Hyper-responders... yet diet doesn't drive serum cholesterol?

[SomeGuy]

What puzzles me as I ruminate on Lean Mass Hyper-Responders (LMHRs):

Given: LDL-P skyrockets shortly after LMHRs go keto.

The science seems clear that dietary cholesterol barely (if at all) affects blood serum cholesterol. (Even Ancel Keys is now said to have agreed with this.)

And yet, the "responder" in “hyper-responder” suggests otherwise.

Put different;y, how could a change in diet from low fat to high fat give rise to both outcomes:

(1) Exert no meaningful effect on LDL, and;
(2) Produce such a remarkable effect on LDL?

There must be a simple way to reconcile these two seemingly contradictory statements, no?

[Justin_Jordan]

I don’t know that they’re contradictory at all.

I can eat peanuts with no measurable health effect and other people will literally die if they do. There’s a lot of variance in the human body. That something doesn’t have a meaningful effect on some and does on others happens all the time.

[SomeGuy]

@Justin_Jordan I’m not referring to individual differences, but to metabolic processes that affect all of us. There seems to be widespread agreement among those in the scientific community (both supportive of keto and not) who state that dietary intake of cholesterol has virtually no effect (15% max) on blood serum cholesterol.

And yet we have hyper-responders whose LDL levels shoot sky high in response to eating fats. Seems like these can’t both be true, no?

[Justin_Jordan]

Note the words ‘virtually’ and ‘meaningful’ in your questions.

You’d need to look at the mechanistic explanations to know whether this is contradictory. But my point was is that the statements ‘peanuts have no effect on lifespan’ and ‘peanuts can kill people’ are not actually contradictory, in the same sense that what you’ve asked isn’t inherently contradictory.

The reason I point out virtually and meaningful is that the explanation for why it might not be contradictory is baked into your question - it’s possible most people have a response that can’t be meaningfully separated from the noise, and some outliers do.

I don’t actually know the answer, but the question as presented doesn’t actually contain unreconcilable facts.

[daddyoh]

I don’t think we know if it is dietary cholesterol or something else about low carb high-fat diets.

Lean Mass Hyper Responders are not like much of the rest of the population in this regard. Maybe there is something that is genetic that is different and those genes are expressed (turned on).

There must be a simple way to reconcile these two seemingly contradictory statements, no?

We don’t know yet.

[SomeGuy]

I appreciate your replies @Justin_Jordan and @daddyoh I think we can all agree that we don’t know

My understanding of most estimates tossed around by those close to the LMHR research is that roughly 30% fall into this category. So I guess my takeaway is that perhaps it’s not as rare as was previously thought. Would be enough to make a “confounder” skewing averages?

To extend the above analogy … It’d be like if 1/3rd of folks had a peanut allergy. This would likely affect the “don’t worry, on average peanuts are safe” on conclusion.

[amwassil]

@SomeGuy My understanding is that if you have a peanut allergy and eat peanuts you’re in for serious repercussions, including possible death. If you are an LMHR, on the other hand, not so much. You have high LDL. So what?

[SomeGuy]

@SomeGuy My understanding is that if you have a peanut allergy and eat peanuts you’re in for serious repercussions, including possible death. If you are an LMHR, on the other hand, not so much. You have high LDL. So what?

@amwassil For those who are LMHRs, you framed the question perfectly … So what?

My current understanding is that, at this time, the lipidology experts who are keen on keto are responding: “Dunno.”

[amwassil]

My current understanding is that, at this time, the lipidology experts who are keen on keto are responding: “Dunno.”

I think Dave Feldman says it’s not a big deal because when you’re metabolizing fat, LDL is the delivery system. He compares it to Fedex. To me this means ‘hyper responders’ just have an aggressive Fedex branch.

[SomeGuy]

I think Dave Feldman says it’s not a big deal because when you’re metabolizing fat, LDL is the delivery system. He compares it to Fedex. To me this means ‘hyper responders’ just have an aggressive Fedex branch.

I believe you’ve accurately described @DaveKeto’s characterization. But my understanding is that this is more of a wish on his part than a fact-based conclusion.

He is typically quite careful to say that he doesn’t know - and perhaps it might turn out to be a big deal after all when more facts are in.

And of course if “off-the-chart” LDL-P levels are as dangerous as some insist, it’s hard to chalk it up to not a big deal. At least an open question at which the science has yet to arrive.

