Assumptions about Dayspring based off the Attia / Feldman Podcast

[brownfat]

Dr. Phinney says something similar, that perhaps 20% of the population is naturally insulin-sensitive and therefore fine on HCLF.

However, that may not be the same 20% who don’t thrive on keto. Dr. Attia has patients who have improved insulin resistance with keto but at the same time due to abnormalities with lipid metabolism develop new issues like crazy high triglycerides or pathological lipoproteins. Being a crappy sugar burner isn’t a guarantee of being a good fat burner.

[PaulL]

Is there any reliable evidence linking lipid numbers to cardiovascular risk? Should we really be as worried as we are? Ravnskov, Kendrick, Diamond, et al. seem to be advocating for clotting abnormalities as the true cause of cardiovascular disease.

[KNHVT]

Ha! That’s pretty funny that I made that mistake in that post! Yes, I meant LCHF!

(I went back and corrected it.)

[KNHVT]

Yes, I think you’ve said it perfectly.

[brownfat]

Is there any reliable evidence linking lipid numbers to cardiovascular risk? Should we really be as worried as we are?

Yes, there is a ton of evidence of varying quality, some of which is considered of best quality - though there is never a 100% guarantee of correctness/reliability, linking lipid numbers to CVD risk. We know with near certainty that increasing LDL-p increases the risk of developing atherosclerotic plaques which are a primary cause of CVD. We know quite a bit about how variations of lipoproteins and their cargo modulate the risk. We also know with near certainty that hyperinsulinemia and poor glucose control are major elements in the other 2 things needed to form plaques, inflammation and endothelial damage.

What we don’t well know is how these factors (and others) combine. Identifying when the common positives of a keto diet, better glucose and insulin, are outweighed by rare negatives, really bad lipid changes, is the challenge. The answer to your last question is thus fuzzy. Most worry too much about bad lipids, but a few aren’t worrying enough. The unlucky few who have major deterioration in lipids without much improvement in glucose/insulin are probably the ones who should worry most.

[atomicspacebunny]

If anything - watch that video of Dayspring. It just reminds me that if LDL is so causal to CAD and such a killer and here we have a “top lipidologist” recommending a high fat diet… something doesn’t jive with that.

My take on this:

Bottom line it is always about the sugar/processed carb intake, vitamin K & D absorption; the high-fat intake is only a small fraction of the equation! What is really “normal” when most of what you have is a kazzilion pieces of data all masked on sugar burner metabolisms, then the confusion ensues…?

The Peter Attia transcript shows comments like:

Attia: “Well, I’m going to keep eating my bacon and eggs like it’s mainlining, and ignoring my LDL-C because my HDL-C is high and my trigs are low, because I’m on a low carb diet, and somehow that makes me special, because no one’s proved that this is wrong.” Wow. That’s not the legacy I want."

Explanation of the dodgy commentary:

Dr. Attia has to be very conservative if peers start questioning the efficacy of his agreements or edorsements and makes most of his opinions on his own n=1’s and patient’s he treats, if by whatever happenstance he could or might be subject to lots of scrutiny and censure (that is changing with time) by peers (what is considered “the respectable medical community”) and the state board of medical examiners if enough complaints are lodged? He certainly does not want to become unpopular with liability insurance providers?

Medical malpractice is big business and highly sought after target for predatory legal professionals!

[dlc96_darren]

I really enjoyed @carl’s interview with Dr. Nadir Ali, in episode 139.

2 Keto Dudes - Episode #139 - Unpacking LDL with Dr. Nadir Ali

He made the statement that really resonated with my simplistic way of thinking. Basically, if high LDL is so bad for us, then why does the body create more of it, when we fast, and fasting is recognized as something beneficial?

[4dml]

My LDL (both C and P) are insanely high - higher than those discussed on the podcast - but everything else is great. After listening to the show, I’ll admit - I’m concerned. I have been moving more toward fish and unsaturated fats, but I don’t know if that’s the right path.

Ben Greenfield did a podcast interviewing Max Lugavere, on the topic of saturated fats, MUFA and PUFA. There are definitely people who are better off limiting their saturated fat intake.

[4dml]

Too bad there is no NUSI to run an RCT to settle this. As it is, we’re all shooting in the dark because there are no RCTs with people who eat low carb, who get “bad” lipid profiles, and then “correct” those profiles using more monounsaturated fat. Until such time as there is an RCT, I personally just ignore my “high” LDL-p.

RCT isn’t necessary. All you need to do is figure out how your body responds. This is a simple experiment. Try it for 3-6 months, get tested, adjust according to the results.

[KNHVT]

I didn’t start gaining weight until my late 40s, and I’m a woman (noting that since women often gain weight more easily than men). And then no matter what I did, I couldn’t lose it.

[PaulL]

hyperinsulinemia and poor glucose control are major elements in the other 2 things needed to form plaques, inflammation and endothelial damage.

And don’t forget about the glycation of red blood cells, making them likelier to clot.

Ravnskov and Diamond, in fact, seem to be coming to the conclusion that the real CVD risk factor is clotting abnormalities. They point to studies of people with familial hypercholesterolemia showing that the ones who get heart disease and die of heart attacks and strokes are the ones with alleles that produce abnormal fibrinogen and factor VIII, whereas the people with FH who don’t have those abnormalities never develop heart disease, and die at perfectly normal ages of other causes.