1/ Ethan would like me to comment on whether I'd take a statin if I had a heart attack, which is commonly considered "secondary prevention"

I can't do that as I avoid discussing use of medication, except (ironically) in a few non-cholesterol Rx.

That said, a few things...
2/ First, I definitely DO NOT want anyone to interpret anything I've said as reflective of analysis with secondary prevention. I'm quite upfront that I prefer looking to lipid research with regard to so called, "primary prevention" (populations without prior heart attacks)...
3/ Second -- and as always -- I want everyone to work with your doctor. Yes, I do think your doctor needs to likewise work with you and your health goals, but this is a given.

If I had a heart attack, I'd definitely be working with my doctor and considering all the options...
4/ I would not dismiss their advice and experience out of hand and would likewise do my due diligence to be a better informed patient on what my next steps are.

But again -- and with emphasis -- I don't genuinely know what I'd do given this area is much less familiar to me.
5/ So to answer @ethanjweiss concerns very explicitly, my not commenting on what I'd do personally should not in any way be taken as implicit advice to *not* take cholesterol lowering medication. I can't emphasize that enough.

👆 And please feel free to retweet this thread.

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More from @DaveKeto

24 Jun
1/ Thank you for the invitation, @chadinabhan.

I've now listened to the episode and was a bit surprised at a few points, but also less so with others.

Cholesterol is a very emotionally charged topic, and understandably so...
2/ For me, this journey started 6 years ago with alarmingly high total and LDL cholesterol following my going on a ketogenic diet. I became obsessed with trying to understand why and begin reading everything I could on lipidology...
3/ I found through a series of experiments there was quite a bit of change I could induce based on dietary patterns. As I developed and executed this "citizen science" research, I turned it around back to the community to hopefully help us in advancing this important topic.
Read 25 tweets
21 Jun
1/ #Thread - Hypothesis on why leanness + low carb likely to lead to high cholesterol

I originally retweeted this with a simple "yep" given how it this relates to the #LipidEnergyModel.

Many have asked me to expand, so this thread will be my simple, layperson-friendly breakdown
2/ Let's have some fun and use a relatable analogy...

Imagine you had exactly two kinds of stores in the neighborhood: bakeries and butcher shops.

You normally get groceries from both, but recently the bakeries were closed down, so now you just get meat only for meals...
3/ Now that the bakeries are down, there's more demand on the butcher shops, so they are having more inventory sent to them.

But then, the neighborhood increased while the number of butcher shops actually decreased, and this required an even higher rate of shipments to restock.
Read 11 tweets
19 Jun
1/ This would be a good opportunity to clear the air on a few things...

Per @DrNadolsky's tweet, we don't know everything we want to know about #atherosclerosis. Almost everyone would agree it is multifactorial, and most of Med would ascribe the central risk driver to LDL/ApoB..
2/ If you see your LDL rise on a #keto/#lchf diet and you're uncomfortable with this, here's a thread I made for that 👇

3/ In the mean time, @DrNadolsky, @DrRagnar and I are literally in the final stages of IRB (knock on wood) to get clinical data via CitizenScienceFoundation.org <obligatory plug>

Clinical data is almost always more valuable than anecdotal data (assuming good design, reputable team)..
Read 7 tweets
16 Jun
1/ This tweet below from @DBelardoMD brought a lot of interesting conversation.

I wasn't going to weigh in, but given I'm pretty vocal on this topic already, here are some respectful additions...
2/ First, I agree glucose going up and down -- in and of itself -- is not inherently a mechanism of concern.

The key questions of interest are by how much and for how long -- and from this, can we determine if there is a dysregulation?
3/ I was listening earlier in a Clubhouse chat to @Dr__Guess discuss her recent study and how "all over the map" glucose levels were for these T2D patients -- which is unsurprising given the nature of the disease.

Read 11 tweets
13 Jun
1/ #ListeningThread — actually didn’t know this, but @BioLayne has a podcast. I actually found it in reverse as I’ve been hunting down all things Hypertrophy - and they have a recent podcast with @YngvaiMalmsteve on the topic so I’ll give it a listen… open.spotify.com/episode/2tgWUE…
2/ @BioLayne “… if you torture the data enough, you can get it to show what you would like it to show.”

This is actually a variation I was one of my favorite quotes of all time.👇
3/ it’s also very prescient in its timing. I was actually just talking with @NutritionMadeS3 yesterday, and why I tend to be more interested in studies that work off open or shared data sets given the level of transparency in the statistical instruments being used…
Read 6 tweets
12 Jun
1/ Great question -- and an important one.

The majority of things I'd "take back" have more to do with my having a simplified version of certain concepts that I now much more about (and would present as such)

But I'll be hit up on those things that are more overtly incorrect...
2/ Probably the biggest is my originally saying "Low Density Lipoprotein's primary purpose" is to deliver fat for energy. I had meant it at the time as the class opposite HDL (thus, all ApoB). Sure, a few slides later I differentiate with VLDL, IDL, and LDL...
3/ But the more appropriate way to have stated the same thing would have been: "The primary purpose of ApoB-containing lipoproteins overall is to deliver fat-based energy."

However, I don't think I'd like this statement as much either given how ApoB impacts immune other mechs...
Read 7 tweets

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