Berry, Norowitz and Feldman on LMHR podcast

(Denise) #1

Probably plenty of you have seen this, but I’m watching it this a.m. and I got excited because I’d never heard Norowitz had/has higher cholesterol than I do, at 545 which I’m all ears now :wink:

Streamed 2 months ago, Denise PS I have no significant plaque btw. No warnings given with the amount of mine at all. I have the test results if anyone wants to know my numbers.

Long term effects of high LDL without any other health issues
(Bob M) #2

Both Norwitz and Feldman are LMHRs (lean mass hyper-responders). They are both very lean.

Norwitz also eats a lot of olive oil, so he is eating plant oils. Still has a high LDL.

(Denise) #3

Ok Bob, I eat I’d say at least 3 tbsp of Olive Oil everyday in my cooking. I also want to stay I have been a stick-person (remember the little drawing of stick people) My whole life, but gained a total of 30 extra lbs plus some illnesses after 1997. Before that, I was very healthy, and active.

Getting on Keto got rid of the extra weight, but I am pretty sure I won’t be dropping things like eggs that are said to raise cholesterol. Now I look like a stick again, only with much more muscle, still a tooth-pick.

So I guess what I’m trying to say is, I really believe I could be a LMHR even though I don’t fit exactly, every evidence of that. Can’t remember off-hand what those differences are, but I’m back at looking into it. I guess I want to know others like myself with high ldl, but they are doing great, as I am too :wink:

(Denise) #4

Nick says at about 27:50 of video that a lot of doctors don’t test for Familial Hypercholestorolemia, they just tell you that (and it IS written on my records I have that!!) that you have it if you have high LDL :frowning: It really burns me up because I know they’ve done none of the tests for FH on me at all!

(Geoffrey) #5

Which of course is no big deal.

(Bob M) #6

@Goldengirl52 They should do a test for FH on you. The problem with FH is supposedly coagulation, not LDL (depending on whom you believe).

These are the anti-LDL folks:

So, if you knew you had FH, you might consider something other than drugs whose primary purpose is to lower LDL.

If you wanted to test whether you are FH or LMHR, you might be able to eat white bread:

I’m assuming the LMHRs would drop their LDL while FH would not, though I don’t know for a fact that’s true.

@Geezy56 That’s definitely my opinion.

(Denise) #7

I just don’t like seeing them put stuff in my record that false information. I get over things quick though and won’t lose any sleep over it.

(Denise) #8

As always, I appreciate the info Bob, and your comments as well @Geezy56.

I’ll take a look at the info you linked to, Denise

(Bob M) #9

Nick was also here:

I listened to it:

Nick was able to drop his LDL a ton…by eating Oreo cookies. More than statins. This was an n=1 study to show elements of the lipid energy model.

Supposedly, if you go to Nick’s YouTube channel, there’s an 8 minute video where they explain some of the concepts.

I think that would be interesting, because I only understand a little bit of it. During the conversation, Nick basically discusses how VLDL is used for fat (trigs) transport, which means trigs go down (because they’re in VLDL) and HDL is somehow fragmented off in this process, meaning there’s more HDL, which is why HDL goes up (and VLDL cause LDL go to up, which is why there’s more LDL).

But their main study of LMHRs has indicated that there is no relationship between LDL (and that EVIL ApoB which is also ridiculously high in LMHRs) and levels they are getting on scans.

(Denise) #10

This sounds very interesting and I will watch it, if only in a part at a time Bob. If Nick is concerned about his high LDL, or maybe more curious than concerned, doesn’t matter to me. I’d like to have lower cholesterol, LDL, just for honestly, peace of mind.

I couldn’t do the Oreo cookies or any sugars as I am a T2 Diabetic, and since just lowering my carb intake I’ve reversed that though I know I’m not cured since I tried something simple like popcorn and my BG shot up, not super high, and went down within the 90 minutes I did checks.

Thanks much, I’ll go take a look, Denise :wink: PS Glad these are 2024 'casts. Get more up to date info on studies.

