Discover and read the best of Twitter Threads about #ldl

Most recents (24)

1/ Posting this hypothesis for posterity:

I now suspect #PlantBasedLowCarb (PBLC) isn't as low carb as originally thought.

Before getting started in this thread, I should emphasize I wouldn't consider this a good or bad thing in and of itself, but it is of interest, ofc... Image
2/ Moreover, I've regularly pointed to people following my work who are both (1) very interested in a low carb diet, but (2) would prefer to keep their #LDL low to consider PBLC as a "third option", as I commonly see it associates with this outcome.

Now to my hypothesis...
3/ PBLC generally has two major features separating it from "typical" #keto/#lchf:

1) More fat sourced from mono and polyunsaturated fatty acids (M/PUFA) instead of saturated fatty acids (SFA)

2) A lot more soluble and insoluble fiber via plants
Read 11 tweets
1/ Very cool experiment and thread by @ScepticalDoctor who did a more #PlantBasedKeto and saw low #LDL #Cholesterol given high MUFA/PUFA relative to sat fat, along with high fiber (which supports my prior thread)

If looking to keep LDL low, this might be worth considering...
2/ As per my various tweets before this one on the topic, and not to beat a dead horse, I feel it is too often "low carb vs plant based" is often assumed the latter *must* be high carb -- thus, "low carb, animal-based vs high carb, plant-based"

... This is a false dichotomy...
3/ There are definitely some of us who are, as I like to say, "cautiously optimistic" with regard to higher LDL as appears to be resulting from metabolic fat adaptation in the context of higher sat fat, lower MUFA/PUFA and low to no fiber. But this risk degree is uncertain...
Read 6 tweets
1/ Interesting thread via @ck_eternity_

I'll add some thoughts in my own thread to follow, but consider reading his entirely first.

As always, this is in the spirit of discourse. Love keeping it respectful and productive on such challenging topic. :)
2/ Before getting started, note the coming #LMHRstudy will effectively be tackling much of these common considerations quite directly as we study #LMHRs who have considerably high #LDL from being fat-adapted with otherwise #CVD healthy metrics (See
3/ While not commonly known, another major carrier protein for chol is Albumin. It's typically considered in light of transporting NEFAs, but its binding sites can (and are) applied to many other lipids, including cholesterol.…
Read 13 tweets
1/ This new MR study by @mendel_random, @mvholmes, et al makes use of UK Biobank data and determines #ApoB increases risk of #AllCauseMortality, and even #T2Diabetes

This is actually relevant timing as we are rapidly approaching the #LMHRstudy.…
2/ If you didn't already know, "Lean Mass Hyper-responders" (#LMHRs) would be considered hypercholesterolemic, with this resulting from being very low carb (typically #keto), and are often lean and/or athletic.

(You can read more on this phenotype at
3/ Setting aside why this population exhibits this (see #LipidEnergyModel for more), the most important question is whether they are at risk.

This MR study builds on the existing conventional expectation that they are, and no less in a dose-dependent manner...
Read 6 tweets

Enfermedades del #Colesterol

¿Por qué el "Colesterol NO HDL" es mejor predictor de #riesgo #cardiovascular que la medición de lipoproteínas de manera aislada?

#AbroHilo 👇🏼
🔺Generalmente, cuando pedimos un perfil lipídico en sangre, básico (HDL, LDL, Triglicéridos), obtenemos el resultado de la cantidad de #lipoproteínas circulantes, pero no sabemos cómo están compuestas específicamente.

🔺De acuerdo a cómo estén compuestas, es decir, qué partículas y qué tamaño tengan, tendrán determinado comportamiento.

Read 10 tweets
#Dislipemias y enfermedades del #Colesterol. Parte I

¿De qué se tratan?

¿Cómo se interpreta un perfil lipídico en un laboratorio?

¿Qué son las #LDL pequeñas y densas y por qué son las que más interesan?

¿Qué es el Colesterol No HDL?

