this post was submitted on 23 Jan 2025
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Thats a interesting paper, unfortunately the endpoints they used where lipoproteins and not all cause mortality. LDL is not the villain it has been made out to be. https://hackertalks.com/post/6054186
I agree if you want to lower your LDL PBF and Seed oils are a great way to do it. I don't agree that lowering your LDL as the only goal is healthy.
Yes! Reducing sugar and carbs is great for metabolic health. Totally agreed
Right, Observational and FFQs.
In this study Low Carbohydrate group was defined as 43% carbs, or 161 Carbs per day. Which is well above a ketogenic metabolism, so does not apply to LCHF/Keto or Carnivore.
Thanks for all the links and papers, its a little overwhelming when you throw so many at once. One paper at a time will make discussion easier. I've look at the data and I'm still comfortable with my choices, and stand behind my statements that ASF is being incorrectly vilified.
You're setting up impossible criteria for what studies you will accept as evidence against your position by saying you will only accept RCT's with all-cause mortality as the end point as evidence. Like I said, nobody does this for studying diet...
You seem to have a double standard for what qualifies as sufficient evidence against your view vs. for your view, as evidenced by the fact you think that the context of a keto or carnivore diet would completely reverse clearly evident trends despite a complete lack of evidence. Where are your RCT's with all-cause mortality as an end point studying the keto diet? Where are your RCT's showing that increasing LDL-C and apo-B does not increase CVD risk over lifespan-scale experiments?
You conveniently chose to ignore the Mendelian randomization studies on LDL-C and apo-B.
Your view on ldl-c and apo-b goes against expert consensus (https://www.lipidjournal.com/article/S1933-2874(24)00240-X/fulltext, https://www.jacc.org/doi/10.1016/j.jacc.2022.07.006, https://pubmed.ncbi.nlm.nih.gov/28444290/), there is very compelling evidence that both, especially apo-b, have a causal role in long-term CVD progression.
While the conversation has been interesting, I feel that continued exchange will not be particularly productive.
Again, I'm not trying to change your mind. I frankly am happy you have chosen a different path.
I literally linked you a RCT in the above post showing LDL being protective for all cause mortality
I do not consider this any more serious evidence than observational. Randomizing observational studies is an interesting way to determine where your next research should be, but not to draw conclusions.
evidence pyramid
Agreed. I don't think either of us are making progress with the other. And that's okay. We can both exist taking separate choices.
This is unfair, because I have provided that information above, I've read all of your links. I don't think you've read any of mine. To be quite frank, I think you've already decided what the right outcome is, you're going through the motions to overwhelm me, but not to engage in an actual intellectual discovery. We're not having a conversation, you're throwing papers at me. That's why we're not progressing
I did read your links, I think it is very interesting but doesn't really move the needle much when we have so much evidence to the contrary
Some Commentary on the linked RCT: https://nutritionsource.hsph.harvard.edu/2016/04/13/diet-heart-ramsden-mce-bmj-comments/. https://ebm.bmj.com/content/21/5/185.full
The study design, in mental health patients, of creating so many artificial foods with corn oil/ omega 6 and no omega 3 as well as the limited monitoring of cholesterol levels and limited length of the study also limits the interpretation of the results. The potential correlation of sudden cholesterol drop with mortality can also be confounded by sudden weight loss, which correlates with diseases like cancer.
Meta analysis of 60 RCT’s linking LDL-C lowering therapies with reduced CVD events:
https://www.atherosclerosis-journal.com/article/S0021-9150(24)01108-0/fulltext
How do you explain how statins reduce risk of CVD events or why those with familial hypercholesterolemia have such high rates of CVD?
It also still does nothing to address apo-b…