Edit: so far, I’m not at all sure I fit the LMHR profile. People that adopt a ketogenic diet are already lean, I wasn’t, I was 30 lbs over being lean. I’m hoping I can find info on lowering cholesterol in me, being a non LMHR. I’ll keep reading because I’m curious what made the Oreos work to lower LDL. Wondering if there are diabetic-safe foods I could eat. And a sleeve of Oreos?? Isn’t that like half a pack of cookies:rofl: and what’s the long term effect, do you have to keep eating cookies Nick :wink:

Well, I’ll learn some things, mainly, that I’m probably not LMHR :wink:

(Bob M) #11

LMHRs shuttle fat using VLDL, via triglycerides. After that fat is delivered to wherever it goes, the VLDL becomes LDL (and apparently HDL? I didn’t know that). That’s why LDL goes up – the fat you’re eating is going to your lipids.

The reason carbs work is that then carbs are used for energy instead of fat. So, your VLDL doesn’t go up, and therefore neither does LDL.

They discuss that people can instead use “healthy” carbs like sweet potatoes instead of Oreos. This will lower LDL. But you’d have to test whether this would be good or bad for your blood sugar and how you feel. Personally, I tried eating sweet potatoes on the days I exercised, and sweet potatoes are problematic for me. But you could be different.

How “overweight” are you? Or are you leaner now? The theory is that if you get lean, you’ll become a LMHR. Nick says he’d like to test this theory in a study, but it’s what they believe to be true. No studies yet though.

You’re also an older woman, which tend to have higher LDL. And, by the way, plenty of the studies I’ve seen for older women indicate higher LDL is better. One function of LDL is as an immune system entity.

From here (PDF download):

Edit: The authors are anti-LDL-causes-death, so may (or may not) be a bit biased.

Uffe Ravnskov, David Diamond, Zoe Harcombe, Malcolm Kendrick. All names I’m familiar with and all firmly on the “carbs are bad or at least not supported by science” and “LDL isn’t causal or at least this isn’t supported by science.”

(Denise) #12

I’m just now waiting for a call-back from my Medicare to see if I might be covered for a CCTA scan. I’m pretty sure I’ve never had that scan, but it sounds so much more thorough, I would like to have one, after reading this from Nicks transcript, I’d rather read than listen as I need to check “definitions” of words to understand ;):
From Nick:
“What they did, or are doing, is taking 100 people like me– lean-mass hyper-responders, or very similar to that phenotype, and they’re following them over one year to see [if] super high levels are [leading to] plaque progression. And I’ll add that we’re not just looking at coronary artery calcium scans (CACs), we’re looking with coronary CT angiography (CCTAs). The distinction there is important because CCTAs look at non-calcified plaque as well. The principal investigator (PI) on this study is an expert in this field and is the one [who] helped design the study, determined the one-year timeframe”.

I just think this would be good for me to have, feedback welcome. I’m not a test freak, like I just want to be tested for every little thing, but still, I want to know about this. I have a 3rd degree AV Node block since '97, pacemaker works so well I forget I even have one, literally. But that is not to do with Vascular, it’s electrical part is how they described it to me…

I’m maybe lean, by an online calculator I am at 20.3 BMI, so not super bony or anything. 5’2", 112 lbs. As I read further, I did see that they said “generally” LMHRs are lean when they start Keto so I guess I still could fit. What I care about most is whether or not high LDL is bad for me if all other health is very good, like trigs, and how much I’m able to do, much more than I ever have done earlier in life, more active with healthy things, activities :wink:

(Bacon is a many-splendoured thing) #13

It is well-known that only about half of the people with FH develop cardivascular problems, and they are the ones with coagulation issues. The people with FH who do not have coagulopathy live to a ripe old age and die of causes other than cardiovascular disease. This has been known since the 1960’s, in fact, and one study I read made the point that it called into question Ancel Keys’s insistence that LDL was a problem. We all know how that worked out, alas!

It’s certainly true in Dave Feldman’s case. He found that eating carbs for three to five days before a blood draw would lower his LDL to a number that wouldn’t freak out his doctor.