#AbroHilo Image
➡️La #enfermedad #cardiovascular es la principal causa de muerte en la población general. Está asociada a decenas de patologías, entre ellas, #diabetes, #obesidad, #tabaquismo, enfermedades autoinmunes, etc; y la que veremos hoy: las dislipemias o enfermedades del colesterol.
➡️Las #Dislipemias son enfermedades causadas por alguna alteración en el metabolismo de los lípidos (colesterol y triglicéridos).
Pueden ser primarias-de causa genética, adquiridas-por determinados hábitos como 🍔🚬 y secundarias-asociadas a otras enfermedades.

#Sigue ⬇️ Image
Read 31 tweets
1/ Still one of my favorite studies in relation to the #LipidEnergyModel. One might wonder what happens to animals who become fat adapted due to fasting for a long period.

Obvious example: Hibernation

#LDL #Cholesterol goes up... does #Atherosclerosis?
2/ They were comparing bears in captivity and the wild. And in both, lipid levels during hibernation are "considerably higher than what is normally found in humans"
3/ In spite of the high lipid levels alongside other risk factors, they found no signs of atherosclerosis in brown bears.
Read 5 tweets
2/ I love that Alan Flanagan kicked off with distinction question re bio markers.

“System Biomarkers in the causal pathway. Systemic biomarkers that can report on the overall picture”
“Biomarkers of disease progression”
3/ “... It seems to be in the wider conversation a lot of these are often conflated to a degree. Or there is misplaced emphasis placed on a particular marker...”

I couldn’t possibly agree with this more!
Read 12 tweets
1/ For a very layperson-friendly video on conventional view of #LDL / #HDL #Cholesterol, and #ApoB, I highly recommend this one from @NutritionMadeS3

It's very visual and IMO fairly true to the more specific position of mainstream lipidology...
2/ Love his opening: "why is this topic so confusing? well, for starters scientists are horrible at coming up with names...there's LDL...and LDL cholesterol and they're different things....but a lot of people call them both LDL....and then there's HDL, VLDL..." (trails off)
3/ He's 100% right. It's why it's so hard to convert this for the lay audience. Lipidology could use a terminology upgrade.

For example, how did "Chylomicrons" manage to get a special exception to the "-DL" acronym party? (Only fellow lipophiles will get that joke... 😐)
Read 7 tweets
1/ Okay, I've been getting lots of pings regarding @DBelardoMD appearing on @RealDoctorMike, particularly given discussion earlier in the video with regard to LDL-C and CVD.

I'll do a reaction thread for now, but I'd like to keep it respectful, ofc...
2/ *First, whether ur a @DBelardoMD fan or not, I have to emphasize I respect anyone willing to move against the grain of their community for where they feel the evidence takes them. While unrelated to lipids, she's endured a lot of unpleasantness for a principled re CVD reversal
3/ 2:08 @DBelardoMD: "Nowadays you want to get your LDL cholesterol as low as possible for cardiovascular risk prevention. So, primary prevention versus also secondary prevention."

->Of course, neither this or statements like these are controversial by conventional med standards
Read 12 tweets
1/ Great new thread by the incomparable, @Lpa_Doc -- covering a number of my favorite topics.

Read his thread and return for my added thoughts...
2/ Vilhjalmur Stefansson is a well discussed explorer among the #LowCarb and (of course) #Carnivore communities.

But even more interestingly, he may have been the first #LeanMassHyperResponder of record*

(* Kinda -- as Sam notes, we didn't advanced lipid panels then)
Read 6 tweets
1/ Long running thought exp'nt:

If a drug did many of the same things with one's lipid profile as a #LowCarb diet, particularly decreasing triglycerides while increasing #LDL #Cholesterol:

1) Would it reduce ASCVD risk?
2) And if so, would it be more acceptable than #LowCarb?
2/ If you haven't heard, SGLT2 Inhibitors have recently emerged and have been gaining a lot of popularity. Data thus far shows they typically:

1) Decrease TG levels
2) Increase #LDL #Cholesterol levels
... yet...
3) Reduce risk for cardiovascular disease
3/ Naturally, that has the attention for those of us interested in how triglyceride trafficking and turnover could be relevant to #LDL increasing for what may turn out to be non-pathogenic reasons (kinda my focus ;) )

But wait -- it get's better...
Read 7 tweets
1/ 😁Thread -- About Me -- 5 year update😁

It's been a busy 24 hours since @joerogan's podcast dropped where @CarnivoreMD discussed our work (mega thx, Paul!). There's been a surge of new followers, so I figured it was high time to do an update for those just tuning in...
2/ I'm a senior software engineer and systems architect having developed a variety of platforms over my career.

