APOE4 hyper-responder. LDL off the charts. What to do?

(Cindy) #26

59 and 70 are GREAT trigs, Gabe. I’ve been reading that when you first go keto, your trigs can elevate for a while, but then the keto diet brings them down very low. Could this be what has happened to you? The keto diet is ideal for bringing down trigs, so you may bring yours down even farther eventually.

(Gabe “No Dogma, Only Science Please!” ) #27

Well those numbers are from the last year, and the 150 reading was right in the middle of it. and I’ve been low carb for 2 years. So I doubt it. My LDL-P is sky-high.

(Cindy) #28

My trigs are much higher than yours high 200’s to low 300’s. I’ve been in full ketosis without a single break for 6-7 months now, and I get bloodwork done soon, so I’ll see what ketosis does soon. All my lipids are high, and I have double genes (MTHFR) that often cause high lipids. I’m hoping that being fully keto will help, but I don’t know yet. For most people, the research says ketosis works. But I could be one of the 5% that it doesn’t work for. I’ll let you know when I find out.

#29

I had my CIMT scan today. Zero plaque build-up. Arteries comparable to that of an average 34 year-old’s (which is 15 years my junior) so that was reassuring. The fact that I haven’t lost any weight in almost 2 months…less so.

(Juliana Szabluk) #30

They all repeat: “cut saturated fat”, “cut saturated fat”. I’ve been reading case after case for about a month. Hundreds of cases so far. One got better after cutting saturated fat. My bet is ketones. They are fat. High ketones = high fat and higher levels for some people. Usually, the pattern is the same, quite different from Dave’s hyper responders: higher LDL, higher HDL, higher trigs, higher apob. My total cholesterol went from 200 to 511. No way this is safe. Lipid panel got worse completely. I’m eating keto + a fruit to keep me off ketosis. I’ll retest and make a post about it.

(Bunny) #31

Not ketones (excessive glucose; glycation/AGES?), nutrigenomic polymorphic anomalies may be what hyper-responders are looking at? Just need to be more aware of type of fat ratios in % being consumed to give you a “normal number?” Then again what is the difference between sugar burner normal and ketogenic normal?

”… Conventionally, LDL-C is estimated by the Friedewald equation, obviating need for an ultracentrifuge. This equation is based on an analysis of 448 patients from 1972 and estimates LDL-C as (total cholesterol) – (high-density lipoprotein cholesterol [HDL-C]) – (triglycerides/5) in mg/dL. …” …More

May need to change type of fats in % being consumed?

Some resources for you:

  1. The Ketogenic diet, Saturated Fat, and Genetics
  1. Cholesterol is required by almost every cell in our bodies. It is so vital we are able to manufacture it. Cholesterol is predominantly made by your liver. Cholesterol is so vital we manufacture the bulk of the body’s requirements.
  1. Cholesterol is the structure which is the base of all our sex hormones, bile acid and Vitamin D is made from. Cholesterol maintains cell walls, allows cellular communication and transportation of substances.
  1. Cholesterol is a poor predictor of heart disease. Half of those with heart disease have ‘normal’ cholesterol levels. Half of those with ‘high’ cholesterol levels have healthy hearts. Most heart attack victims have cholesterol within the “NORMAL” range.
  1. HMG-CoA Reductase
  1. ”… When you consume a diet high in cholesterol, your body naturally produces less endogenous cholesterol, and the total overall amount is insignificantly changed . …” …More
  1. Dr. Ronald Krauss on LDL Cholesterol, Particle Size, Heart Disease & Atherogenic Dyslipidemia
  1. SNP’s PPAR-alpha & PPAR-gamma
  1. APOE4 – THE GENE THAT CAN’T HAVE SATURATED FATS
  1. Apolipoprotein E – ApoE explained: We all carry two copies of the APOE gene. The combination of alleles determines our ApoE3 genotype. There are six possible combinations (genotypes) for ApoE:
  • E2/E2
  • E3/E3
  • E4/E4
  • E2/E3
  • E2/E4
  • E3/E4
  1. Super-sticky ‘ultra-bad’ cholesterol revealed in people at high risk of heart disease: “… They found that MGmin-LDL is created by the addition of sugar groups to ‘normal’ LDL – a process called glycation – making LDL smaller and denser. By changing its shape, the sugar groups expose new regions on the surface of the LDL. These exposed regions are more likely to stick to artery walls, helping to build fatty plaques. As fatty plaques grow they narrow arteries – reducing blood flow – and they can eventually rupture, triggering a blood clot that causes a heart attack or stroke. …”
  1. CDEP: Regular Flossing Lowers Serum C-Reactive Protein
  1. Ketogenic Diet & C-Reactive Protein: A Marker of Inflammation
#32

