@DoctorTro

Physician | Father | CMO @GoTowardHealth | ❤️‍🩹I help companies ⬇️ healthcare costs |💪🏻I help patients lose weight, improve diabetes | https://nitter.cf/t.co/9COUe2aacl

We see patients NATIONWIDE
Joined December 2010
This is really the whole issue for me. I actually like nattokinase. I recommend it. I think some of the data are interesting. But you have to apply the same evidentiary standard to the things you like and the things you don’t. You said: “Please show me the 5 year statin study showing a significant AR reduction of MACE in 10% of treated subject” Look at VESALIUS-CV. It randomized 12,257 high-risk patients without a previous MI/stroke to repatha or placebo and followed them for a ~5years. At 5 years, 3-point MACE went from 8.0% to 6.2% with decreased cardiovascular mortality and decreased all-cause mortality (not hierarchically significant) So now I’ll ask you the same question. Where is this for nattokinase? Where is the adequately powered, multi-year randomized trial showing nattokinase reduces MI, stroke or cardiovascular death? It doesn’t exist. And I’m not saying that means nattokinase doesn’t work. I LIKE nattokinase. I’m saying you are willing to use physiology, surrogate endpoints, imaging and clinical judgment when the therapy is one you believe in. So am I. You also said: “It seems to me that as the prescribing physician you should be able to provide for your patient the research that demonstrates the medication will provide a clear benefit which outweighs any harm.” We do. We literally put our evidence reviews online for anybody to read for free. We discuss LDL, ApoB, CAC, plaque imaging, statins, ezetimibe, PCSK9 inhibitors, absolute risk, benefits, harms and uncertainty. We have nothing to hide here. toward.health/pcsk9-inhibito… toward.health/understanding-… toward.health/why-cac-matter… toward.health/ezetimibe-keto… We also have long discussions with patients, answer all questions, and ask what they want to do. WHAT THEY WANT TO DO. This is called shared-decision making. But then you said: “Prove to me that your patients will benefit as a result of taking the ezetimibe you prescribed for them” This is where the double standard becomes impossible to ignore. You’re asking me to PROVE that an individual patient will benefit from ezetimibe. Okay. Can you prove that the individual customer buying nattokinase from you will benefit? Of course you can’t. There is no randomized nattokinase cardiovascular outcomes trial showing that the person buying your product will avoid an MI, stroke or cardiovascular death. There isn’t even a large randomized nattokinase MACE trial from which you could reasonably make that claim. Yet somehow the requirement to “prove to me that your patient will benefit” seems to stop when the intervention is nattokinase... which you sell. That is exactly the inconsistency I’m pointing out. For ezetimibe, you demand proof of benefit for the individual person. For nattokinase, you accept surrogate data, mechanistic reasoning, carotid imaging and clinical judgment. You can’t have it both ways. And again... I’m not criticizing nattokinase for having incomplete evidence. I recommend nattokinase. I’m criticizing the fact that you are applying an evidentiary standard to ezetimibe that you clearly do not apply to your own product. Because ezetimibe actually has considerably more cardiovascular outcomes evidence. cardiac events decrease, plaque volume decreases... Then we have coronary imaging. PRECISE-IVUS actually measured coronary plaque. Plaque regression occurred in 78% of patients receiving atorvastatin plus ezetimibe compared with 58% receiving atorvastatin alone. Nattokinase has interesting surrogate data too. One small randomized study using 6,000 FU/day reported a 36.6% reduction in carotid plaque size over 26 weeks. A larger 1,062-person study using 10,800 FU/day reported reductions in carotid plaque and CIMT. I think those findings are interesting. That’s one reason I’m open to nattokinase. But that larger study was retrospective. And when nattokinase was tested in a double-blind placebo-controlled trial of 265 people for about 3 years, there was no significant difference in CIMT progression or carotid stiffness. So again... I am giving nattokinase every benefit of the doubt. I am simply asking you to give your discussions that same courtesy. Then you said: “Further, I find it disturbing that you and Adrian would prescribe ezetimibe to #LMHRs with no empirical evidence of a coronary benefit.” There is no randomized trial proving ezetimibe prevents coronary events specifically in LMHRs. Correct. There is also no randomized trial proving nattokinase prevents coronary events specifically in LMHRs. Actually, there isn’t a nattokinase cardiovascular outcomes trial remotely comparable with IMPROVE-IT in ANY population. So what is the actual rule? If the rule is that we cannot use a therapy in an LMHR without an LMHR-specific randomized cardiovascular outcomes trial... then nattokinase fails your own standard too. If the rule is that physicians can integrate broader randomized outcomes data, mechanistic evidence, plaque imaging, surrogate endpoints, safety and individual patient characteristics when phenotype-specific outcome trials don’t exist... then ezetimibe clearly qualifies too. That is the hypocrisy. Not that you like nattokinase. I like nattokinase too. The hypocrisy is demanding a level of proof from a generic medication that you do not demand from a product you personally sell. Pick an evidentiary standard... then apply it to everything.
