·
Nobody profits from telling you the body heals itself. So nobody tells you. Your taste buds are new every 10 to 14 days. The tongue reading this flavour is a fortnight old. Your stomach lining rebuilds every 3 to 5 days. Last week's gut is already gone. Your skin turns over every 4 weeks. You grew a whole new surface this month. Your white blood cells renew in days. Tonight's immune army was not on watch last week. Your red blood cells retire every 120 days. Four months, and the entire fleet is replaced. The fat built into your cell membranes turns over too. Years of stored seed oil can slowly be walked back out. Your liver just gets on with regenerating. It holds no grudge about the bad years. Your skeleton rebuilds over roughly ten years. The bones made in the worst years are not the ones you finish with. Every one of those rebuilds is made from what you feed it. Feed it meat, fat, sunlight and sleep, and it builds you strong. Feed it sugar, seed oil and the sofa, and it builds you soft. The body you will have next year is under construction right now. What you give it today is what it builds you into.
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Tellit Likeitis
Tellit Likeitis@Tellit007·
Turnover replacing cells is not the same as the disease process undoing itself. Your arteries get new endothelial cells every day too, and plaque still sits there if ApoB retention keeps outpacing clearance. If self-repair alone did it, chronic disease would not exist. And if carnivore would fix it, why is there zero hard cvd outcome data to prove it? Interesting...
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Tellit Likeitis
Tellit Likeitis@Tellit007·
@SamaHoole turns real cell biology into a coaching pitch: feed it right and it heals, so buy the "fitawakening" plan that tells you what right means. Fun times! The turnover numbers are broadly accurate. Skin cells, red blood cells, stomach lining, they do renew on roughly those schedules. His post is self defeating. If the body is this mean self healing machine, who the heck needs to restrict themselves to carnivore, right? This is how he spins it. The fallacy sits in what gets built on top of that biology: a binary where meat, fat, sunlight and sleep builds you strong, and sugar, seed oil and the sofa builds you soft, as if diet quality and physical activity are the same variable, and as if there are only two settings instead of a dose-dependent spectrum. Real physiology does not work as a switch. It works as an accumulation, shaped by how much of each input arrives and how often. There is a bigger gap underneath that one. If the body simply repairs itself from the right inputs, chronic disease should not exist, and it clearly does. The reason is that renewal replaces cells. It does not undo whatever process is already running in the tissue those cells sit inside. Arterial wall cells turn over constantly, and plaque still accumulates when ApoB particle retention keeps outpacing clearance, the mass-delivery-versus-removal mechanism lipidologists like @Drlipid describe. A new endothelial cell does not reset the plaque sitting beneath it. None of that argument requires cutting out grains, legumes or fruit. Feed it meat, fat, sunlight and sleep describes ordinary, uncontroversial nutrition advice, not a case for carnivore specifically. Note that carnivore still has zero randomized trials and zero long-term outcome data. Unlike Mediterranean pattern eating which has PREDIMED: 7,447 high-risk patients, randomized, roughly 30 percent fewer heart attacks, strokes and cardiovascular deaths over 4.8 years. Never give up. Never surrender.
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Sama Hoole@SamaHoole

Nobody profits from telling you the body heals itself. So nobody tells you. Your taste buds are new every 10 to 14 days. The tongue reading this flavour is a fortnight old. Your stomach lining rebuilds every 3 to 5 days. Last week's gut is already gone. Your skin turns over every 4 weeks. You grew a whole new surface this month. Your white blood cells renew in days. Tonight's immune army was not on watch last week. Your red blood cells retire every 120 days. Four months, and the entire fleet is replaced. The fat built into your cell membranes turns over too. Years of stored seed oil can slowly be walked back out. Your liver just gets on with regenerating. It holds no grudge about the bad years. Your skeleton rebuilds over roughly ten years. The bones made in the worst years are not the ones you finish with. Every one of those rebuilds is made from what you feed it. Feed it meat, fat, sunlight and sleep, and it builds you strong. Feed it sugar, seed oil and the sofa, and it builds you soft. The body you will have next year is under construction right now. What you give it today is what it builds you into.