Five years ago next month I saw my cholesterol levels skyrocket on a ketogenic diet and was extremely interested as to the mechanisms behind it...
3/ I began learning everything I could about Lipidology and the system that moves #cholesterol around in our body. To my surprise, it has many structural things in common with a network (a very advanced one, mind you), but soon I was manipulating my own lipid levels easily.
Read 20 tweets
1/ Thread -- Let's Get the Data

Many medical professionals (like my good friend and colleague, @DrNadolsky) feel strongly that #LowCarb-ers may be acting very recklessly by allowing their #LDL #Cholesterol to be much higher than the guidelines allow.…
2/ And this may well be the case.

Certainly if "diet induced" high LDL is the equivalent to genetically high LDL, such as those with #FamilialHypercholesterolemia (FH), then there should be likewise rapidly progressing #atherosclerosis.
3/ "The sine qua non of FH is severe elevation of total and LDL cholesterol levels."…

Often heterozygous FH is considered where LDL is 190 to 500 mg/dL, with homozygous being above 500.
Read 14 tweets
1/ #ListeningThread

My interview on @IanCramer's podcast is up.

It's been many months since we recorded, so I may give it a re-listen...
2/ Ha! When @IanCramer has me give a little background on how I got into this space, I give one of the clumsier setups I think I've given in an interview. Not the best intro for the energy model either- but you can always check out the general poster here:
3/ @IanCramer asks me for a "50,000 foot view of my thesis" where I walk it into the "high LDL where metabolically induced" context.

This leads me into introduction of how #LDL particles relate to the immune response as illustrated by @siobhan_huggins…
Read 8 tweets
Got a high #LDL #cholesterol test result while on #keto? Likely this is a false alarm, but it can have far reaching consequences. Your doctor might put you on statins to lower your LDL or you stop Keto. Often the LDL value is calculated and this is problematic when on Keto. 1/8
Most labs calculate your LDL with the The Friedewald because measuring the LDL level is more expensive and bit complicated. The calculation is as follows;
LDL chol. = total chol. – HDL chol. – (triglycerides/5). 2/8
It is well know that this method doesn't work well with high triglycerides (TG) values. In those cases the lab measures the LDL value instead. Lesser known is that the same applies with low TG values of <100mg/dl (1.13 mmol/L). 3/8
Read 9 tweets
1/ Retweeting for balance from my good friend and colleague, @DrNadolsky

To be sure, I agree large LDL particles can be participants in atherogenesis.

The real question is whether they are independently initiating and/or accelerating atherosclerosis (regardless of context).
2/ Existing medical consensus is that yes, regardless of context, more LDL=more risk of CVD, full stop.

Myself, I believe context does indeed matter. Which is why I suspect we haven’t yet gotten a study to meet the #LCCholesterolChallenge…
3/ In short, I think the context of why we get particular lipid patterns (such as atherogenic dyslipidemia) helps to expose the underlying root cause of atherogenesis.

I often refer to this as “lipid profile centric” thinking vs “lipoprotein centric” thinking.
Read 4 tweets
1/ So the experiment I'm considering is a crossover (possibly even dbl x-over) where I consume a baseline diet throughout, save the intervention of either (1) high SFA food such as butter or heavy cream vs (2) extra virgin olive oil (EVOO). 1 and 2 matched for calories.
2/ I speculate my Total and #LDL #Cholesterol will decrease on the EVOO compared to the SFA-centric intervention.

