Discover and read the best of Twitter Threads about #lmhrstudy
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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...
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...
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...
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
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 ✅
Epi: When randomly grabbing a large population of Americans, we find those who generally weigh more generally have higher BP ✅
3/ Rx -- interventions that generally reduce weight, also generally reduce BP ✅
And lastly, 🧬 -- most genes that associate with lower weight will generally have lower BP ✅
Now obviously we have more advanced tools these days than weight scales and BP cuffs...
And lastly, 🧬 -- most genes that associate with lower weight will generally have lower BP ✅
Now obviously we have more advanced tools these days than weight scales and BP cuffs...
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...
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.
Function vs dysfunction (or successful regulation vs unsuccessful regulation) having an upstream impact on lipid levels should be strongly considered.
3/4 But currently, it is assumed these influences are either irrelevant or the impact known -- at least to the extent that it is commonly assumed high LDL is pathogenic in every context (hence, little need to prospectively study metabolically healthy populations with high LDL)
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.)
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
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
Answer is: Both are possible.
Now that said, it is way more common for people to only consider (1) and not (2)
I regularly do my best to get folks to consider (2) as well -- and have been doing so for several years now.
Now that said, it is way more common for people to only consider (1) and not (2)
I regularly do my best to get folks to consider (2) as well -- and have been doing so for several years now.
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
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..
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..
3/ In other words, to confirm/disconfirm the contribution of LDL-P independently to atherosclerosis, we'd want to look to populations without a likely form of disorder or dysfunction (be it genetic or acquired).
Obviously, I think LMHRs provide a unique opportunity on this...
Obviously, I think LMHRs provide a unique opportunity on this...
📍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…
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.
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.
-- Until now.
🧵 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
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.
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.
And to my surprise, this system is already very familiar to me as a software engineer given it is a distributed object network.
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.
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...
👆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...
3/ As an analogy - if someone were to make a video that outlined:
"Myth: LDL-C < 70 will keep you from ever having a heart attack" -- and then knocked it down, it would rightly be considered a strawman position of proponents more knowledgeable and representative of the whole.
"Myth: LDL-C < 70 will keep you from ever having a heart attack" -- and then knocked it down, it would rightly be considered a strawman position of proponents more knowledgeable and representative of the whole.
🧵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
🔖 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
and
- #Triglycerides of 70 mg or lower
Which is actually common for lean, very folks on #lowcarb/#keto folks. doi.org/10.1093/cdn/nz…
- #LDL #Cholesterol of 200 or higher
- #HDL #Cholesterol of 80 mg or higher
and
- #Triglycerides of 70 mg or lower
Which is actually common for lean, very folks on #lowcarb/#keto folks. doi.org/10.1093/cdn/nz…
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) doi.org/10.3389/fendo.…
(⚠️Please note this is a single case report and should be considered anecdotal, ofc) doi.org/10.3389/fendo.…
🧵 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
nature.com/articles/s4385…
High adiposity associates with:
- ⬆️ #ApoB & #LDL-C
- ⬆️ #triglycerides
- ⬆️ levels of all fatty acids
How does this relate to #LEM? Let's unpack... /1
nature.com/articles/s4385…
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...
🙌 Okay, it's Nov 1 -- I'm back! 🙌
A catch up 🧵
✅ Social Media Hiatus was nice (I recommend)
✅ #LMHRstudy near recruitment goal
✅ 3 new research endeavors in works!
✅ Possible film project next year
Read on for the unpacking... /1
A catch up 🧵
✅ Social Media Hiatus was nice (I recommend)
✅ #LMHRstudy near recruitment goal
✅ 3 new research endeavors in works!
✅ Possible film project next year
Read on for the unpacking... /1
2/ The Social Media Hiatus...
I was originally shooting for a few weeks away, but it stretched into two months.
Honestly, I have to really credit @MichaelMindrum for inspiring me to really commit to this. It was easier than I assumed given the ongoing research efforts.
I was originally shooting for a few weeks away, but it stretched into two months.
Honestly, I have to really credit @MichaelMindrum for inspiring me to really commit to this. It was easier than I assumed given the ongoing research efforts.
3/ The #LMHRstudy is nearing recruitment completion!
That said - we still have some participants to go to put us over the top!