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Tellit Likeitis
Tellit Likeitis@Tellit007·
@sayerjigmi You're calling an 82 person trial with no placebo arm a landmark and skipping the placebo controlled one that already read out. NAPS: 265 patients, 3 years, double blind, same measure, opposite answer. Stay awake my friends.
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Sayer Ji
Sayer Ji@sayerjigmi·
They Ran Nattokinase Against a Statin. The Enzyme Won. A landmark randomized trial put a fermented-soybean enzyme head-to-head with simvastatin — and on the one measure that predicts heart attacks and strokes, the pennies-a-day enzyme shrank plaque more than three times as much as the drug. sayerji.substack.com/p/they-ran-nat…
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Tellit Likeitis
Tellit Likeitis@Tellit007·
@sayerjigmi runs GreenMedInfo's supplement funnel and a paid Substack, and he is selling an 82 person trial as proof an enzyme beats a statin. Classic supplement-versus-drug substitution play. The trial exists. Ren et al 2017 randomized 82 patients to nattokinase or simvastatin 20mg, 76 completed, and the nattokinase arm shrank carotid plaque more (36.6% vs 11.5%) and raised HDL where the statin did not move it. What the post leaves out: no placebo arm. Active comparator only, two treatments, no untreated control, so neither group can be shown to beat doing nothing. The correlation between nattokinase's plaque drop and its cholesterol drop was not even significant (r=0.35, P=0.09) in an arm of 39 people. Noise dressed up as a mechanism. The trial that actually answers this question already ran. NAPS, Hodis et al 2021: 265 patients, three years, double blind, placebo controlled. Carotid thickness progression came back identical to placebo. Statin evidence does not rest on a 26 week open trial against 20mg of an older drug. Ask a lipid specialist like @DrNadolsky where the real evidence base sits: the Cholesterol Treatment Trialists meta-analysis, 170,000 patients across dozens of trials, event reduction scaling with ApoB lowered. Choose wisely my friends.
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Sayer Ji@sayerjigmi

They Ran Nattokinase Against a Statin. The Enzyme Won. A landmark randomized trial put a fermented-soybean enzyme head-to-head with simvastatin — and on the one measure that predicts heart attacks and strokes, the pennies-a-day enzyme shrank plaque more than three times as much as the drug. sayerji.substack.com/p/they-ran-nat…

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Rx Readmore Livemore
Rx Readmore Livemore@SopitaSirirata1·
@Tellit007 Every time I accessed to X, I searched your post firstly. Thanks for your tremendous efforts to provide evidence based medicine to debunk a lot of health misinformation. Really appreciate your work here.
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Tellit Likeitis
Tellit Likeitis@Tellit007·
X buried this account and hoped no one would do the math. 97 percent. That's the calculated decline in views per post over roughly six weeks, with dated screenshots on both ends. April and May: 12,000, 12,000, 13,000, 14,000, 14,000, 20,000, one post at 165,000. July: an average of 406. Same account. Same subject matter. Same format. Fascinating. No policy citation. No explanation. Every attempt to get a real answer from X "support" hits the same canned loop, a support bot that repeats the identical help article twice regardless of what gets typed back, pointing to a report form that returns "page cannot be reached." Meanwhile the accounts this project exists to counter, the ones selling unproven protocols off a chart with no outcome data behind it, do not appear to have this problem. A platform that cannot explain why evidence gets throttled while unproven sales pitches do not is not neutral. It is despicable, and it should say so instead of hiding behind a broken link. Never give up. Never surrender!
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Pablo Corral MD
Pablo Corral MD@drpablocorral·
12/12 for #LMHR and Keto-CTA “trial” Congrats, great achievement 🙌
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Tellit Likeitis@Tellit007·
@LDLSkeptic Peter Anderson, @PeterJAnderson_, asked a sharp, legitimate mechanistic question on this thread and handed you the actual citation to answer it. You called it a thoughtful approach and moved on without touching what the paper actually says. Remarkable. The paper he cited doesn't say clotting factors are an independent, superior alternative to LDL-C. It says hypercholesterolemia enhances arteriolar thromboembolism specifically by reducing nitric oxide, and restoring nitric oxide completely reverses the cholesterol-driven clotting effect. That's elevated cholesterol causing the clotting problem, not competing with it as a separate explanation. Mr. Anderson asked exactly the right question. The reply that followed never engaged with it. This is the third version of the same move from this account in a matter of weeks. TG/HDL was going to replace ApoB. Clotting factors generally were going to replace LDL-C. Now fibrinogen specifically is going to replace LDL-C again, each time skipping the mechanistic literature showing the "replacement" variable sits downstream of the thing it's supposedly replacing. Credit where it's due: Anderson raised the one question on this thread that actually mattered. It went unanswered. Isn't it ironic.
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David Diamond@LDLSkeptic

