Tellit Likeitis

What actually separates a scientist from a grifter? Because both have financial interests. Both are selling something. So why does one deserve your trust and the other deserves your skepticism? It's not the money. It's what the evidence does when money pushes back. A scientist working inside the Bradford Hill framework builds a case from converging lines of evidence: consistent associations across populations, dose-response relationships, biological plausibility, genetic data, and most importantly, experimental evidence where changing the exposure changes the outcome. When those RCTs show their hypothesis is wrong, scientists update. The evidence has overruled careers, textbooks, and billion-dollar assumptions before. That's the system working. A grifter's financial model collapses if the evidence is true. So the evidence can never be true. The carnivore coach needs saturated fat to be harmless despite ApoB elevation, so every lipid trial is "industry-funded." The plant-based absolutist needs animal protein to be poison, so every null result in their pet hypothesis disappears. The functional medicine practitioner in the middle sells tests and protocols nobody needs, so "root cause" deflection never ends and statins are always the villain. The conclusion never changes regardless of what the data shows. That's not skepticism. That's a business model dressed as skepticism. The moral distinction is this: a cardiologist's reputation is built on whether their patients live longer. That constraint is real and merciless. The CTT collaboration tracked 170,000 people across randomized trials and the answer is visible in hard endpoints: cardiovascular events, mortality, measurable disease. A clinician who ignores that data watches patients die. That's accountability with consequences. None of these grifters face that constraint. Testimonials are curated. Failures disappear. The carnivore who died of a heart attack at 52 never makes the highlight reel. The plant-based absolutist whose client developed irreversible neurological damage from B12 deficiency because supplementation "isn't natural" isn't in the case study. The business runs precisely because there's no RCT demanding accountability from any of them. Both scientists and grifters have financial skin in the game. Only one has to be right to stay in business.

@BrianWiley_ That is all I needed to know. Thanks. You measure it. The clinical team handles it. You are the coach. Readers: a keto coach who can not act on elevated ApoB is not your cardiovascular safety net.

Can't and won't go into detail on that, that's the clinical team's call. I will just tell you it is addressed; it's not dismissed as you think. And that list is a sample, the entire panel is run. I refuse to interact with you further. You think we’re just a bunch of ApoB- and cholesterol-denying lunatic charlatans, and that’s the farthest thing from the truth. All of these questions you have asked could be answered with a little research into Me and our practice. If you have any other questions, visit the website, download the app, do some homework, and if you have further questions… call us.

When I was 100 pounds overweight, I was told: “Eat less fat, avoid red meat, use smaller plates.” I lost 100 pounds and kept it off for 17 years… Eating meals like this where the fat & red meat barely fit on a larger plate.

@BrianWiley_ Follow up question: You list the ratio. That is not the same thing. When absolute ApoB comes back elevated, what do you do with that number?

@BrianWiley_ You list it. That's good. But when a client's ApoB comes back elevated after going low-carb, what do you do with that number?

You got healthy. That is real and it matters. Your clients may not have your ApoB. Without measuring it, you do not know. A coach who helps people lose weight without telling them to track the one marker that predicts silent plaque accumulation is leaving the most important question unanswered. The fix is simple. Add ApoB to the panel. Then you are actually making people healthy.

@Tellit007 I don't know what to tell you. I got healthy, I help other people get healthy, and I'm blessed to work at a place that gives me this opportunity. What exactly do you do to contribute to making people healthy? Trolling and posting thousands of ApoB tweets is not it.

@pziegler1986 @TomsWorld01 The HORUS study found atherosclerotic plaque in 34% of pre-agricultural mummies across four continents. Humans doing what humans have done for 100,000 years still got atherosclerosis. The ancestral argument is one reply up. Not a laughing matter.

@TomsWorld01 @Tellit007 Because keto is effectively what humans have done for 100,000s years - this grain heavy Western diet is only a recent phenomena. It's why I laugh at posts like the author's. We'd have been wiped out as a species if what he/she is saying is actually true.

A patient's blood sugar improves on carnivore. Their ApoB climbs to 180 mg/dL. The coach calls it a win. Nobody measured the ApoB. This is the keto grift in one sentence: confusing the symptom fix with the disease fix. When insulin signalling is broken, carbohydrates raise blood glucose more than they should. Reducing carbohydrates removes a proximal glucose source in a system that cannot manage it. Blood sugar improves. That improvement is real. It is also a symptom response, not disease reversal. T2 Diabetes is driven by chronic energy surplus causing fat accumulation in the liver and pancreas. That is Roy Taylor's Twin Cycle Hypothesis. The DiRECT trial confirmed it: 298 participants, caloric restriction, 46% T2D remission at 12 months. The intervention was not low-carbohydrate. It was caloric deficit. Carbohydrates were not the variable. Energy balance was. The fat in the liver and pancreas resolves with energy deficit regardless of macronutrient composition. Keto produces energy deficit partly through appetite suppression. That is the mechanism. Not carbohydrate restriction per se. The grift lives in the gap between the short-term glycaemic win and the long-term cardiovascular picture. The patient whose A1c improves while ApoB rises is not winning. They are trading one risk for a larger one that nobody is measuring. Managing carbohydrate intake in established T2 Diabetes is a legitimate glycaemic tool. Selling it as a cure while directing patients away from the interventions that address energy balance and cardiovascular risk is where the science ends and the sales pitch begins.