So again, *please* visit LMHRstudy.com to see if you or someone you know is eligible for the study.
That said - we still have some participants to go to put us over the top!
So again, *please* visit LMHRstudy.com to see if you or someone you know is eligible for the study.
1/ Two things..🧵
1️⃣ We need to complete registration!
You / someone you know:
👉Had LDL 160 or under before keto
👉LDL increased to 190 or more on keto
👉HDL 60 or more
👉Triglycerides 80 or below
👉2 or more years on keto
Go to LMHRstudy.com & see if u/they qualify
1️⃣ We need to complete registration!
You / someone you know:
👉Had LDL 160 or under before keto
👉LDL increased to 190 or more on keto
👉HDL 60 or more
👉Triglycerides 80 or below
👉2 or more years on keto
Go to LMHRstudy.com & see if u/they qualify
2/ Participants get:
🧬 Genetic testing
🩸Wide spectrum bloodwork
🫀 Advanced #CCTA scans
🚨🚨🚨YOU can help us get our target of 100 participants. Please do!
👉👉👉LMHRstudy.com
🧬 Genetic testing
🩸Wide spectrum bloodwork
🫀 Advanced #CCTA scans
🚨🚨🚨YOU can help us get our target of 100 participants. Please do!
👉👉👉LMHRstudy.com
3/ Please consider:
✅ Retweeting this tweet thread
✅ Sharing this thread or its contents in #Keto and #Carnivore #Facebook groups
✅ Sharing on #Instagram
✅ ... and, of course, you may already know people personally who fit this profile -- please reach out to them!
✅ Retweeting this tweet thread
✅ Sharing this thread or its contents in #Keto and #Carnivore #Facebook groups
✅ Sharing on #Instagram
✅ ... and, of course, you may already know people personally who fit this profile -- please reach out to them!
1/ Medical Case
👉53y M, #LMHR w LDL 394, HDL 111, TG 40 for 4y on #keto diet
👉BMI 21.6
👉Prior to keto LDL was 98 mg/dl
👉CCTA shows no plaque, CAD-RADS = 0
👉Parents both lived to >80y w/o cardiac events Family hx of neurodegenerative diseases, including 2x of 👉Parkinson’s
👉53y M, #LMHR w LDL 394, HDL 111, TG 40 for 4y on #keto diet
👉BMI 21.6
👉Prior to keto LDL was 98 mg/dl
👉CCTA shows no plaque, CAD-RADS = 0
👉Parents both lived to >80y w/o cardiac events Family hx of neurodegenerative diseases, including 2x of 👉Parkinson’s
2/ Patient doesn’t want to abandon diet because it makes them “feel my best.”
You’ll notice, there’s no poll associated with this case. Medicine isn’t a democracy and not all medical opinions on Twitter are equally informed. However, I wanted to share this case ...
You’ll notice, there’s no poll associated with this case. Medicine isn’t a democracy and not all medical opinions on Twitter are equally informed. However, I wanted to share this case ...
3/ ...as a juxtaposition to the extremism I’m seeing ON BOTH SIDES: LDL/ApoB is benign v. lower is better (period). Neither is the case. A bit of nuance…
With respect to “LDL/ApoB is benign,” all things being equal, the data don’t support this view. It’s a risk factor...
With respect to “LDL/ApoB is benign,” all things being equal, the data don’t support this view. It’s a risk factor...
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..
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.
(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.
The population of #LMHRs have extremely high levels of ApoB. But this pattern is a mix of very *low* TRL and very high TPL.
1/ Two weeks ago we released our paper on the #LipidEnergyModel (#LEM) along with our video abstract for it. I'm pleased to say it has led to many great connections and expanded discussion.
I'm going to recap on a lot of these in this thread. 🧵 ...
I'm going to recap on a lot of these in this thread. 🧵 ...
2/ First and foremost, thanks to everyone for their extraordinary support in retweeting our announcement, sharing our paper, and letting researchers know of this model.
3/ As we state many times (including within the video abstract), this model doesn't describe all possible influences on cholesterol levels. For example, other things can impact LDL-C such as M/PUFA-to-saturated fat composition, fiber, genetics, medication, etc.
