Nutrition Made Simple! - 2023-12-11
Is it safe to have high LDL as long as it's large and "fluffy"? Is LDL size a key determinant of risk? Subscribe for more free nutrition and health tips: https://bit.ly/2toMJ9u Connect with me: Facebook: https://www.facebook.com/DrGilCarvalho/ Twitter: https://twitter.com/NutritionMadeS3 Animations: Even Topland @toplandmedia References: 1-https://jamanetwork.com/journals/jama/article-abstract/374290 2-https://pubmed.ncbi.nlm.nih.gov/15296705/ 3-https://www.ahajournals.org/doi/epdf/10.1161/CIRCULATIONAHA.108.819359 4-https://europepmc.org/article/med/10499189 5-https://www.ahajournals.org/doi/10.1161/CIRCULATIONAHA.111.073684 6-https://academic.oup.com/jcem/article/88/10/4525/2845681 7-https://www.ahajournals.org/doi/10.1161/CIRCULATIONAHA.105.565135 8-https://www.sciencedirect.com/science/article/pii/S0021915006002590 9-https://www.lipidjournal.com/article/S1933-2874(21)00248-8/fulltext Disclaimer: The contents of this video are for informational purposes only and are not intended to be medical advice, diagnosis, or treatment, nor to replace medical care. The information presented herein is accurate and conforms to the available scientific evidence to the best of the author's knowledge as of the time of posting. Always seek the advice of your physician or other qualified health provider with any questions regarding any medical condition. Never disregard professional medical advice or delay seeking it because of information contained in Nutrition Made Simple!. #NutritionMadeSimple #GilCarvalho 0:00 Intro 1:40 Small LDL is associated with risk 3:48 LDL size vs number 7:09 ApoB, lipoproteins and risk 9:16 Eliminating confounders 11:22 Genetic lessons 14:25 Small LDL keeps bad company 15:25 Summary & Takeaways
7:32 over 90% of ApoB particles are LDL [however in a previous video, the same expert said that in most people LDL-C doesn't track well with ApoB, unless your LDL-C is very high or very low, so i'm left a little confused as to which one i should test, also considering that idk the ideal ApoB ranges.].
7:41 here are the more atherogenic ApoB particles (the bigger ones are less atherogenic).
11:08 small and large LDL particles are equally atherogenic [this seems to contradict what i wrote in the line above].
11:20 the LDL in familial hypercholesterolemia is large [and not oxLDL, i might add], yet the people with such condition have early events and cardiovascular disease.
11:59 we used to think that small was worse than large.
12:31 large and small are equally associated with heart attack, stroke, and events.
Regarding your first question, I could not find when he said the LDL-C doesn't track well with ApoB for most people, can you give me the timestamp from the other video? The only reference I remember and could find was him explaining that if you have a high amount of Triglyceride Rich Remnants, that this was the cause for the discrepancy between ApoB and LDL-C as it relates to risk, but this was not typical.
LDL and LDL-c are two different things. LDL is the number of LDL particles,LDL-c is the amount of cholesterol inside these LDL particles. If you want the most accurate one-measure apoB and the lab usually has the intervals for that. Quick google search says less than 100 mg/dL( some other sources say 40-120 mg/dL) is good. The lower the better.
@@nichtsistkostenlos6565 the video is titled "What causes heart disease? | Dr. William Cromwell" and the part on the discordance between LDL-C and ApoB starts at 10:05.
@@nichtsistkostenlos6565 i have found the part of the video you're looking for but for some reason my comment reply isn't publicly visible :( oh, this one reply is visible! let me edit it real quick: the information you're looking for starts at 10:05 (in that other video by Gil with the same expert).
LDL-C refers to the cholesterol content carried by the apolipoproteins, whereas LDL-P refers to the number of LDL particles.
In most people, apob tracks well with ldl-p
Covering every excuse from their book! Good job!
Chemical engineer here. Another important point is that large particles can carry more relative cholesterol, though he doesn’t talk about it in this video. Let’s say we have two different size trucks (particles). Truck A can carry 100 cholesterol units, while Truck B can only carry 1 cholesterol unit. Therefore, for two given mixtures, A/B, who both have the same total cholesterol, mixture A will have only 1 truck relative to mixture B, who will have 100.
In other words, the total amount of LDL-C is much less important than the total number of trucks. LDL-C is only important to the degree that it increases total particle number. Bottom line is that we have been measuring the wrong variable all along.
Important to point out that the reason that particle number is important is because it’s the number of collisions with the wall that really matters.
I am super early!
Love from an other (soon to be) dietitian from Greece!
Keep up the great work mate for both the public and us scientists all around the world!
Thank you for covering this important and misunderstood topic, Gil.