You are asking why they are not dropping like flies. Three problems with that framing. First, there is no registry. No tracked cohort of long-term keto adherents with serial ApoB measurements and adjudicated cardiovascular endpoints. The absence of a visible signal in an unmonitored, self-selected group is a data gap, not evidence of safety. Second, atherosclerosis is silent for decades. Elevated ApoB at 40 does not produce the MI until 58. The keto community does not have the 30-year follow-up data. FH registries do. Lifelong elevated ApoB, SMR 2.29 under 70. That is what the long timeline looks like. Third, hunter-gatherers. HORUS study: 137 mummies, four continents, pre-agricultural, no processed food. 34% had atherosclerotic plaque. The ancestral diet did not protect them either. The flies are on a delay.

@Tellit007 Unlike other interventions, Keto advocates are usually people that regained their health from the diet. They don't 'sell' anything. Second if this army of ticking time bombs of undiagnosed heightened ApoB was a real risk, why are 10-20 year Keto folks not dropping like flies?

Your ApoB is excellent. Genuinely. That was noted in March when you shared it. The point is not about YOUR ApoB. It was about the proportion of patients on high-saturated-fat diets who see ApoB rise. Your result does not refute a population finding any more than one person smoking to 90 refutes the lung cancer data. And the coaching page is still there.

@Tellit007 I have shared this you, are doing so much trolling you forgot?

@BrianWiley_ Your bio links to toward.health/health-coaching. That page lists you by name selling an 8-week group coaching program and a 24-week one-on-one coaching program. The AI did not make a mistake. You have a coaching business.

@Tellit007 You are a sad little person, not even sure why you follow me...I am a Health Coach, that is true, but I do not have a health coaching business or sell a "protocol" You should know these AI posts clearly state they can make mistakes.

@BrianWiley_ lost 100 pounds and turned it into a coaching business. The 100 pounds is real. The science is not. Let's check the product. He sells low-carb health coaching as a protocol, with the personal transformation story as the pitch. The post above is the sales material: dietary advice was wrong, he proved it, steak is the answer. Seventeen years of personal adherence is the evidence. x.com/i/status/20247… It is not a trial. It is a testimonial. No control group. No ApoB measurement. No cardiovascular endpoints. Saturated fat reliably raises ApoB in a meaningful proportion of patients, and high ApoB seeds arterial plaque regardless of how the weight came off. A person can lose 100 pounds on any protocol and still be accumulating silent atherosclerosis if ApoB is elevated. The weight is visible. The plaque is not. @DrNadolsky publishes on exactly this intersection. @BrianWiley_ posts steak. One of those methods produces data that can be challenged, corrected, and replicated. SELECT: 17,604 patients, 20% fewer major cardiovascular events. SURMOUNT-1: 2,539 patients, 22.5% mean body weight reduction. Both trials ran ApoB panels. Both reported hard endpoints. The plate is larger. The evidence is not.

GLP-1 drugs took years to protect your heart. Stopping them erases it in months. BMJ Medicine this week: 333,687 veterans, up to 3 years follow-up. Those who stayed on GLP-1s continuously cut their cardiovascular risk by 18% compared to sulfonylureas. Those who stopped for a year saw cardiovascular risk climb 14% compared to continuous users. Two years off: 22% higher risk, benefits virtually gone. The researchers call it metabolic whiplash. Half of patients stop within the first year. Cost, side effects, access. The drugs are not failing those patients. The system around them is. This matters for how the debate is framed. GLP-1s are not a course of antibiotics. They are not a short-term fix with a defined endpoint. Obesity and type 2 diabetes are chronic, relapsing conditions with a cardiovascular price tag. The drug manages the condition. Stopping the drug stops the management. The disease does not stop with it. SELECT already showed semaglutide cuts major cardiovascular events by 20% in 17,604 patients, including in people who did not lose weight, suggesting a direct cardiovascular mechanism beyond adiposity. This BMJ Medicine study adds the discontinuation data: the protection is real, it is ongoing, and it is reversible in the wrong direction. The grifters will use this study to argue dependency. They have it exactly backwards. Needing continuous treatment for a chronic disease is not dependency. It is medicine working as intended.

You just told 80,000 people that butter doesn't clog arteries. What does the ApoB data from your butter-eating patients look like? Not asking for vibes. Asking for numbers.

