Dave Feldman Profile picture
Engineering / Lipidology / Citizen+Formal Science 🎗 https://t.co/tKrrIdG1Yf (501c3) 🟡 https://t.co/EhKewtOfxz 🩸 https://t.co/D1LrI2dtIi
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May 21 10 tweets 4 min read
1/🧵 If Plaque #ApoB-48 > #ApoB-100

Quite a rabbit hole so far...

First, let me say that data on this has been a bit limited. But *IF* we do ultimately confirm there are more ApoB-48 (B48) than ApoB-100 (B100) in ASCVD plaque, it would be a very big deal.

Let's unpack... Image 2/ First, thanks to @TuckerGoodrich for pinging me on these pubs and pressing the discussion.

But also credit to @CaloriesProper on tweeting this a couple years ago (I missed it then)

To understand why this would be so important if true, some review...
Apr 14 4 tweets 4 min read
1/ Chat on Triglyceride rich #LDL

#Me: Why would triglyceride rich LDL particles be more atherogenic than triglyceride poor LDL particles?

#ChatGPT: Triglyceride-rich LDL (low-density lipoprotein) particles are more atherogenic (i.e., more likely to contribute to the… twitter.com/i/web/status/1… 2/

#Me: Couldn’t it also be possible that triglyceride rich LDL are ultimately the result of metabolic dysfunction and that better explains its association with atherosclerosis?

#ChatGPT: Yes, that is also a possibility. Triglyceride-rich LDL particles are often associated… twitter.com/i/web/status/1…
Apr 13 10 tweets 6 min read
1/🧵 I'm definitely a fan of both @DominicDAgosti2 and @DrRagnar (obviously), so I was excited to see them chatting about #lipids, #LMHRs, and Dom's consideration of increasing carbs to lower his #ApoB

If no one minds, I'd like to add some thoughts...

2/ First -- I'm extremely excited to share @DominicDAgosti2 may be the most notable N=1 I've waited for regarding #ResistanceTraining change & #LDL/#ApoB in a #ketogenetic context

Those who've followed me for a while know exactly what I'm talking about...
Mar 24 5 tweets 4 min read
🧵Followup on #salt comment last night:

Took 3 readings of my blood pressure this morning:
Average: 106/73

- Male, 49
- Moderate exercise
- Moderate-high stress career
- Supp 6-10g of salt daily when #keto* to relieve fatigue, cramping (for >5 yrs) 2/ So everyone on #keto should be like me and take copious amounts of #salt?

Well, sorry, but the answer appears to be:
👉 Your results may vary.... a lot.

On the little-to-no salt side, check out @KetoCarnivore's recent discussion on this
Mar 23 25 tweets 10 min read
1/ #Metabolism, #lipids, and #ASCVD

Okay, I want to revisit and breakdown my position on this crucial topic and the challenges in communicating it.

⚠️ Get comfortable, as this could get long.

Ready? Let's go... 2/ First, it's worth reviewing why there's a high level of confidence low density lipoproteins (LDLs) drive atherosclerotic cardiovascular disease (ASCVD)

For an excellent, lay-person video, I recommend @NutritionMadeS3's from a couple years ago 👇

Mar 12 5 tweets 2 min read
Maybe. I hope so.

Let me just say a major problem with the #diet and #nutrition space is just how many sides seek to oversimplify these things.

And as unpopular as it is to say it, I think there's way too much focus of folks having extremely quick success as though it's common. I know it's well intentioned.

But I also know many people in my own family who have struggled their whole lives to lose weight and assume if they don't have this near instant drop to their goal weight like <fill in the blank success story> then they are doing it all wrong...
Mar 11 16 tweets 8 min read
1/ My thoughts on #Satiety & @DietDoctor 🧵

If you've followed me a while, you know I try to avoid the "diet debates" (tho not always successfully)

However, I have been getting a high frequency of DMs/messages/calls regarding DD's new endeavor for a #lowcarb alternative 2/ Let me first start off by saying I don't think any diet is inherently superior to all others.

I *do* think the #lowcarb diet is under-utilized for populations that can uniquely benefit from it.

However, I also believe most of us have many more options than is often assumed.
Mar 9 7 tweets 2 min read
1/ Yes-- I've been meaning to literally do an entire talk on Simpson's Paradox because the concept is really quite simple.

Here's an example:
✅Hypothesis: higher body weight causes higher blood pressure.

💡If we only had scales and BP cuffs, we'd certainly see the relationship 2/ Let's further point out we could demonstrate it over three lines of evidence: observational (epi), interventional (Rx), and genetic (🧬)

Epi: When randomly grabbing a large population of Americans, we find those who generally weigh more generally have higher BP ✅
Mar 5 4 tweets 2 min read
1/4 "also is the LEM (Lipid Energy Model) mutually exclusive with high LDL being atherogenic?"

Yes and no.

Yes -- in that the two should be treated as separate questions. It may well be that LEM is true, yet high LDL is independently atherogenetic and vice versa.

However... 2/4 No -- in that it was actually metabolic dynamics having an impact on lipid profiles that led me down the road we're at now.

Function vs dysfunction (or successful regulation vs unsuccessful regulation) having an upstream impact on lipid levels should be strongly considered.
Feb 7 12 tweets 4 min read
1/ Got lots of pings on this one (including from @theproof)

But it's worth unpacking just how many variables are in play and why I obsess so much about controlling for them when the shifts are relatively small... 2/ If you're just tuning in, I've done over 50 experiments with many of them hypercontrolled (like below) where I literally eat to an exact meal plan with exact timing, have nearly identical exercise, and try to sync sleep schedule as best as possible. cholesterolcode.com/the-oxldl-repl…
Feb 2 5 tweets 2 min read
1/2 Example 1:
🚬 Imagine if the average person from the moment they're born were taught to be 2 pack a day smoker.

