ajaMD

Retired and rewired vascular surgeon

[ajaMD @AlanAnnenberg]

@DavidBCollum Shame they didn't get stung for housing Ralph Baric's Covid laboratory.

[ajaMD @AlanAnnenberg]

@MBAeconomics1 @SirSilverQuack If Trump and Bessent don't revalue gold, they certainly will revalue the dollar when the Fed turns on the printer.

[ajaMD @AlanAnnenberg]

@DowdEdward Probably jabbed the Cialis in his turtle.

[ajaMD @AlanAnnenberg]

@grok @4boysontheloose @afshineemrani Your data is accurate .Your interpretation particularly regarding "modest "benefit in primary prevention is disingenuous. Now maybe you are just regurgitating what the authors wrote but ARR of .07% or .09% is not modest regardless of what a "peer reviewed" journal states.

[ajaMD @AlanAnnenberg]

@grok @4boysontheloose @afshineemrani @grok, that is some pretty mystical stats. Who paid for the study?

[ajaMD @AlanAnnenberg]

@grok @4boysontheloose @afshineemrani @grok, I asked Perplexity the same questions. I think you have embellished most of this data.

[ajaMD @AlanAnnenberg]

No, it's directly observed—not extrapolated or modeled. WOSCOPS randomized 6595 men to ~4.9 years pravastatin vs placebo. Record linkage tracked them to 20 years total. All-cause mortality: 34.7% vs 38% (HR 0.87); CV death down 21%. Post-trial statin use equalized and stayed modest, yet the early-treated arm showed sustained lower events. Classic legacy effect from reduced cumulative ApoB exposure shifting plaque trajectory.

[ajaMD @AlanAnnenberg]

@grok @4boysontheloose @afshineemrani @grok, did you not quote the WOSCOPS: CHD death/nonfatal MI ARR 2.4% (~5 yrs) for primary prevention?

[ajaMD @AlanAnnenberg]

@grok @4boysontheloose @afshineemrani @grok ,so that 20 year number was an extrapolation of five years of treatment? That's pretty tricky.

[ajaMD @AlanAnnenberg]

@grok @4boysontheloose @afshineemrani @grok ,so taking a statin to reduce Apo B for twenty years reduce all cause mortality by 3.3%. That means 3 out of 100 treated. In 20 years can you give me the data on the NNH taking a statin?

[ajaMD @AlanAnnenberg]

@grok @4boysontheloose @afshineemrani @grok but you are saying that if I take a statin for 5 years ,I can then disconinue it and have twenty years of reduced risk? No physician has ever conveyed that to me. And I'm a retired vascular surgeon.

[ajaMD @AlanAnnenberg]

@grok @4boysontheloose @afshineemrani @grok, This makes no sense. If " Protection endured after most stopped therapy " then explain why statins are needed. ApoB doesnt just come and go at moments in the lifetime of a patient.

[ajaMD @AlanAnnenberg]

@grok @4boysontheloose @afshineemrani @grok, show me the long term follow up that confirms the benefit over 5 year average?

[ajaMD @AlanAnnenberg]

@grok @4boysontheloose @afshineemrani @grok, how can you say truthfully that a ).9% ARR is a modest risk reduction?

[ajaMD @AlanAnnenberg]

The ~0.6% ARR all-cause mortality in primary prevention meta-analyses (avg 4.4 yrs) means ~1 death prevented per 167 treated. Treating 100 patients prevents ~0.6 deaths on average, not 2.5—that figure doesn't match the data and may reflect a different endpoint, relative risk, or higher-risk subgroup.

Benefits are larger for major vascular events/MI (~0.7% ARR, NNT ~140) and scale directly with baseline risk and LDL drop. Truly low-risk primary prevention has modest absolute gains; moderate/high-risk patients see better NNT. Guidelines target therapy accordingly, with ApoB/Lp(a)/inflammation for refinement. Individualized shared decisions remain essential.

[ajaMD @AlanAnnenberg]

@grok, but you just stated quite correctly that Lp(a) is 6x more atherogenic than LDL and accumulates preferentially early on. Yet ApoB is the driver for statins and statins have no benefit on lower Lp(a). So it seems that statins don't really get to the root cause of atherogenesis. They are not effective for Lp(a), and are 15-40% effective in reducing inflammation. You care to comment ?

[ajaMD @AlanAnnenberg]

@grok @4boysontheloose @afshineemrani @grok, but that's not a modest reduction in all cause for primary prevention. You have to treat 100 patients to get 2.5 patients who benefit over 5 years. You comment ,please.

[ajaMD @AlanAnnenberg]

@grok @4boysontheloose @afshineemrani @grok, not very impressive in primary prevention . All cause death is 3.3% ARR. Can you breakdown the subtypes of all cause death.

[ajaMD @AlanAnnenberg]

@grok @4boysontheloose @afshineemrani @grok, please demonstrate the absolute risk reduction of death,MI events in the large trials lowering ApoB with statins. I'm not interested in relative risk reduction . I'm interested in both primary prevention and secondary prevention.

[ajaMD @AlanAnnenberg]

Histologic studies confirm apo(a) co-localized with ApoB in plaques, proving Lp(a) retention. Lp(a) is ~6x more atherogenic per particle than LDL and can accumulate preferentially early on. However, Lp(a) particle counts are typically far lower than LDL, so the majority of total subintimal apoB substrate in most people still comes from LDL. Lp(a) adds distinct prothrombotic/inflammatory effects via apo(a). Both drive atherosclerosis; measure ApoB + Lp(a) for complete assessment. Lowering ApoB remains foundational.

[ajaMD @AlanAnnenberg]

@grok @4boysontheloose @afshineemrani @grok, but aren't there histologic studies that demonstrate ApoA components with ApoB components thereby strongly suggesting that the majority of thrombogenic substrate subintimally results from lipoprotein (a) and not LDL?

[ajaMD @AlanAnnenberg]

@grok @4boysontheloose @afshineemrani @grok, does lipoprotein(a) carry ApoB?

[ajaMD @AlanAnnenberg]

@grok @4boysontheloose @afshineemrani @grok, how do we know that the retained substrate is LDL?