But I'll also be getting other metrics of interest such as free fatty acids, Lp-PLA2, as well inflammatory markers like hsCRP, Ferritin, etc.
3/ Of special interest will be my getting oxLDL throughout and am curious if we'll see a difference in proportionality.

Will EVOO be higher, lower, or the same in relative proportion to LDL-P?

Here's a poll in case you want to venture a guess yourself...
Read 4 tweets
1/ My presentation to @stanford on the Lipid Energy Model is now up at my channel.

It was a great honor to be invited and discuss my research, experiments, and this hypothesis in depth.

Lots of discussion on #LDL #HDL #Cholesterol #ApoB and #LipidTriad
2/ For many of you who have followed my work for a while, this will feel like review. But this presentation challenged me to tie everything together as best I could for a non-#keto/#lchf audience at a university level. Given the feedback /retention, it appears to have gone well..
3/ Of course, there's quite a lot that it *not* covered, and indeed I wanted to squeeze a bit more into it. Sometimes I wish I could summarize the energy delivery throughput and cross my fingers everyone at a certain level will get it. But that's been the biggest challenge...
Read 6 tweets
1/ Live Read Through Thread

1st... a setup:

A while ago I guested on @NutritionDanny's podcast #SigmaNutritionRadio. Alan Flanagan and I discussed #Lipids, #LDL #Cholesterol, #Atherosclerosis, etc. If you haven't already listened, I highly recommend it
2/ Today @NutritionDanny let me know they have an article out rebutting my points found here:

As always, I encourage you to read their article with an open mind. Then feel free to come back here for my first impressions.

Let's get started...
3/ Oh -- the beginning of the article includes a tweet from a #ListenThread I did when the podcast was dropped. That can be found here:
Read 28 tweets
1/ This study is extremely fascinating, but also not too surprising. Lipids/Lps drop during infection of CV.

#LDL #cholesterol

Low Serum Cholesterol Level Among Patients with COVID-19 Infection in Wenzhou, China…
2/ "Findings The absolute value of white blood cells, neutrophils and lymphocytes were
lower than healthy controls ( P <0.05), more significantly, the patients had sharply
decreased total cholesterol (TC), HDL-cholesterol and LDL-cholesterol levels..."
3/ Results
1. Serum lipid levels generally decreased at the initial stage of infection
2. More significant decline in cholesterol level in primary cases
3. The changes of serum lipid are independent of gender and age
4. The serum lipid changes in a critically infection case
Read 8 tweets
1/ We’re wrapping up a nine week, around the world filming schedule for #TheCCDoc, where we chatted with @lansberg, @DrAseemMalhotra, @bschermd, @KenSikaris, @eatmostlyfatali, @DrPaulMason, and @zoeharcombe to name just a few of the 36 interviews so far.…
2/ We’re now turning our focus to the US where our first stop will be #LowCarbDenver #LCD2020.

If you’re attending and a medical professional with insights on #cholesterol, #HeartDisease, and/or have patients seeing a rise in their #LDL, register here:
3/ Importantly, we’re looking to get a wide spectrum of opinion. Whether you are pro LDL-lowering, a skeptic, or anywhere in between, we want to hear from you.

This documentary needs to have input from each side of this important topic for the benefit of the viewers.
Read 4 tweets
1/ #ListenThread -

My guest appearance on #SigmaNutritionRadio just dropped where I have a very friendly #debate with @NutritionDanny and Alan Flanagan on #LDL #Cholesterol, #ApoB, #Atherosclerosis, #AllCauseMortality & much, much more!
2/ I did this podcast semi-sleep deprived and between interviews for #TheCCDoc. But I know my main hopes going in were to emphasize:

(1) Why I favor the "Lipid profile-centric" model over the "Lipoprotein-centric" model.
(2) How this is relevant to "the triad" ⬆️LDL⬆️HDL⬇️TG

(3) Why this triad is of particular interest to all of us as it relates to not just cardiovascular disease, but in particular -- all cause mortality (ACM)

I honestly couldn't remember how well I did in getting these core points across, thus relistening now...
Read 64 tweets

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