Discover and read the best of Twitter Threads about #ldl

Most recents (24)

Ya comienza #SIAC23 ♥️
La LOCOMOTORA del corazón de las Américas en MARCHA!! 💪💪

Te cuento mis sesiones favoritas de la mañana!! 👀 para los q les interesa prevencion CV/ cardiometabolismo ☺️

🧵🧵👇🏻👇🏻👇🏻👇🏻 @SIAC_cardio
Comenzamos #SIAC23 con #HTA
- Andrés Rosende ⏩HEARTS
- @DanielPiskorz ⏩HTA telemonitoreo
- Wyss Fernando ⏩Control de la TA
- Antonio Coca⏩Demencia e HTA
@SIAC_cardio @siacprevent Image
🔜9:15 IMPERDIBLE: Fármacos no cardiovasculares #SIAC23
- @FranklinCuevaMD ⏩ enf Neurologicas
- Fabian Chávez ⏩ Anestésicos
- Jean Pierre Carrión ⏩Opioides
- @cardiologiamn ⏩ enf psiquiátricas
@SIAC_cardio Image
Read 6 tweets
1a) Welcome to a live-tweeted, #accredited #tweetorial from @nationallipid #NLA23 in #Atlanta on advances in #hyperlipidemia management #LLT. Our expert returning faculty is Pam R. Taub, MD @PamTaubMD #cardiologist from @UCSDHealth ImageImageImage
1b) Dr. Taub is a clinician/scientist and is a frequent contributor to our #accredited programs. She is the founding director of the Step Family Foundation Cardiac Rehabilitation and Wellness Center at #UCSD.
#FOAMed #cardiotwitter @MedTweetorials #MedEd #lipids Image
2) This program is supported by an educational grant from Esperion Therapeutics & is intended for #HCPs. Statement of accreditation & faculty disclosures at Earn 0.75 hr 🆓CE/#CME by following this 🧵!
Read 48 tweets
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……

#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……

#Me: Is it possible that almost the entire amount of atherogenesis associated with high triglyceride rich LDL is due to dysfunctional lipid metabolism and the diseases that result in these profiles rather than the LDL particles themselves?

#ChatGPT: Yes, it is possible that……
Read 4 tweets
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...
3/ When chatting with Dom in SD last year for dinner, he mentioned focusing less on maintaining such a sizable muscle mass as he typically does, and I predicted he'd likely see his LDL/ApoB as considerably higher with this change if still #keto. This podcast appears to confirm...
Read 10 tweets
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?
If genetically low LDL/ApoB had universally a net benefit -- this would be strong evidence that indeed this particle is pathogenic -- which is to say, disease-causing overall (not just atherogenic)

But does existing genetic data support this hypothesis? Is there clear longevity?
Read 5 tweets
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
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.
2️⃣ As always, be aware these data are observational.

And as I say often👇

(Always worth a mention of Bradford Hill and his criteria, btw)
Read 4 tweets
1/🚨New Episode🚨
The Lipid Panel Reimagined: #MindtheGap Segment

How do you interpret the #lipidpanel to help inform patients' risk for #cardiovascular disease? Do you use #ApoB? 🧐

2/ Unfortunately, our patient is stuck in "bumper-to-bumper" #cholesterol traffic 🚗!

See traffic analogy to understand why ApoB can give us information that LDL-C may not:

#Mindblown! 🤯
3/ Overall, LOWER ⬇️ is better for both #LDL-C and #ApoB in terms of reducing #CV disease risk!

But #discordance between LDL-C vs. ApoB is actually quite common!

Take a look at the orange line to see how ApoB confers a higher CVD risk over time 👇
Read 5 tweets
📍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…
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.
3/ But this is understandably a challenge given how much progress on this research has been accomplished outside typical channels ("Citizen Science").

-- Until now.
Read 7 tweets
🧵 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.
3/ At the same time I learned as much as I could about Lipidology - which focuses on how the body moves lipids (like cholesterol) in the blood.