Interesting. I thought HDL was a different lipoprotein. So far as I know, the progression is VLDL to ILDL to LDL (and to oxidised LDL if the dwell time is long enough). I’ve never heard that HDL was to be found in that progression.

(Denise) #14

Somehow this isn’t very appealing to me this a.m., but thanks for the heads-up @PaulL
Are you sure you didn’t mean “rotten old age” :rofl:

(Bob M) #15

Hi Paul, I was thinking I’d have to listen to the whole thing again, to find out exactly what Nick said. Thankfully, they have a transcript:

My interpretation was wrong, though. Somehow “surface components include cholesterol, which then gets transferred to HDL particles”. Not sure how that works. Do you know?

Also, the other thing I can’t figure out is why this only occurs for LMHRs. My limited understanding was that we overweight/not lean folks use some fat reserves for our energy transport mechanism, and this has a different pathway than VLDL. Thus, our LDL doesn’t go as high. But I don’t know where I got that info. Not sure if it was a Dave Feldman lecture (seen him a few times at KetoFests) or something else.

(Bob M) #16

Found a few references, but nothing describing why higher LDL would result in higher HDL:

But found this, which I’m going to have to read:


(Denise) #17

yes, I love their transcripts as well as I can go back and read again which the need comes up quite often :slight_smile:

(Bacon is a many-splendoured thing) #18

That passage you quote is closer to what I understood to be going on. However, that bit about cholesterol being transferred from LDL to HDL is news to me, though it certainly makes sense. And I notice that it’s the cholesterol from the lipoprotein container that he seems to be talking about, and I only recently learned that there was cholesterol in the container, which, again, is not surprising.

I’m not versed in what is supposed to go on generally for everyone versus what happens specifically to LMHR’s. It gets confusing, because some lipid numbers are usually calculated, rather than measured, and I’m not clear whether chylomicrons are separate from VLDL, or whether they turn into VLDL. I believe I may have heard both. One understanding is that chylomicrons carry the energy (as fat) from the current meal, so if they turn into VLDL, then that would explain high triglycerides. But Feldman makes it sound as though VLDL is carrying fatty acids from adipocytes in the case of LMHR’s, but does that mean that the liver makes the VLDL but then they go and pick up more triglycerides from the fat cells?

In any case, the contents of chylomicrons do not appear in lipid results if the blood draw was done fasting, because they have a very short dwell time. But what if the patient forgets and eats before the blood draw? If the chylomicrons and the other LDL are all the same lipoprotein, there might not be any way to distinguish between them. (HDL is supposed to have a different type of lipoprotein as its container.) That might inflate the triglyceride number, mightn’t it?

To quote Moonstruck, “I’m so confused!”

ETA: It does seem to make sense, as the Norwood paper you linked posits, that lean people would have higher LDL and HDL, since there would certainly be a greater need for shuttling triglycerides around the body. They would be taken to cells needing energy by the LDL and returned to the liver in the HDL (according to Feldman, the cholesterol is merely along for the ride). So eating in a way that minimises fasting triglycerides would certainly promote this. And most of the rest of us are probably fat enough that our LDL doesn’t need to work nearly as hard.

(Bob M) #19

Well, I took a look at my fancy NMR LipoProfile…and it has a calculated LDL-C. Hmm. Of course it tells all kinds of other stuff including sizes for HDL, LDL, VLDL, and particle counts (though no particle count for VLDL). Oddly, even when I had relatively low LDL, I’ve always had “high” LDL-p.

I think I either permanently damaged my liver or have some genetic aberration, because my HDL, even when above 50, has bad HDL size:

My HDL markers on this scale are always plastered to the right, which means my LPIR score (a purported measure of “insulin resistance”) is always bad. (I found a calculator for this,and if I move my HDL to the left a bit, I get a much better LPIR score; but my HDL never move.)

Anyway, maybe this helps answer my question:

Maybe you’re correct, in that people who aren’t lean don’t “need” to stress the system and therefore this results in less VLDL and LDL?