Here’s the video of my presentation at Low Carb USA. I’ve already posted on the ApoE4 group that sponsored it and the many amazing events surrounding the conference.
In this video, I was able to do a much deeper dive in the beginning, to better help the audience understand the nature of the lipid system and the importance of “ride sharing” for lipoproteins — in layman’s terms. 🙂
Special note: In case you thought this week hit its quotas for blog posts, just wait until you see what we have coming in tomorrow…
Just a comment, I do not eat pork or shellfish at all and I would love to be able to compare those who do to those who don’t especially since the keto group pushes pig bacon so hard. I believe our bodies are designed to eat certain animals and not others (some are food and some are not food just like poison ivy is not food but broccoli is). The okay animals are: fish with fins and scales (so no shellfish or calamari or whales or shark), animals that both chew the cud and have a split hoof (not pig, not monkey, not dogs, not rabbit, not possum, not bears). and only certain insects like grasshoppers (but I have never eaten one that I know of haha). Its based on scriptures in the bible – Leviticus 11 and Deuteronomy 14. I am not trying to bring religion into it as much as asking what if this is correct info and we aren’t getting the full benefit of our health. My son and I did a Science fair using petri dishes and swabs of meat to ask which is better for you beef or pork and he won Best of Show! We looked at things under the microscope and did a lot of research and it seems scientifically on a very low scale test, pork is nasty stuff. For whatever its worth…
Pretty interesting, Sally. Yes, it would be cool to see if your data provided any difference in regards to lipids relative to the pork and shellfish diets.
That’s interesting because in Leviticus 7:22-24 it says not to eat the fat of ox, sheep, or goat:
23 Speak unto the children of Israel, saying, Ye shall eat no manner of fat, of ox, or of sheep, or of goat.
24 And the fat of the beast that dieth of itself, and the fat of that which is torn with beasts, may be used in any other use: but ye shall in no wise eat of it.
This may not have anything to do with saturated fat though, because the Bible does not restrict butter and cheese, which are richer in them.
2 Samuel 17:29:
29 And honey, and butter, and sheep, and cheese of kine, for David, and for the people that were with him, to eat: for they said, The people is hungry, and weary, and thirsty, in the wilderness.
And it does not seem that all sorts of animal fat are forbidden, such as ones in bone marrow:
Isaiah 25:6:
6 And in this mountain shall the Lord of hosts make unto all people a feast of fat things, a feast of wines on the lees, of fat things full of marrow, of wines on the lees well refined.
But Israel, being a nation with a longer history of agriculture, may have a lower prevalence of APOE4 and other genes with sensitivities to saturated fat.
I watched this video, and I am a bit puzzled. As a functional medicine physician, I play with people’s blood glucose and lipid panels for a living. I recommend diets and I watch things change. I will definitely give people a heads up to stick to their diet very closely for the 5 days before a NMR test.
But here is my question: We start with the understanding that ApoE4 carries fat and is inflammatory (so might lead to many long term issues that come about as a result of chronic inflammation), and so we recommend that patients with ApoE4 reduce animal saturated fat and coconut fat to optimize lipid parameters (reduce LDL-P and sdLDL).
There is no discussion of this in your blog. I heard you say that your carotids are clean – how about markers of inflammation? Doesn’t ApoE4 turn on our inflammatory genes? Does this not matter if your diet is ketogenic?
My personal experience (very superficial I now realize) is of a 25% drop in LDL-P and sdLDL and also TG when I replaced coconut oil with avocado oil. Unfortunately I also did something else at the same time, which was 3 rounds of the fasting mimicking diet, which eliminated my insulin resistance.
Dr. Gundry says cheese (which he says ApoE4 people love inordinately) will blow up your LDL-P and needs to be avoided at least for 3 days before your test if you want nice numbers. In my experience (which needs to be more tightly controlled, I now see) most patients drop their lipid numbers on a high fat diet, except ApoE4 patients for whom it rises. I have felt that it is more related to high HbA1C in the average person on a SA diet. Once that is controlled, you get a number of other effects.