And to my surprise, this system is already very familiar to me as a software engineer given it is a distributed object network.
Read 15 tweets
🧵1/8 Here's an easy thread for reference on our current papers. 👇👇👇

🔖 Bookmark this!

We cover:
- High #LDL on #lowcarb/#keto
- Lean Mass Hyper-responders (#LMHR)
- The Lipid Energy Model (#LEM)

- And, ofc, our #LMHRstudy underway right now
2/8 The #LMHRpaper was our first describing the #LMHR phenotype

- #LDL #Cholesterol of 200 or higher
- #HDL #Cholesterol of 80 mg or higher
- #Triglycerides of 70 mg or lower

Which is actually common for lean, very folks on #lowcarb/#keto folks.…
3/8 Our second paper brings a case report on a single #LMHR with extremely high #LDLc (~500 mg/dL) for 2.5 years, their eating patterns, and current CT angiography.

(⚠️Please note this is a single case report and should be considered anecdotal, ofc)…
Read 9 tweets
1/ Alright, let's chat the #NHANES (IV)

As usual, I'll give my caveats this is back-of-the-envelope on data I wrangled via CDC on this expansive dataset -- and it's associational, ofc (observational)

So what are the lipids like for those who live to 100yr in NHANES?
2/ Remember, these aren't the lipid levels taken *at* age 100+, it's what their levels where at the time of examination 15-20 years prior.

This is very relevant when considering reverse causality given this extreme gap in time for all who were reaching centenarian status.
3/ First up -- #LDL #Cholesterol.

Yes, 73% of you correctly guessed 130mg/dL is the mean average for these 32 individuals (lipids taken age 85 or earlier).

LDL mean average: 130 mg/dL

0% 25% 50% 75% 100%
72.0 102.5 126.0 154.0 215.0

Read 9 tweets
1/4 Back-of-the-envelope:

There are now 32 NHANES participants with lipids & mortality data who have lived to at least age 100 (age + followup > 100yr.), thus earning the designation of "centenarian"

What was mean avg #LDL-C for this group from their bloodwork 15-20yrs prior?
2/4 What was the mean average #HDL #Cholesterol (#HDL-C) for this group from their bloodwork 15-20yrs prior?
3/4 What was the mean average #Triglyceride (TG) levels for this group from their bloodwork 15-20yrs prior?
Read 4 tweets
🧵 New paper on comparing advanced lipid testing (NMR) with body fat (adiposity) - ht @nicknorwitz

High adiposity associates with:
- ⬆️ #ApoB & #LDL-C
- ⬆️ #triglycerides
- ⬆️ levels of all fatty acids

How does this relate to #LEM? Let's unpack... /1…
2/ "Adiposity-related hypertriglyceridemia is mainly driven by increased numbers of triglyceride-rich VLDLs (which carry the largest proportion of triglycerides in blood). Concurrently, the cholesterol in these lipoproteins also seem to be higher at higher adiposity levels."
3/ And these next sentences are key -- take special note of the underlined text... Image
Read 7 tweets
Interesting study on #LDL #cholesterol via #SoybeanOil.

- Uses LDLr “knock out” mice, thus poor clearance

- Yet lower #LDL observed anyway

- Differences for “conventional” vs “modified” oils

- Conventional same plaque levels as SFA control

Ht @KCKlatt…
“After 12 weeks, the mice fed conventional soybean oil had much lower levels of VLDL and LDL cholesterol… compared to the mice fed lots of saturated fat. However, to the researchers’ surprise, the mice on those two diets had the same amount of plaque buildup in their arteries…”
Naturally, I’m especially interested in how much impact this diet had on resulting oxidative potential of newly synthesized lipoproteins and how much (or how little) of these reduced Lp-X levels could be a result of scavenger receptor removal in particular.

cc @TuckerGoodrich
Read 3 tweets
🚨 NEW! Lean Mass Hyper-Responder Editorial🚨

👉 10 MD & PhD authors from 4 countries🌍coming together for 1st of it's kind Consensus Statement on #LMHR