Dr Cromwell is amazing at breaking down this complex topic! I'm not a clinician nor a statistician but even I could follow his nuanced explanation.
So many people are still attached to the belief that you don't have to be concerned with LDL as long as they are large particles. It's definitely gonna take some time to change this common misconception.
Most people have no idea that there is difference type of LDL particles. 😂
What do you mean by 'in absence of genetic perturbations'?
How many people have this?
Gill and Cromwell were not talking about genetic outliers, but the association between apoB, large, small LDL particles and ASCVD in the entire population, not just a subgroup.
Small dense (damaged) ldls are typically damaged via glycation and/or oxidation. It cannot bind to receptor so stays in body with nowhere to go. Typically seen with high triglycerides.
Sdldl is a Hallmark of metabolic syndrome
Do you have any references for this? Thank you!@@adriansrfr
@@Godfryd23this is true!
One of the best clear and concise summaries of particle size, particle number, and interactions as it relates to CVD risk. Thanks.
A clear concise explanation of a very complex topic. Reinforces the importance of lowering Ldl and Apo B.
That was very good, thank you. Although baffling not even a mention of Lp(a), even when discussing the most concerning ApoB containing particles. Lp(a) certainly should have been included.
Definitely the most concise and understandable explanation I’ve heard of why risk tracks with number versus size, as well as how the confusion over particle size got started in the first place.
Fantastic explanation of a very confusing subject. Sure wish he would have also addressed the added risk of the dreaded Lp(a) particles. Maybe a great follow up topic?
Pairing with a creator with a very good ability to explain complex statistical topics (like 3Blue1Brown or Stand-up Maths, for example) to explain the suppressor variable effect would be fantastic. There wasn't enough time in this conversation to dive into it but I think presenting the exact way that that it affected the particle size analysis would be fascinating and help people really come to a personal and complete understanding of this subject. Some might wave this explanation off as that the extra analysis isn't honest and just serves to let the researchers arrive at the conclusion they wanted to arrive at. That's not the case, but bringing the viewers to a place where they can really internalize why that extra analysis is necessary would really solidify the point and the message. Also, math is awesome!
Excellent presentation. My doctor is one who still believes large particles are less concerning than small. I've been reading several studies on cholesterol, but most seem to concentrate on cardiovascular outcomes. I would love to have you address overall mortality in relation to cholesterol levels.
Its not the size that matters, its how you use it. Thanks doc for the reassurance. 😂
You're a breath of fresh air..
My mum just sent me an article dr. William davis (he claimed to be a cardiologist) saying how bad grains are.. and how eating pork and bacon is not what causes cvd..
And how small size ldl is the real problem..
I knew I couldn't me misled ...so headed over to your channel..
He literally lacked basic understanding of established science..
Some supposedly educated commenters who claimed to be mds themselves even said "high ldl is a result of bad metabolism.. it's a symptom like fever".. and that "plaque is there to heal after the clotting.."..
Gill, I appreciate the scientific rigour in all your videos and your passion to improve scientific communication. I strongly feel it would be much better if you use a professional camera to shoot your videos and also change the display picture of the youtube channel which is very over exposed and you are not at all visible.
Thanks for explaining this topic.
How long does the oxidized small particle stay in the blood stream ?
I got the impression that you wanted to say that LDL is not that significant unless you are insulin resistant, suffering from metabolic syndrome or are diabetic. You kind of hinted at that but maybe I'm reading to much into it. Enjoying your videos. Thanks.
14:15 he just says that a lot of ldl is bad no matter the size. And about metabolic issues was that some of them are associated with high LDL. You misstated the point
Best nutrition channel in the world
Excellent video! This was very interesting.
So what is a max number of pattern B small dense LDL that would be considered a real concern?
Can you get Dr. Cromwell to comment on how he currently treats elevated Lp(a) levels as there is no approved drug to lower that LDL type . Thank you.
High lp(a) risk (above 100mg/dl) is addressed by crushing ApoB via diet and statin even in absence of other risk factors as per European Heart assoc consensus statement
We already know that our LDL lab results really measure LDL-cholesterol: the cholesterol within the particles. It's used as a sort of proxy, to guess at particle numbers. It doesn't measure particle numbers. Is this really a useful number, when particle count is what truly matters? Is ApoB the only useful number available, and why isn't it used routinely? By the way, the latest research has clearly shown that LDL-cholesterol does NOT directly cause cardiovascular disease. I believe Dr. Carvalho has a video on this.
I have perfect LDL and my HDL is a little low. But my LDL particle number is above range at 1667 nmol/L. My doctor never explained the numbers or what they mean. This is all new to me. Thanks for the simple explanation !