Anyways, sorry for the rambling. I am in the business of needing to give people advice and so I wonder about causing unanticipated harm with saturated fat via inflammation caused by ApoE4.
Hi Myrto—
I’m not sure if I agree that ApoE4 is specifically pro-inflammatory. I have many followers who are 4/X or 4/4 who are hyper-responders with very high LDLc/p, yet with extremely low inflammatory markers.
My liver enzymes are normal or optimal. AST, ALT within range, hsCRP typically <1.0. Normal CMP, CDC, etc. The one thing I haven’t been able to isolate is my higher Ferritin numbers (though I have normal iron panels and no genetic hemochromatosis) — so technically, that could be inflammatory, but it could also be genetic.
Per my point above, I don’t believe ApoE4 is *independently* inflammatory. It may be that it has more aggressive processes compared to E2 and E3 alleles, but that is a question more of outcome of response than origin of the problem.
I think generally replacing SFA with PUFAs will reduce LDLc/p, but I don’t consider this a net benefit given the higher oxLDL outcomes as a result. For more on this I suggest reading/watching Chris Masterjohn’s content.
I have a lot of compelling data at this point that ApoE4 status is a component of a resulting LDLc/p outcome, but actually a pretty small one overall (see my LCUSA presentation to ApoE4 group http://cholesterolcode.com/low-carb-usa-2017-presentation-video/). The biggest is existing composition of the diet (fat vs carbs) and body/health of the person (lean and/or athletic cholesterolcode.com/are-you-a-lean-mass-hyper-responder/).
Dave, it’s neat how you and many of the APOE4 followers you know manage to keep inflammation low despite very high LDLc/p. I remembered how you mentioned in the “Why everything you’ve been told about cholesterol is WRONG! A conversation with Dave Feldman” podcast with Dr. Paul Saladino that you seemed to have the best blood work when you are on a very high saturated fatty acid ketogenic diet. Low inflammatory markers and fantastic liver enzymes.
All the APOE4 people on the APOE4 info website I have followed all say they need to reduce saturated fat in order to lower inflammation as well as insulin resistance, oxidized LDL, and triglycerides.
Is there a particular way you and these other APOE4s do this? SFA to MUFA/PUFA ratio, % of calories from SFAs, protein intake, dietary cholesterol, total calories, medications, supplements, exercises? Are there possibly other genes you guys might have that would offset the effects of APOE4?
Regarding the APOE4 group, are they reducing saturated fat because they’ve demonstrated an effect in themselves, or is it an assumption going in that if you’re APOE4 you need to and that’s why they’re doing it? I know some, like Gundry, discuss research surrounding saturated fat and APOE4 but one criticism I’ve seen is that this research focuses on saturated fat from dairy, and dairy is a bit of a potential beast of its own (e.g. it may not be the saturated fat per se, but the source it’s coming from). I would also wonder about the context of the overall diet, and the context of the person in question (e.g. health context). I’m not saying these would for sure be relevant, just that they’d be questions of interest for me.
I’d be interested to see a study on this in a ketogenic (dairy free) diet context in the future, for sure.
As for Dave, I’ve never heard him say he’s doing anything special, besides eating a primarily whole food ketogenic diet. He’s a bit on the protein dominant side (I think around 30%), but he’s also done higher fat carnivore so I’m sure you could ask for the inflammatory markers from that.
Before trying to investigate what’s special for APOE4s who seem to tolerate high saturated fat well, I’d first want to know if they might not be the norm in that context. I don’t know for sure which it is in this case, but I feel it’s worth asking, regardless. If the APOE4s in the group you mentioned said it were common to see much higher inflammatory markers when including higher SFA, that went down to normal upon switching to MUFA, and this was independent of dairy inclusion – I’d find that interesting, for example.
They are reducing saturated fat because they’ve seen their blood markers go in the wrong direction, and after replacing most of their saturated fats with MUFAs, their blood markers improved. Some did eliminate dairy afterwards, but there had been others who never had it before or after.
That’s definitely interesting – thanks for the further info. 🙂