1/ I had the debate between @NutritionMadeS3 & @ifixhearts on in the background while working. Really enjoyed it
First and foremost, both gentlemen were very cordial and professional. No ridicule, name-calling, or any other emotive personal attacks, etc..
First and foremost, both gentlemen were very cordial and professional. No ridicule, name-calling, or any other emotive personal attacks, etc..
2/ Which -- as you all know -- I'm a strong advocate for.
@NutritionMadeS3 represented the pro-LDL/ApoB lowering position well. (Note I've linked/tweeted his videos several times)
@ifixhearts brought forward the importance of metabolic health, and fault in it getting ignored...
@NutritionMadeS3 represented the pro-LDL/ApoB lowering position well. (Note I've linked/tweeted his videos several times)
@ifixhearts brought forward the importance of metabolic health, and fault in it getting ignored...
3/ One important difference I was especially interested in-> do we have enough data in hand to feel confident high LDL/ApoB is a strong independent risk factor regardless of metabolic health. Generally @NutritionMadeS3 appears to favor "yes", @ifixhearts favors "unsure" to "no"
1/ Always honored to have your added opinions, @Lpa_Doc and I'll again mention I'm a tremendous fan of your work (and the #OxPL assay, btw)
The #LMHR phenotype is potentially providing a new window of investigation into lipid metabolism, but its high LDL risk level is unclear...
The #LMHR phenotype is potentially providing a new window of investigation into lipid metabolism, but its high LDL risk level is unclear...
2/ ... Hence the importance of the #LMHRstudy (still recruiting, btw -- see LMHRstudy.com for details)
In the mean time, we regularly and often emphasize everyone should work with their doctor and understand the guidelines recommend against high cholesterol...
In the mean time, we regularly and often emphasize everyone should work with their doctor and understand the guidelines recommend against high cholesterol...
3/ ... There are many like this pt who are in the unusual position of having a severe medical condition that appears to be uniquely resolved through a very carb restricted diet.
With respect, the patient didn't immediately refuse any form of treatment...
With respect, the patient didn't immediately refuse any form of treatment...
1/ #Study #MegaThread
A new study dropped with a trove of data I've long waited for around #CCTA/#CAC scans and #LDL #Cholesterol
✅ >23k studied (!)
✅ Largest sample of CCTA w/ ≥190 #LDL to date (!)
✅ Very uniform study population
Let's unpack...
jamanetwork.com/journals/jaman…
A new study dropped with a trove of data I've long waited for around #CCTA/#CAC scans and #LDL #Cholesterol
✅ >23k studied (!)
✅ Largest sample of CCTA w/ ≥190 #LDL to date (!)
✅ Very uniform study population
Let's unpack...
jamanetwork.com/journals/jaman…
2/ First, be sure to check out this short thread from the lead author, @MaBMortensen.
2 quick notes:
a) While there'll be lots of data appreciated by LDL skepticism, @MaBMortensen maintains LDL-C is still "an important causal RF"
b) Usual epi caveats, etc
2 quick notes:
a) While there'll be lots of data appreciated by LDL skepticism, @MaBMortensen maintains LDL-C is still "an important causal RF"
b) Usual epi caveats, etc
3/ Okay, so if you've followed me a while, you know just how incredibly thankful I am of studies that seek to avoid common risks of selection bias (Even if entirely unintended).
This study had the distinct advantage of categorically scooping its population directly...
This study had the distinct advantage of categorically scooping its population directly...
1/ A very busy time
But in this late moment of calm before the weekend, I'm finding myself truly humbled that our #LMHRpaper is finalized and has crossing so many interested eyes.
I hope many will agree with us this phenomenon is well worth researching.
cholesterolcode.com/our-paper-on-l…
But in this late moment of calm before the weekend, I'm finding myself truly humbled that our #LMHRpaper is finalized and has crossing so many interested eyes.
I hope many will agree with us this phenomenon is well worth researching.
cholesterolcode.com/our-paper-on-l…
2/ Via @nicknorwitz: "... this paper has stimulated vigorous discussion, risen to the top of its journal for all time reads, and is among the top 15 trending papers across all American Society of Nutrition associated journals for the year 2021." nutrition.org/15-trending-nu…
3/ There's quite a bit more work in the pipeline from the many great collaborators I have the honor to be working with. We're passionately working on a #LipidEnergyModel paper, the #LMHRstudy (currently underway), and a couple other projects I can't announce just yet...