⛔️ Now imagine a fraction were born into families that were 0 pack a day smokers.

Would we expect that latter group to have greater longevity than the former? 2/2 Example 2:
Now imagine most people averaged 100 #LDL cholesterol over their lifetime.

But a fraction were born with a genetic mutation that kept their average at 20.

Would we expect that latter group to have greater longevity?
Feb 1 4 tweets 2 min read
1/4 Interesting study regarding #LDL-C vs all cause mortality*

✅NHANES -- so it's #OpenScience 👏
✅Lowest LDL-C associates with highest ACM
⚠️ No short term censoring (more on this below)

(*had in my reading list, but forgot until ht
@BobJohnson462) nature.com/articles/s4159… 2/4
A couple notes...

1️⃣ Many assume the higher ACM associated with LDL-C is due to "reverse causality". It's a hypothesis, to be sure, but one I think worth exploring.

Thus, it would have been ideal of the authors tried at least one or more analyses censoring 2-3 years.
Jan 30 7 tweets 3 min read
Yes, read it when it came out.

For those who've followed my work and know where I'm coming from, WHY would I fully expect LDL-TG (triglyceride content per LDL particle) to closely associate with atherosclerosis?

(By now this should be a very easy question.) 2/ Let's start with causal directionality.

Which of the following are possible?

1) High LDL-TG is causing higher atherosclerosis

2) One or more things are causing both higher LDL-TG and higher atherosclerosis
Jan 26 4 tweets 1 min read
I don’t want to bias the results, but I’ll concede my answer would depend on the population criteria. For example, I’ve known many who are into fitness (or just now getting into it) that are seeing better results on PE.

To be sure, that’s anecdotal, and it’s hard to know for sure if they were getting adequate protein in the first place…
Jan 9 5 tweets 2 min read
Great comments today via @Lpa_Doc -- please note his precise language. 👇

I'm going to thread 🧵 this and his other comments and then add some of my own...

/1 2/ "My point is, there is no athero or chronic vascular inflammation without a lipid disorder."

I have a nuanced difference with Sam on this -- but the important point here is that we need to disentangle the disorder/disfunction from the athero to test..

Dec 25, 2022 8 tweets 2 min read
🎄My Holiday N=1 Overeating Survival 🧵

Here are the observations I give my own family members based on what's I've learned in my N=1 experiments.

1) Nothing beats proximity.

The further I'm away from food, the less likely I am to eat it. Not just across town, but in the room. 2) Like many (but probably most), eating something outside my diet commitments on a holiday almost always results in my continually breaking that commitment from then on.

Some things I can "cheat" on (like "normal" pizza). Some I can't (like "normal" chocolate chip cookies).
Dec 19, 2022 4 tweets 2 min read
Wow — i’m currently traveling for the holidays and tweeted this out before getting on the road (currently at a stop). I guess this is actually a topic with a lot of interest…

some quick answers to questions… Yes, this was one of the things that got brought up. It’s actually where a lot of the arguing originated because naturally everyone wants to reassure everyone else not to feel insecure. But some chimed in that it isn’t “how the real world works”…
Dec 15, 2022 4 tweets 2 min read
Yes -- let's take a moment to talk reverse causality as this is often confused. #thread 🧵

@NutritionMadeS3's point is that some diseases result in *both* mortality and lower total & LDLc.

Thus, the root cause is upstream of each (such as some forms of cancer, potentially). /1 2/ Hence the value of stratifying away a period of early deaths for a given population (aka "censoring")

Thus, if you exclude all deaths in a given population that took place during the follow up period up to year X, then this helps to address reverse causality.
Dec 13, 2022 7 tweets 5 min read
📍Big milestone!📍

The Nov/Dec @LipidJournal just dropped!

🚨Featuring the #LMHReditorial 🚨
via @nicknorwitz et al

It focuses on #LMHRs, both in consideration of their high #LDL and an urgent call for expanded #research.

Why is this important?... /1
doi.org/10.1016/j.jacl… 2/ Certainly the biggest impact is bringing this phenotype well into the spotlight.

If you've been following my work from the beginning, you can appreciate just how much energy I've put toward putting this phenotype in front of Lipidologists.
Dec 9, 2022 15 tweets 7 min read
🧵 Dec 9th anniversary thread

On this day in 2015 I received a lab result that would alter the course of my life.

Just two weeks earlier I had gotten my very first bloodwork after half a year on #keto that showed my total and #LDL #Cholesterol had nearly doubled (!)… /1 2/ With that first test I was overcome with shock and curiosity — much more former than the latter.

I wanted to get a repeat test to confirm this wasn’t a lab error.

I wasn’t ready to give up #keto, but I was miserable enough that I ate considerably less.
Nov 29, 2022 9 tweets 4 min read
1/ 🧵 I like a lot of @NutritionMadeS3's videos, but I'll concede this one was a little mixed, so I wanted to share some notes (it gets better by the end)

As always, I hope this will be received by everyone in a productive, respectful manner. 2/ myth: “CAC score of 0 means no plaque”

👆I feel this is another statement that is extremely categorial and unrepresented by the vast majority of knowledgable proponents for CAC.

We were chatting about this before on the debate questions...