This is a video everybody eating low carb/keto/carnivore needs to see. Influencers in that area only showing people half of the information, despite it is nothing incredibly new, comming to dangerous conclusions. There has been boycotting of statins, mistrust in primary care providers and their advice, self interpretation of blood test results if you look at the comments of such videos. Difficult to see, yet ineffective discussing with those people. Half truths are extremly dangerous. Thank you for this video, an honour to hear from such an expert that my understanding of the topic is not wrong.
I have a question though that has not been answered in this interview. In what cases does the determination of particle size sense in order to not overlook elevated risk, when you have somebody witout risk factors? As Dr. Cromwell was explaining the idea to look at particle size was given by the fact that there are individuals without otherwise detectible risk factors having myocardial infarctions.
Family history would come to my mind. In diabetics and insulin resistance you would have elevated TG, so that would give a hint at small particle size, thus not needing advanced lipid testing? Or am I wrong in that regard?
Sorry but I don't see anything disproving low carb diets. Listen carefully at 14:34. If you focus on the problem of metabolic syndrome (in other words, talk about the obesity epidemics rather than familial hypercholesterolemia), then indeed what happens is a huge amount of small dense LDL. And if the problem is insulin resistance, then fasting and low carb are proven ways to solve it.
@@ChappySinclair
You misunderstand me. Not saying it is a gimmick. I did low carb myself for a time.
I‘m against spreading medical misinformation. Every diet has a downside. You need to know what it is to counter balance it and to estimate the risk vs benefit going on such diets.
You can adjust the fats in low carb if you find your LDL-C rising to much.
It also might not be the diet that is causing high LDL-C, a big part is genetics. But with the misinformation out you simply might dismiss it as harmless not listening to your doctor about it.
We are also talking about long term consequences of high LDL-C, not short term, arteriosclerosis develops over decades. Short time elevated LDL-C is not that tragic, long term is. If you read about the critique on low carb you will find exactly that, the worry about long term effects.
It is also an option to do a diet long term + taking medication to counteract the negative effects of high LDL-C.
The worst thing to do is ignoring a problem by just talking it away as if it does not exist.
@@ChappySinclair people improve when they stop overeating, stop eating ultra processed foods, and stop drinking alcohol. If low carb is the best way for someone to stick to these things, that's great! But at the end of the day, regardless of your diet, if your healthcare provider flags something in your blood work you should probably do something about it (including getting a second opinion if needed).
@@markotriesteThe entire country of Switzerland is proof against low carb 😂. They eat bread 5 meals a day and give zero F's. Low rate of obesity and diabeetus. Difference is they have real bread. Low carb is an American thing. We don't have real bread here, it's more like an industrial foam 😢
@@dudea3378Even the home baked bread with simplest and best ingredient still spikes my blood sugar. Life style is another important factor. Europeans move much more on regular basis
it's a question of ""Foam cells, also called lipid-laden macrophages, are a type of cell that contain cholesterol. These can form a plaque that can lead to ... " and how particle sizes pro[de]mote this trigger mechanics,"
TriGlycerides are just as good a proxy for metabolic [insulin] disease as any other.. This idea of confounders [supressor variables] obscuring causation might mean something to him, but to me it is only the cross correlation that is confounding his hand waving argument. Mathematically these are the eigenvalues of the co-variance matrix of paramenters [ this is distinct from Factor Analysis yet more multivariate calculus]
Is there a study or meta analysis that supports this new interpretation of small ldl risk?
I am 62 & have high dense particle numbers & normal cholesterol levels. I started taking niacin supplements but don’t know if I can continue due to the flushing it causes.
Great video! Many thanks for this Dr Carvalho
I heard Niacin (B3) can lower LDL. Is it True? Then why we still need Statin?
Is testing for particle size useful if you have a low LDL level? Mine is calculated to be 39 mg/DL. Total cholesterol is 120 mg/DL, and HDL is 61 mg/DL.
my trig - 41mg/dl, ldl - 96mg/dl, hdl- 69mg/dl, small dense ldl - 49mg/dl. Am doing low carb diet.....can low saturated fat diet help to reduce small dense ldl?
Thank you for the amazing content Gil! The part about FH is really interesting too.
so why do lipid panels universally prioritize LDL-C over LDL-P in how they report results?
Would really love to know his thoughts on Lp(a).
Me too
Me 3! Mine was 380 nmol/L last time I checked. It was 243 nmol/L last June, 293 in September, and last time I checked in April it was 380. No telling how high it is now. Getting new blood work done tomorrow.
Excellent as always. Thanks to both of you!
