Positive LMHR paper


(Bob M) #21

They did do FFQs (food frequency questionnaires), so they have some idea what they ate, which is how they got an estimate of saturated fat intake.

Granted, there are a lot of issues with this. For instance, “saturated fat” has long-chain (supposedly worse) and short-chain (supposedly better) versions and even chained (supposedly worse) and odd chained (supposedly better) versions. And I’ve often thought of trying to compare “saturated fat” version “PUFA” and cholesterol, but to do this in the real world is so much of a challenge, I’ve given up even trying to determine a plan as to how I could do it. (1) you really have no idea how much of anything you’re getting, even if you eat high (long chain) saturated fat containing foods like cacao; (2) you really don’t know calories either, which play a role (eat fewer calories, TC, LDL go up, HDL down; eat more calories, TC, LDL go down, HDL up; eat any carbs, LDL goes down). And there’s a 3-5 day lag for LDL to change, meaning you’d have to be very specific over those days. And, there’s an error in lab testing for these things, as I’ve gotten the same tests done at the same time, and gotten slightly different results.

Also, I think he says that this is the most calcification they’ve seen over a year. But how many studies of CCTA over a year are there?

I am not against vegan or vegetarian. But some people, like me, have a problem with fiber and vegetables. If I eat too many salads, I get IBS, constipation, all heck breaks loose. So I limit salads to maybe one per week. If I eat some plants, I again get problems.

And eating keto, as Peter indicates, has helped me in so many ways, I would be here for a long time listing them. Just the mental aspect alone – no mood swings, no depression, infinite energy – are reasons to stay keto. Many of the people in this study aren’t doing keto to lose weight, but instead to help something else, like Crohn’s disease, IBS, etc. That’s why Nick Norwitz started keto - Crohns. The dude did not need to lose weight.

Anyway, I’m off to do family work.


(E P) #22

I’m an LMHR, or at least I was when I was breastfeeding. LDL almost 300, TG about 50 and HDL about 100. As soon as my baby weaned, my LDL immediately dropped to 100. I was testing monthly.

Does that anecdote help or hurt the lipid energy hypothesis? I’m not quite smart enough to parse it out exactly.


(Joey) #23

Sorry, FFQs are a scientific “red line” for me. Garbage in; garbage out.


(Werner) #24

Any thoughts on this critique of the paper?
Essentially asserting sloppy science.


(Bob M) #25

Here’s more info:

Basically, Dr. Budoff takes issue with saying that this is the fastest atherosclerosis ever recorded. He states that there was no relationship between keto, LDL, or ApoB and atherosclerosis. The people who had atherosclerosis to begin with did get more. He recommends, for these people, they look into why. Is there high inflammation? Can you take aspirin and/or a statin (which obviously the LDL lowering is meaningless, so these are doing something else)?

Now, he did mention Lp(a), but I have ridiculously high Lp(a), top 1 or 5% depending on which study you’re looking at, and a zero score on CAC.

He did say they have a ton of data, such as Lp(a) and a bunch of other types of plaques, which they will be analyzing to attempt to decipher why some people – the ones who started with atherosclerosis – have (much) higher plaque development.

Edit: I did not realize it, but they have a transcript. So, you can read the interview instead of listen to it, and you can see the graphs they are discussing (I listened to it on a podcast during my workout).

Edit2: Here’s what he says: “In the medical literature in PubMed, you see mostly scientists addressing scientists, so it’s a civil discussion, and it’s scientifically based. I think we lose that a little bit with Twitter or now known as X.” Uh, duh. Elon Musk, who owns Twitter/X, called a Thai rescuer a pedophile because the rescuer thought Mr. Musk’s idea of using a submarine was not useful:

When that guy is in charge of Twitter/X, that’s what you’re going to get. No decorum.


(Peter - Don't Fear the Fat ) #26

This study has caused a right stink. Wow people are really hating on it. Calling it bad science poor research, incomplete paper etc etc … Yeah like Ancel Keys did great work?
Can only assume it’s touched a nerve. Excellent :grinning:

Don’t know about you guys but my blood pressure has improved on a high fat diet.


(Bob M) #27

And if you were in charge of this study and wanted to know how much saturated fat the participants were eating you would do…what?

You can complain all you want, but at some point, you have to decide how to track what people eat. Right now, FFQs are pretty much all we have.


(Joey) #28

I would refrain from bothering with FFQs and conduct meaningful scientific exploration instead.

Handing folks a clipboard and asking how much of various menu items they ate over the past few years does not produce useful data.

Perhaps it’s just me, but I can’t recall what I had for dinner a couple of nights ago. So what’s the point in asking what I ate last year? :man_shrugging:


(Alec) #29

My opinion is that you don’t need to be “lean mass” to be a hyper responder. Their research focuses on what they call the LMHR phenotype, which they define. But I think it would be a mistake to think that only lean mass people “hyper respond” to keto/carnivore diets in terms of blood lipids.


(Werner) #30

Latest update on the paper.

https://x.com/janellison/status/1914774541110534616?t=6UFwRcbGFqM3gzoarEKNQQ&s=19