👉 Published in official Journal of the National Lipid Association @LipidJournal

A thread 🧵👇… Image
2/ A bit of background to catch some of you up

Over the past 6 years a population of people has emerged who demonstrate ⬆️ LDL on a #ketogenic diet in the context of ⬇️TG +⬆️HDL

Phenotype was first observed by @realDaveFeldman and (historically) named Lean Mass Hyper-Responders Image
3/ 1 year ago, we started researching #LMHR more formally, and in this year, we've published 4 prior papers

Cohort Study
Case Report
Cholesterol drop protocol
Lipid Energy Model
Read 11 tweets
Join us tomorrow for the launch of a new #accredited #tweetorial on the primary care management of #hyperlipidemia covering the relationship between #LDL_C & major #CV events, CV risk categories, recommended LDL-C treatment goals, & oral therapeutic options for lipid-lowering
1) Welcome to a new #tweetorial on the primary care management of #hyperlipidemia. Our returning @cardiomet_CE expert author is dedicated #SoMe education advocate Kevin Fernando, FRCGP FRCP Edin, FAcadMEd MSc Diabetes @drkevinfernando
2a) This is the next instalment of @cardiomet_CE's 10-part #tweetorial foundational series on #lipid management! It is accredited for #CME/CE and intended for #physicians #physicianassociates #nurses #nursepractitioners #pharmacists.
#FOAMed @MedTweetorials #cardiotwitter
Read 45 tweets
1/ Yes, the topic of a "hyper-response" with high #LDL #Cholesterol (LDLc) on #keto has been coming up a lot this summer, particularly for #LMHRs -- and that's a good thing. More discussion and research desired!

I'll try to unpack the key differences in 3 standing hypotheses...
2/ Conventional: higher LDLc "hyper-response" (HR) mainly due to higher consumption of saturated fat (SF)

@DrNadolsky hypothesis: HR due to higher SF, but also genetics

Me: HR affected by many things, but generally more influenced by Lipid Energy Model (LEM) than SF or genetics
3/ Starting with a few key influences we all agree on...

These things likely have a significant detectable increase on LDL compared to reverse:

1) Swapping unsaturated fat with SF
2) Reducing fiber
3) Less resistance training
Read 8 tweets
1/ 🚨New N=1 Experiment: #IsItSaturatedFat🚨

Yes, I'm doing a new N=1 -- and it's going to be a biggie!

My good friend and colleague, @DrNadolsky completed his recent #MakingLMHR experiment concluding the added 2 sticks of butter as the reason for his LDL increase. Image
2/ He's already conceded he's left out all the context on aiming for #LMHR profile, the relevance of RER, and the #LEM (so no need for people to keep pinging me on the IG video). I've chatted with him privately and we'll leave it at that. 👍

3/ However -- this actually affords us a huge new opportunity.

@DrNadolsky's claim isn't just his own, it's just about everyone else's outside the low carb community.

Simply stated: high #LDL #cholesterol seen in #LMHRs is predominantly due to high consumption of saturated fat.
Read 6 tweets
1/ I want to give huge props to @DrNadolsky for doing this #MakingLMHR experiment!

Yes, I know some of my followers may be blocked -- so I'm including an image as well.

If you're interested in how this experiment came about -- read on... 🧵 Image
2/ We've had an ongoing debate on how much (or little) #saturated fat consumption is responsible for high #LDL #cholesterol levels we typically see for #LMHRs.

Whereas I (we) believe #LEM to have greater relevance overall.

Which led to the experiment👇
3/ Could @DrNadolsky emulate the #LMHR phenotype while *not* being fat adapted? (or at least, to get his #LDL #cholesterol that high?)

He consumed two sticks of butter a day to test this! 🧈🧈

Yes, the experiment went more toward my prediction, so alas, I won't be flying there.
Read 7 tweets
🚨 #LeanMassHyperResponder lowers LDL 🚨

1/ First off, this thread is long with lots of nuance.