Interesting talk. Essentially, small-LDL is associated with insulin resistance and in that way, has high risk of CVD. But genetically induced high number of large-LDL (as in the case of FH) in the absence of insulin resistance represents high risk of CVD too. What about diet-induced low number of small-LDL (as in the case of keto diet: low carb, high fat diet) in association with high number of large LDL? Is the risk of CVD in this case high or reduced?
If someones total cholesterol is high but everything else is fine, (hdl high, ldl fine but on the higher cusp), would thid be affected by health polyunsaturated fats? My mother does not eat meat or processed foods just rarely chocolate and cakes....no butter but olive oil
Thanks for clarifying how both small dense and large fluffy LDL can both be problematic in for different reasons/circumstances. I have very few small dense but I am a hyper-absorber and don't clear LDL well at all, so it sounds like my larger LDL can become an issue if they hang around long enough. That being said, doesn't any LDL only have a 5 day life anyway?
I believe both can be problematic if you have some underlying issues already yes. Diabetic, insulin resistance, high blood pressure, smoking, other metabolic issues then both large and small LDL can be bad, however, my understanding is small LDL takes for it to be processed by the liver. If large LDL is hanging around to long and you have some damage it is more likely it could be bad yes
I have recently learned of oxidized triglycerides and how many studies about their atherogenety were performed. I wonder why there is no mention of them in atherosclerosis cause discussions like this? Are they irrelevant or debunked?
8:05 So LDL are danergous because they are small enough to get under the inner layer of the artery wall?
I think I just had a "A HA" moment that helps me tell these *DL's apart.
Hi Gil, what do you think about Dr Gregor’s science based book How not to die? Lots of meta analysis.
Labcorp offers LDL particle (LDL-P) tests. But what numerical ranges in particle size and number are we supposed to refer to when interpreting our results and assessing possible risk? Dr Cromwell seems to have numerical sizes and ranges in mind associated with risk…how can we learn what those ranges are? (or appear to be at this point in time based on the current state of research?)
When Dr Cromwell talks about one particle blocking another, is he referring to a testing error or a data analysis error? He seems to say it's a data analysis error. I thought the test LDL-P results are very straightforward: a direct count and size measurement is provided with no ambiguity and that's it. What am I missing here?
Just a thought, for that recent keto-CTA study that found on average the keto group had many times the plaque accumulation of an otherwise similar group not on that diet, but interestingly the keto members with super high LDL did not have more plaque accumulation than those with just very high LDL, is a possible explanation that the super high LDL group had no more LDL particles, but just the ones that they had blew up to very large size, elevating their LDL test score? Did they test these participants for number of LDL particles, not just total LDL?
What about low ApoB and LDL and higher sdLDL-C
So, all LDL particles are atherogenic, but some more than others, and the fewer of both, the better?
No - all LDLs are equally atherogenic
@@nanduthalange77367:40, is VLDL not LDL? "VLDL not so much." I'm still sticking with what I said unless someone clarifies this. Also I did not say "equally."
It appears that he is saying the small particles seem to be worse because there are too many of them, and the bigger ones seem worse because they are equivalent to a few small particles.
I think until they don't explain the mechanism of action of how these particles interact with and enter the artery walls, it is all a mathematical model.
No we do not know that. All are dangerous, but we have yet to understand exactly how relatively dangerous each is. @@nanduthalange7736
@@rsalehi6568 He said the larger ones, VLDL and chylomicrons "not so much because they're so large they don't get into the artery wall."
Small dense (damaged) ldls are typically damaged via glycation and/or oxidation. It cannot bind to receptor so stays in body with nowhere to go. Typically seen with high triglycerides.
Sdldl is a Hallmark of metabolic syndrome
@georgehornsby2075 - 2023-12-11
Incredibly clear communication by him without oversimplifying. You may have competition...
@MindVersusMisery - 2024-02-02
I know that you were just joking, but I'd like to say that in pursuit for truth, there shouldn't be competition, but cooperation. 🙂
@kraka2oanIner - 2024-11-18
@@MindVersusMisery YES. Antithetical to our monetary (capitalist) SYSTEM. Cooperation is KEY.
@Madasin_Paine - 2025-05-26
Indeed these two are very good at educating people and it proves that even the most complicated subjects can be made understandable to the general public if people have this sort of mastery and keep on improving it.
That said, I wonder if it would have been useful to repeat the maximum that like dissolves like?
As has been mentioned many times this deposition of this cholesterol is in the arteries more than it is in the veins. But the other thing is since both the small and the large particles both carry so much LDL that their solubility isn't much different despite their size which in a way makes sense. Although intuitively I would think the smaller ones would absorb better because they would have greater surface area.
maybe there is slightly more take up by the arteries of the small particle but it would have to be another level of refinement in the study as he referenced earlier by the hand covering the hand example.