@DrBPHealth is targeting the smoke and selling the fuel. He has a paid Substack and 50+ clinics selling the idea that national organizations are lying to you about seed oils. That is the product. Here is what the product does not include: Mozaffarian et al. pooled 8 RCTs, PUFA replacing saturated fat. CHD event reduction: 19%. That trial existed before this post. It will exist after. Remarkable. The omega-6 inflammation mechanism is real. What does not exist is a cardiovascular outcomes trial showing seed oil avoidance reduces MACE. CANTOS tested inflammation directly: 10,061 patients, canakinumab, 15% MACE reduction, zero all-cause mortality benefit, higher fatal infection rate. That is the best the inflammation hypothesis has to offer. Butter does not have a trial at all. ApoB loads the arterial wall. The wall inflames. Saturated fat raises ApoB. Seed oils do not. @DrMarthaGulati publishes. @DrBPHealth posts. One of those methods produces data that can be challenged, corrected, and replicated. What he doesn't tell you: the eight trials.

@ChewieWins No need to wait. If their diet is already consistently spiking ApoB we have all the data already 👍

@Tellit007 Curious if current Carnivore trend results in spike and rise of cardiovascular issues in this group in decades to come

@Square1Wellness @zoeharcombe @I_mitochondria You called this pair brilliant. The study @I_mitochondria keeps citing has ten subjects, no control group, and no cardiovascular outcomes. What makes it brilliant: the n, or the conclusions?

Two brilliant minds together talking, "How and why Insulin Resistance drives chronic disease" with Dr. Isabella Cooper and Dr. Zoe Harcombe, Bravo! @zoeharcombe #healthcoach #insulin @I_mitochondria zoeharcombe.com/2026/03/dr-isa…

@Square1Wellness is selling a paid coaching practice off the back of two women running a podcast behind a paywall. Fine. The science attached to it is worth looking at. Let's go! Isabella Cooper's PhD study: ten subjects. No control group. No randomization against a comparator intervention. No cardiovascular outcomes measured. What @zoeharcombe calls "meticulous in execution" is a crossover design where subjects switched states. That design cannot tell you whether this prevents heart disease in anyone. The mechanism is real. Hyperinsulinemia matters. None of that is disputed. What does not exist: a single RCT showing that the keto protocol built on these mechanisms reduces cardiovascular events. SELECT enrolled 17,604 patients. The cardiovascular outcome is 20% fewer MACE. Keto does not have a trial. It has a PhD with ten people and a Bravo from a health coach. Anyone who wants to know the difference between a mechanism that interests a biochemist and one that passes a cardiovascular outcomes trial should read @drpablocorral. The short version: one of those is Cooper's PhD. The other is SELECT. Ten subjects. No comparator. No outcomes. Brilliant.

@ApoDudz Love it! 🤣

😂 🎯

@DoctorTro runs a telehealth clinic that charges patients to deprescribe their cholesterol medication. Telling those same patients to stop asking about cholesterol is not a medical insight. It is a business model. x.com/i/status/20247… "Stop asking what's my cholesterol. Start asking what's my insulin." The clinic that profits from this advice is the one you are being told to text. ApoB is the particle that carries cholesterol into the arterial wall and drives plaque formation. PCSK9 loss-of-function genetics: carriers with lifelong low ApoB have 88% fewer coronary heart disease events. CTT Collaboration: 170,000 patients, 26 randomised trials. Cardiovascular events fall with every reduction in ApoB-containing particles. This evidence does not disappear because insulin is also worth measuring. And if insulin resistance is the root problem, the intervention with the best outcomes data for fixing it is a GLP-1 receptor agonist. SELECT: 17,604 patients, 20% fewer major adverse cardiovascular events. SURMOUNT-1: 2,539 patients, 22.5% mean body weight loss, insulin resistance markers improved. @DoctorTro's clinic does not lead with those options. It leads with a text number. @Drlipid has spent decades explaining why the answer to "stop asking about cholesterol" is: because ApoB is what seeds the plaque, regardless of what your insulin is doing. The gaslight accusation in this post is aimed at the doctors following that evidence. Stop asking about cholesterol and start losing the CVD battle. Classic @DoctorTro x.com/i/status/20247…

Genuinely useful data. A 15% Lp(a) reduction is real and worth knowing. The framing is worth examining though. This is a biomarker signal with no cardiovascular outcomes data attached. The authors themselves said it warrants study in major trials powered on hard outcomes. Those trials have not been run. Meanwhile the same low-carb high saturated fat dietary pattern raises ApoB. PCSK9 loss-of-function genetics: 88% fewer coronary heart disease events across a lifetime of lower ApoB. CTT Collaboration: 170,000 patients, 26 randomised trials, cardiovascular events reduced with every 1 mmol/L LDL-C reduction. That is convergent hard outcome evidence from multiple independent lines. The selective attention is notable. Fifteen percent Lp(a) reduction with zero outcomes data generates excitement. The ApoB consequences of the same diet, with decades of hard outcome evidence behind them, do not appear in the thread. Muvalaplin and olpasiran are in Phase 3 with 80-90% Lp(a) reductions. If outcomes matter for Lp(a), they matter equally for ApoB. One standard applied consistently would be useful.

We saw this Lp(a)-lowering effect of a low-carb/high-fat diet in our trial, with rather remarkable consistency sciencedirect.com/science/articl…