As a follow-up to my post yesterday, I raised the issue of clotting factors as superior measures of CVD risk compared to LDL. In the film "Cholesterol Code", Dave Feldman was astonished to see that plaque was not well developed in the LMHRs and their subsequent research has shown that LDL does not correlate with plaque development. If he had paid attention to my presentations at CoSci or if he had read any of my papers he would not have been so astonished. Here is one slide of mine that shows one clotting factor, fibrinogen, is an age-independent risk factor for coronary heart disease and stroke. One would think that they should've assessed clotting factors in the LMHRs, but apparently, they did not. Why they didn't is a mystery to me. @BenBikmanPhD @DrPaulMason @Alabdulgaderaa @ifixhearts @FatEmperor @zoeharcombe @ProfTimNoakes @MaryanneDemasi @SinatraMD @DwightLundell @DiljanMansoor @markkaplan20 @KenDBerryMD @PeterJAnderson_ @ApoDudz @dramerling @ElieJarrougeMD @JeffryGerberMD @TuitNutrition @bigfatsurprise @GrassBased @shashiiyengar @drozcanyuce @SbakerMD @DominicDAgosti2 @ElieJarrougeMD @grahamsphillips @doctortro @bscherMD @BudoffMd @AdrianSotoMota @drjenunwin @drericwestman @lowcarbGP @_coach_al @nicknorwitz @lowcarbGP @realDaveFeldman