My goalposts have been fixed in place since my first talk 15 years ago. Again, I'm not anti-meds or anti-lipid lowering meds. I'm only for the accurate portrayal of benefits, which we have published numerous times and I've provided here. Are you not able to see my copy/paste of Ridker's portrayal of Crestor benefit as a 54% reduction of MIs, when the real reduction is 0.41%? If NK advocates used relative risk to sell their supplements I would criticize them as well.
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DoctorTro retweeted
Good Morning Tennessee! Ready for day 2 of LC4BH
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Eating healthy is a duty to yourself and to your family Stop being a victim of corporate monster selling you addictive slop Start cooking meats, fish, chicken, eggs and lamb
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I can't believe this day has finally arrived. Everyone inside @wideeyetv knows just how much I was hoping we would get here! I'm just so incredibly grateful to everyone for all their support 🙏 And if you haven't seen it yet -- GO! Watch here: amazon.com/gp/video/detail/B…
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Patients deserve better than blame. They deserve a clinician who takes their hunger, cravings and lived experience seriously. I wrote about why this fight is personal. toward.health/why-obesity-an…
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Ever wonder why counting calories doesn’t work for most people? There are actually a few reasons…
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A 14-patient study looked at ezetimibe for high LDL on keto, finding a 53.2% median reduction. Discover why patient selection and study limits matter before drawing conclusions. Read the full interview: toward.health/interview-towa…
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Please provide the evidence that metabolically health people will benefit from LNT (lifelong nattokinase therapy) By the way I am favorable of it, I want to merely see the nature of the logical and intellectual consistency
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Bringing metabolic health to Tennessee!
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I can own my tone without walking away from this fight. I lived at 350 pounds. I watched what obesity did to my family. Here is why the fight over obesity and nutrition is personal to me. toward.health/why-obesity-an…
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This is exactly correct 👍🏻
N-acetylcysteine (NAC), an OTC supplement, is useful for many conditions, from lupus to OCD and even alcoholism, by delivering cysteine, a sulfur amino acid. But it may be useful only because most people don't eat enough animal protein, which has a cysteine content of up to 6%, with dairy having the highest. It seems possible that many of the conditions which NAC treats may be caused or exacerbated by low dietary protein. Vegetarians are particularly likely to have a sulfur amino acid deficiency, and the RDA for protein is too low.
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DoctorTro retweeted
Drugs decreasing plaque volume: high-intensity statins, PCSK9 inhibitors, ezetimibe (+statin), icosapent ethyl. These also reduce cardiac events (MACE). Numerically lower CV deaths: statins, icosapent ethyl, some PCSK9i data, colchicine, bempedoic (primary prev). Statistically lower events: all listed lipid drugs + colchicine (MACE trials). All-cause mortality: robust for statins; mixed/numerical for others (IPE, alirocumab); not for ezetimibe, bempedoic overall, colchicine. Unclear event/mortality but used by metabolic docs: nattokinase, K2/MK7.
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Bret, please allow me to correct you. There has also never been a study on lean-mass hyperresponders, who started ezetimibe on a Thursday of a blood moon, who also had an uncle whose barber lost an eye in the war that demonstrated 1.23562 more years of life and no side effects while adjusting for calories.
"There's no RCT showing statins or ezetimibe extend life in lean mass hyper-responders. So doctors who prescribe them are misled." The first part is technically true. But here's why the conclusion doesn't follow. 🧵
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Why did LDL drop 53% on ezetimibe in keto patients? A 14-patient series showed marked drops, but selected responders do not tell us what happens for everyone. Read the full interview: toward.health/interview-towa…
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Clarification and apology - I said on @LCMDPodcast that Ezetimibe lowered cardiovascular mortality in a clinical trial - it HAS NOT done this - it was remained neutral for cardiovascular mortality while decreasing cardiac events. I mixed this up with Icosapent Ethyl which DECREASED cardiovascular mortality and events.
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DoctorTro retweeted
This may be the most idiotic influencer alive
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🤖 Made with AI
Replying to @DoctorTro
Bashes original creator for saying “most people don’t need 100s of calories in liquid since they’re already fat and unhealthy” Cites studies of people on maintenance diets and “94 health males” to prove his point when most people are overweight and obese. You’re a retard.
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Why did LDL drop 53% with ezetimibe in 14 keto patients? A new case series shows marked response in selected individuals, but does not prove mechanism or heart outcomes. Read the clinical interview: toward.health/interview-towa…
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This may be the most idiotic influencer alive
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PMID: 25825943 33684506 27935520 35710164 31935149 36753292 39633044 19403641
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For lazy gymbros and peptide maxxers @grok summarize the above evidence
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