As an LMHR myself, I don’t currently plan on doing much differently. I’m not eating a ton of saturated fats (maybe around 25% of my total fat intake), so there’s not much room to reduce. Eating statins isn’t going to happen. So that leaves me with Dave’s wishes and my hopes.

Some say that once weight loss stabilizes, the LDL-P might return to less lofty levels. Frankly, although I lost 20 lbs, I seem to have stabilized and I wasn’t terribly overweight to begin with (hence the “lean” part of LMHR). BMI from mid/low-20s to the low 20s.

Will likely schedule another CAC at some point and keep NMR testing along the way. But meanwhile, I’m feeling phenomenal, so it’s hard to fight what seems like success

[Justin_Jordan]

To extend the above analogy … It’d be like if 1/3rd of folks had a peanut allergy. This would likely affect the “don’t worry, on average peanuts are safe” on conclusion.

You’d think.

But the peanut allergy is (intentionally) dramatic.

More applicable is the standard (I mean no keto) advice for carb intake. It’s clearly bad advice for a very minimum a large part of the population, and maybe everyone.

But it’s still the advice.

The LMHR stuff falls into a new category so it’ll take a while for the standard advice to change, if it ever does.

[brownfat]

The science seems clear that dietary cholesterol barely (if at all) affects blood serum cholesterol. (Even Ancel Keys is now said to have agreed with this.)

And yet, the "responder " in “hyper-responder” suggests otherwise.

Put different;y, how could a change in diet from low fat to high fat give rise to both outcomes:

(1) Exert no meaningful effect on LDL, and;
(2) Produce such a remarkable effect on LDL?

Diet definitely has a large effect on LDL even though ingested cholesterol doesn’t. Many people find prolonged fasting strongly raises LDL and I expect it is the carbohydrate restriction that is the primary cause of increased lipoproteins/cholesterol on a keto diet. Most consider the increase in HDL very desirable. Some of us think an increase in LDL can also be desirable under some circumstances typical when keto such as low inflammation and low insulin.

Dave Feldman’s theory is the rise in LDL is due to its role transporting lipids and the increased need for transport when one is primarily burning fat and not glucose. Seems like a possibility to me although I don’t think he explains why there is such variation in how LDL levels change among people eating keto.

[SomeGuy]

@brownfat You make excellent points. Very helpful in squaring the circle for me.

… although I don’t think he explains why there is such variation in how LDL levels change among people eating keto.

Perhaps this remains the core conundrum. That is, when a growing number of folks like ourselves enter into a ketogenic eating pattern, how can two diametrically opposed lipid results (lower LDL-c/LDL-p vs markedly higher LDL-c/LDL-p) be “good” for each n=1 involved, regardless?

No doubt there’s a good answer out there. One may be that it just is good for everyone, regardless … with scientific details to follow.

Another is that it’s not good for either one or the other group … and which group is which might still surprise us all down the road

[anon81060937]

Us LMHRs are producing what’s missing in abundance to keep us in ketosis and amplify our metabolism. Hence why those who aren’t producing what’s missing will succumb to low carb and their addictions or hack away with supplements.

It’s good that you can see that there is a missing piece in the very complex puzzle.

[SomeGuy]

Us LMHRs are producing what’s missing in abundance to keep us in ketosis and amplify our metabolism. Hence why those who aren’t producing what’s missing will succumb to low carb and their addictions or hack away with supplements.

It’s good that you can see that there is a missing piece in the very complex puzzle.

Not entirely clear to me where you’re going - but happy to hear more about the point you’re getting at. Thanks.

[April_Harkness]

Per Dave Feldman…I am the highest lmhr…thus far that has been found. Maybe not for long. LDL 822. I was just informed THE entire CARDIOLOGY DEPT at Northwestern Hospital will be presented with my case. The entire dept at a major hospital. They just sent my blood work to Mayo. And soon I’ll have more tests done that my cardiologist will not order paid for by concerned citizens who want to overturn the lipid hypothesis.

[SomeGuy]

You are our LMHR rockstar.
Live long and prosper.

[April_Harkness]

[Fangs]

wow that is so interesting, you are a ‘subject’ now…cool

[SomeGuy]

@April_Harkness Costume is awesome. Can’t quite see pointy ears, but we certainly trust you.