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Ethan J. Weiss
Ethan J. Weiss@ethanjweiss·
I don't know these guys (John and Calvin). Never met them. Never even exchanged a word. But wow they nailed it. All you need to know here is that the LMHR crew actually produced a feature-length documentary on the study before the study was even complete. I have wasted far too many words on this garbage dump so instead of wasting more, I will let someone way more articulate say it instead.... youtube.com/watch?v=wE0BQD… I strongly think that no clinical or medical decision should be based on these crude, unadjusted exploratory models. And even then, an author of this study described the finding that LDL-C exposure and ApoB levels were not associated with plaque progression as “incredibly robust.” This characterization is statistically indefensible and clinically irresponsible. This is not a subtle disagreement over interpretation. It is a basic misunderstanding of no-association results—or it’s just spin for that claim. The design is not robust. The exposure definition is not robust. The measurements are not robust. The statistical modeling is not robust. The null inference is not robust. The reporting is not robust. The interpretation is not robust. And the conclusion is not robust. There’s nothing remotely robust about this finding except the author’s insistence that it is. And this definitely raises some serious questions. This study does not meet basic statistical standards and cannot support the claim that LDL-C exposure or ApoB did not predict plaque progression. The paper’s statistical case is a complete shambles. It is fatally flawed, statistically indefensible, and actively misleading. And remember, this is the scientific foundation of The Cholesterol Code documentary, promoted as being grounded in science. Well, this is the kind of science it’s grounded in. How do I drop this mic?
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Tellit Likeitis
Tellit Likeitis@Tellit007·
Thank you. I appreciate your support!! Unfortunately almost nobody is now seeing my posts. I put a lot of effort in it but if only a handful of wonderful people are seeing them, that makes it hard to continue. There is no actual support on X anymore. @elonmusk made sure of that. Just bots and dead links. Very sad.
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Achilles Stephens
Achilles Stephens@farawaydeployed·
@Tellit007 Keeping fighting the good fight. This is one of the accounts I actually look forward to seeing posts from.
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Tellit Likeitis@Tellit007·
Mark Kaplan spent a thread listing four cholesterol drugs, Zetia, niacin, torcetrapib, and Repatha, and framed each one the same way: the number went down, no one lived longer, and in one case people died faster. The conclusion offered was that lowering LDL-C and ApoB is a manufactured pattern, not medicine, and the real answer is testing fasting insulin, HOMA-IR, triglyceride to HDL ratio, and hs-CRP instead. Precious. @markkaplan20 has this account blocked, so what follows is not a quote of his post, it's a response to a post forwarded by a reader. Credit to @DrSandipRoy for flagging it. "Zero lives saved" is doing a lot of work here. IMPROVE-IT's actual primary endpoint, the composite of cardiovascular death, heart attack, stroke, and hospitalization, was reduced from 34.7 percent to 32.7 percent, statistically significant. When researchers later counted every event instead of just the first one, the reduction held at 9 percent. All-cause mortality alone did not move, that part of the chart is accurate. But that is not a scandal, it is what happens when a trial sized for its composite endpoint gets held to a different standard afterward. All-cause mortality pools every cause of death, cancer, accidents, infection, everything, which dilutes a cardiovascular-specific effect and typically needs a far larger pooled sample to reach significance. One endpoint not moving because the trial was never built to detect it doesn't erase a different endpoint that did. Now for what our grifting buddy Kaplan conveniently skipped. Ezetimibe added to a statin does something specific: it lowers LDL-C and ApoB by blocking intestinal cholesterol absorption, which means the same target can often be hit at a lower statin dose. A lower statin dose means fewer dose-dependent side effects, for the same LDL-C and ApoB reduction. IMPROVE-IT is the hard outcome data behind that specific combination, not a surrogate marker, an actual reduction in cardiovascular events across 18,144 patients. Torcetrapib is the one entry on his list that isn't being spun. It did raise mortality, and the trial was stopped for exactly that reason. What's missing is why: off-target toxicity specific to that molecule, raising blood pressure and aldosterone, not a drug class effect. Later CETP inhibitors without that toxicity didn't repeat it. None of this asks what Kaplan's own protocol has. Fasting insulin under 5, HOMA-IR under 1, trig/HDL under 1, hs-CRP under 1, sold through a company with a waitlist and five names on the founding team. Where is the randomized outcomes trial showing Kaplan's protocol reduces heart attacks or death? It does not exist. His checkout button does though. The same standard being demanded of Zetia should apply here first, no? Choose wisely, my friends.
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Sandip Roy@DrSandipRoy

Kinda not true what he tries to prove: "This is the pattern. Zetia: LDL down. No lives saved. Repatha: LDL down 60%. No mortality benefit. $14,000 per year... All lowered the number. Not one saved more lives." Tagging my two fave med-data nerds @Tellit007 and @ScottAppliedSci

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Tellit Likeitis@Tellit007·
@SamaHoole is slipping fast. Blood is not a deep fryer, and arteries are not pipes waiting for beef tallow to congeal. Remarkable. Atherosclerosis is not a melting-point problem. It is a biological one: ApoB-carrying particles travel dissolved in blood as lipoproteins, not as solid fat, cross into the artery wall, get retained, oxidize, and trigger an immune response that builds plaque over years to decades. None of that requires blood to drop to 30 degrees. It requires particles crossing into the vessel wall, which happens fine at 37. Nobody pulls a solid lump of Tuesday's dinner out of an artery because that was never the claim to begin with. Plaque is oxidized lipid, dead immune cells, calcium, and fibrous tissue, not a grease clog. The kitchen physics is correct. It is also answering a question no one in cardiology asked. Fun times.
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Sama Hoole@SamaHoole

If saturated fat clogged your arteries, you'd have far more immediate problems. Beef fat sets at around 30 degrees. You run at 37. So for the clogging to start, your core temperature has to fall seven degrees first. At 35 you are shivering uncontrollably. At 33 you are confused and slurring. At 30 you are unconscious, your heart is arrhythmic, and you have far bigger concerns than what you had for breakfast. The plaque theory only works on a patient who is already dying of something else entirely. Nobody has ever pulled a solid lump of Tuesday's dinner out of an artery, because the only body cold enough to hold one has stopped needing arteries. Turn the heating on. Have the steak.

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