But here’s the bottom line:

👉 I dropped my #LDL by over 400 mg/dL
👉 Previously ~500
👉 Now it is under 100

(Yes, you read that correctly)

Here’s how I did it… Image
2/ The method was quite simple:

Add in some carbs.

This shouldn’t be a news flash for anyone following our work on the Lipid Energy Model

We published on this intervention with the #LMHRpaper case series here:…
3/ I’m an example of an LMHR that eats a relatively low saturated fat diet at baseline. Even when >80% of my fat intake is MUFA/PUFA, my LDL can run >500. Thus, it’s not simply the sat fat. Even when fiber intake has been >30g with net carbs <30g, my LDL can easily run >350 Image
Read 19 tweets
1/ I'd love to take an opportunity to expand on this important topic, and if I may, suggest something important to watch for with some newly emerging data.

To @MichaelMindrum point, I too believe the #ApoB will demonstrate higher association with #ASCVD than #LDL #Cholesterol..
2/ But to be sure, ApoB can be best represented as:

(1) Non-LDL ApoB lipoproteins
- and -
(2) LDL ApoB lipoproteins

The first category is predominantly chylomicrons, VLDL, and IDL -- which associate very highly with ASCVD.
3/ You can think of category (1) as "Triglyceride Rich Lipoproteins" (TRL, aka "remnants") and category (2) as "Triglyceride Poor Lipoproteins" (TPL)

The population of #LMHRs have extremely high levels of ApoB. But this pattern is a mix of very *low* TRL and very high TPL.
Read 6 tweets
📊Polls ahead of #KetoSaltLake

Poll (1/4)
Lean Mass Hyper-responders (#LMHRs) are defined by:

+⬆️#LDL #Cholesterol at 190mg (5.17mm) or higher,
+⬆️#HDL-C 80 (2.07) or higher &
+⬇️#Triglycerides of 70 (0.79) or lower

In your opinion, cardio risk level of this profile is likely
Poll (2/4)
Many demonstrating the #LMHR phenotype (but not all) consume a diet...

High in animal protein
High in red meat
High in saturated fat

In your opinion, if we were to further stratify the #LMHR population to those with the above diet, their cardio risk level would be...
Poll (3/4)

When did you first hear of the Lean Mass Hyper-responder profile?
Read 5 tweets
9) Many risk factors modulate the propensity of LDL-C to traverse the endothelium and enter the arterial intima. See 🔓….
10) It now appears that the passage of #LDL into the #intima is not a merely passive process whereby the concentration in blood & the permeability of the endothelium determine LDL accumulation.
11) It’s #Transcytosis (an active process), through a vesicular pathway involving #caveolae, scavenger receptors (#SRB1) and activin like receptor kinase 1 (#ALK1). Hence for a given blood level of LDL-C the amount of atherosclerosis is variable.
Read 36 tweets
1) Welcome to an #accredited #tweetorial on the role of ⬆️ #LDL-C levels in the pathogenesis & pathophysiology of #ASCVD. I am Kausik Ray MD FRCP @profkausikray, Professor of Public Health & Cardiologist @imperialcollege London AND President of European Atherosclerosis Society
2) This #tweetorial, accredited for #CME/CE and intended for #physicians #physicianassociates #nurses #nursepractitioners #pharmacists is supported by an educational grant from Esperion Therapeutics. See faculty disclosures at
3) #Atherosclerosis starts in childhood, progresses in fits and spurts and presents in middle to late life in the form of major adverse cardiovascular events #MACE.
Read 4 tweets

Related hashtags

Did Thread Reader help you today?

Support us! We are indie developers!

This site is made by just two indie developers on a laptop doing marketing, support and development! Read more about the story.

Become a Premium Member ($3.00/month or $30.00/year) and get exclusive features!

Become Premium

Too expensive? Make a small donation by buying us coffee ($5) or help with server cost ($10)

Donate via Paypal Become our Patreon

Thank you for your support!