🚨 Tro is moving the goalpost and manipulating study results to affirm his low carb bias - the exact same thing the KETO CTA study authors are doing. 🚨
1. Moving the goalpost = The primary outcome of interest is not PAV change. It’s NCPV (as per their own study protocol and it was the main point of our commentary letter. The NCPV increase after 1 year was 18.8mm^3 for the KETO dieters. That’s almost a 4x INCREASE in plaque for their PRIMARY outcome vs other healthy cohorts (e.g. NATURE CT study)❗️🤦🏽♂️
2. The reason NCPV is more appropriate in this context is because statins tend to increase the amount of calcified plaque (to help stabilise it), thus changing the composition of plaque to be more protective. Using PAV is inappropriate in this context as it includes both calcified and non calcified plaque - people on statins may still increase PAV even if non-calcified plaque volume hasn’t increased much. This is backed by the PARADIGM cohort itself (PMID: 30789215); “However, under the effect of statins, CACS progression indicates only calcified PV progression, but not non-calcified PV progression.” When we look at the PRIMARY OUTCOME, the data is not good for these keto dieters.❗️
3. You keep bringing up the nonsensical point of: “why didn’t they find a correlation between their LDL and plaque progression?” As we explained in the commentary letter —> in order to detect a robust dose response relationship, you need sufficient variability in exposure = analyse those with high LDL vs those with low LDL.❗️You need a large enough exposure contrast. Checking for an association between LDL and plaque progression when everyone has high LDL is a meaningless analysis without a low exposure group. It’s like assessing if skin wrinkles is associated with age, but the only age brackets you’re testing are those who are aged 70-85 years old 🤦🏽♂️
4. Even if you want to hang your hat on a made up outcome (Percent Atheroma Volume) that wasn’t mentioned in the protocol as being an outcome of interest 🤔 —> the low risk group in PARADIGM were still overweight on average (BMI 24.9), had more hypertension (40ish%), diabetes, smoking, largely inactive and 70% had atypical chest pain - so if your argument is now that “metabolically healthy” fit and lean Keto dieters who have a CAC score of 0 at baseline, with no other risk factors for CVD other than high LDL/ApoB —> progress plaque at the same rate as metabolically unhealthy, hypertensive, diabetic and overweight medicated smokers following a generally unhealthy diet —> then it’s not looking good bruv. ❗️What you’re saying is the healthiest keto dieters with high LDL gain plaque at the same rates as your average overweight hypertensive Joe… And you think LDL is not an issue? Sorry you can’t be this stupid. 🥴
5. When you look at PAV change across the entire KETO cohort (0.8% increase), that’s HIGHER than the HIGH risk group in PARADIGM (most were overweight, 70% were hypertensive, 50% had diabetes and 32% were smokers).❗️
You’re doing the same thing these researchers tried to do
@realDaveFeldman @nicknorwitz - change the narrative, avoid the primary outcome of interest and spin very alarming study results to suit your low carb bias. But quite frankly you failed just as catastrophically as them. 💀
No matter how you try and frame it, no matter what insults you use, you remain out of your research interpretation depth and facts remain facts =
🚨These “metabolically healthy” lean keto dieters increase their plaque at similar or faster rates than metabolically unhealthy cohorts and MUCH faster than healthy cohorts.🚨
@drgarymcgowan @Richie_Kirwan @PatrickElliott0 @DrNadolsky @drmatthewnagra