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@ayeshavisk41781

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Buy Bitcoin.

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@AaronLiv_

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[illuminatibot @iluminatibot]

Bitcoiners were right about everything, it's all happening!

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1. The title overstates the findings
•Title says: “Plaque Begets Plaque, ApoB Does Not”
•But the data do not conclusively prove that ApoB “does not” — only that in this very specific cohort over a short duration, there was no strong correlation between ApoB levels and plaque progression.
•There’s no causality testing, and no comparison with a low-ApoB group. So, the conclusion is too strong for what the data show.

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2. Extremely specific population (lean mass hyper-responders)
•Participants had very low triglycerides, high HDL, and extremely high LDL and ApoB due to long-term ketogenic diets.
•This is a non-standard metabolic phenotype, and the results cannot be extrapolated to the general population.
•Yet the discussion implies broader implications — that’s a logical overreach.

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3. No proper control group
•All participants were already on low-carb diets for at least 2 years (often 5+).
•There was no matched control group with lower ApoB but otherwise similar profile.
•That makes it impossible to isolate ApoB as a variable — there’s no baseline to compare against.

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4. The CAC results are glossed over
•About 20% of participants developed new CAC (coronary artery calcifications), which is plaque progression.
•The authors dismiss this because it didn’t correlate with ApoB, but:
•All subjects had very high ApoB, so correlation might disappear due to a ceiling effect.
•It’s still clinical progression, which undermines the idea that these people are “immune.”

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5. Study duration is too short
•1 year is not enough to assess long-term atherosclerosis risk.
•Atherosclerosis is a slow process, and short-term plaque stability does not imply long-term safety.
•The authors emphasize “most plaques didn’t grow,” but some did — and it matters.

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6. Bayesian analysis is used selectively
•They used a Bayesian framework with priors assuming ApoB is harmful, to test whether the data contradict that.
•But they did not test the reverse — whether the data actually support the “ApoB doesn’t matter” view.
•This is a biased use of Bayesian logic, not a neutral analysis.

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7. Possible survivorship bias
•Participants were long-term keto adherents who likely already “survived” the early adverse responses.
•People who react badly to keto + high LDL probably quit the diet early, so they’re not in this sample.
•So the cohort may be resistant outliers, not representative.

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8. Narrative bias in the discussion
•The authors repeatedly state this study “challenges the lipid hypothesis” and “calls into question the role of ApoB.”
•But the evidence is narrow, short-term, and observational — it should be described as a hypothesis-generating study, not a paradigm-breaker.

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9. No inflammation markers measured
•They did not collect data on hsCRP, IL-6, or other inflammation markers.
•ApoB-related damage may be mediated via inflammation, so by not measuring it, they ignore a critical pathway.

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10. No analysis of plaque composition
•The study focused on calcification and total volume, but didn’t assess plaque vulnerability, lipid core, or fibrous cap.
•So we don’t know if the plaques became more stable or more dangerous.

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Summary:

This paper is a very interesting exploratory study of a rare, keto-adapted, hyper-responder population. But:
•It overstates its conclusions based on short-term, narrow data.
•It does not disprove the ApoB hypothesis — it only fails to detect a correlation under very specific conditions.
•It contains logical gaps, lacks proper controls, and shows evidence of narrative bias.

It’s worth studying further — but it’s not the revolution it’s trying to be.

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@BTC_broo They say that their bags are „pumping”