1/ If you want to hear a great discussion on the #LMHRstudy from my colleague,@DrNadolsky (who is most definitely pro-#LDL #Cholesterol lowering), I highly recommend this podcast that just dropped via @Plant_proof.
I'll add just a few quick thoughts...
I'll add just a few quick thoughts...
2/ Firstly, this may be the most I've heard myself talked about in a podcast I wasn't in (😂 weird, but understandable given the context).
But while certainly critical in many respects, I felt both @DrNadolsky and @Plant_proof provided a lot of good context...
But while certainly critical in many respects, I felt both @DrNadolsky and @Plant_proof provided a lot of good context...
3/ @DrNadolsky bring up my oft-repeated phrase, "cautiously optimistic" [in the context of higher LDL/ApoB as a seemingly resulting from metabolic fat-adaption]
Worth repeating that mine is a hypothesis and should be treated as such, hence the "cautious" part of the phrase...
Worth repeating that mine is a hypothesis and should be treated as such, hence the "cautious" part of the phrase...
1/ This is especially important timing.
As many of you know, we're conducting a study on #LMHRs (link later in thread) who not only have extremely high #LDL #Cholesterol, but many (likely most) have diets quite contrary to this advice by the @American_Heart.
Let's unpack...
As many of you know, we're conducting a study on #LMHRs (link later in thread) who not only have extremely high #LDL #Cholesterol, but many (likely most) have diets quite contrary to this advice by the @American_Heart.
Let's unpack...
2/ First, and most importantly, we do not know what the outcome of this prospective study is. So while I'll be outlining commonalities we observe with #LMHRs, this isn't an explicit endorsement of the diet nor any altered lipid levels as a result.
With that said...
With that said...
3/ We have a lot of data between our standing survey, submissions to CholesterolCode.com, and CC and LMHR Facebook groups (7.7k and 7.5k members, respectively).
Diets are often:
1) Low to no fruits & veg
2) Low to no grains
3) High animal protein
4) Low in plant oils
Diets are often:
1) Low to no fruits & veg
2) Low to no grains
3) High animal protein
4) Low in plant oils
1/ Wow -- it's been quite a week! I announced the #LMHRstudy six days ago. And in case you missed it -- visit here for more details:
CitizenScienceFoundation.org/study
I'm going to provide some updates and answers to frequent questions of the last several days...
CitizenScienceFoundation.org/study
I'm going to provide some updates and answers to frequent questions of the last several days...
2/ "Dave, can you get me in the study?"
No! You have to contact Lundquist directly through the proper channels and they will decide based on the study design whether you qualify as prescribed by existing eligibility criteria we all determined in advance.
No! You have to contact Lundquist directly through the proper channels and they will decide based on the study design whether you qualify as prescribed by existing eligibility criteria we all determined in advance.
3/ While myself, @DrNadolsky and @DrRagnar developed the protocol in collaboration Lundquist, we in no way can (or should) influence any decision making regarding individual considerations -- and that's a good thing. We want this study as fair and objective as possible.
1/6 I'd like to both retweet and add on to @NutritionMadeS3's point here...
Again, and with emphasis, my position is one of cautious optimism. That's an explicit acknowledgement of uncertainty, even if I have a leaning toward the positive in this context...
Again, and with emphasis, my position is one of cautious optimism. That's an explicit acknowledgement of uncertainty, even if I have a leaning toward the positive in this context...
2/6 I discuss this at length in 13-15 of my pinned tweet
Hence the importance of #LMHRstudy
I'd hope this were self-evident, but if I were completely certain high LDL + high HDL + low TG = low risk in fat-adapted context, there'd be no effort for a study
Hence the importance of #LMHRstudy
I'd hope this were self-evident, but if I were completely certain high LDL + high HDL + low TG = low risk in fat-adapted context, there'd be no effort for a study
3/6 I've chatted with @NutritionMadeS3 and others on evidence I consider very compelling regarding the connection of health and illness for lipid metabolism and their impact on lipid profiles. But I likewise stress we'd be better served with prospective data in this context
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...
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...
... 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...