I’m in the same boat e3/e4. I did the cac test and a CIMT. I follow Craig and Maria Emmerich Keto. After having the APO E gene test I was told to go low fat diet. I’m choosing to follow the advice of Craig. Especially since I’m feeling so much better. He says to NOT worry about cholesterol numbers while actively losing fat since we are releasing it (into our bloodstream?). Wait until weight stableizes and you’ve lost the fat. I’m giving it 6 months and then rechecking CIMT test. Insurance doesn’t pay for the CIMT and I didn’t need a referral (in my area of the US anyway). It’s $200-250 but I feel it will be worth it to know how my arteries are doing. IF they are building up more calcium I’ll have to look into other things. I have started to restrict saturated fat and I’ve gotten back into some form of exercise even though the Dr says I can eat 100% low fat and exercise for hours daily and it won’t be enough. She wants me on Repatha and says it’s been a huge help for people with e4. Time will tell. Good luck to you. I will read all the other post now. :wink:

(Bunny) #33

Very important to know, thank you for your post! :slightly_smiling_face:

(Cindy) #34

Hi Gabe, sorry I’m so slow to answer. Life got too too crazy for the last few months.

I got my full genome done at 23andme.com . I think it cost around $199 and it gave me complete genetic info that I could upload to 2 other websites to get even more info from. But it immediately gave me my status on APOE, BRCA, and several other important genes. I can now go to my doctor and show genetic evidence for some health issues I’ve had all my life, such as normal TSH and T4 but super low T3 because I genetically lack the enzyme that converts T4 to T3. It’s amazing how much info our genome gives us.

(Bacon is a many-splendoured thing) #35

How do we know that cholesterol is dangerous? The original research was done by force-feeding rabbits, which are obligate herbivores, animal cholesterol. I don’t see that as having valid implications for human beings.

Many studies of heart-attack victims show that the majority of them have lipid profiles in the normal range.

A number of epidemiological studies have shown an inverse correlation between LDL and cardiovascular risk, especially in the elderly and in women. While that doesn’t mean that LDL necessarily has a protective effect, it does tend to show that high LDL does not cause cardiovascular disease.

Studies of people with familial hypercholesterolemia show that about half never develop cardiovascular disease, despite their elevated lipid levels. The ones who do develop cardiovascular disease have been shown to have polymorphisms of fibrinogen and clotting factor VIII that make their blood much likelier to clot. Diamond and Ravnskov have proposed that such clotting anomalies, particularly in conjunction with glycated hemoglobin, may be the root cause of all cardiovascular disease.

So again, and seriously, what evidence do we actually have that links cholesterol to cardiovascular risk? The Minnesota Coronary Study, the Women’s Health Initiative, the Framingham study, and several others that were designed to show that cholesterol causes cardiovascular disease all failed to do so. Yet the persistence of the diet-heart hypothesis would tend to indicate that there is some evidence for it out there somewhere. Wouldn’t it?

(Bob M) #36

Another post by Dr. Malcolm:

In this, he goes over some studies where they test the risk factors in various calculators, and turns out the calculators are awful at determining risk (and they use these calculators to determine whether you should be on a statin!).

Dr. Kendrick states the following:

“On a similar note, a group of researchers in the UK decided to look at data gathered on 378,256 patients from UK general practices. They wanted to establish which factors were most important in predicting future risk. The paper was called ‘Can machine-learning improve cardiovascular risk prediction using routine clinical data?’”

Out of 48 factors, where does LDL come out? The 46th WORST factor. Only two factors were worse than it.

I think if you want to increase your odds, don’t be concerned with “high” LDL or “high” LDL-p. Instead, reduce stress, eat a low carb/keto diet, reduce any inflammation (no seed oils), if you can stomach aspirin, take it, exercise if you can and like it, etc. Have a support system, family if possible or if you’re religious, volunteer there. Do anything to reduce clotting, as that’s most likely what’s causing heart disease.

(Bob M) #37

The Repatha studies have been abysmal in overall death rate. In one study, more people died taking Repatha than died on placebo (not statistically significant, but still). And, like statins, Repatha probably does something other than lower LDL that is the true “benefit” (to the extent it has one).

(Bacon is a many-splendoured thing) #38

@ctviggen Thanks, Bob, for turning me on to the estimable Dr. Kendrick. Yet another reason to spent interminable amounts of time on the computer! But how can you resist gems like this:

Moving back to medical scientific research, which is more my area. Much of what is going on here is a complete disaster, but nutritional science is particularly awful. A complete mess. I have virtually given up reading any paper in this area as they just annoy me so much. I simply look at the authors involved, and I know what the paper is going to say. This does save time.

(Bob M) #39

I still agree with this…though I would probably drop off “as that’s most likely what’s causing heart disease”. Clotting is important, but some people do have atherosclerosis. (I was looking at ApoE4 and saw this thread.)

(Bacon is a many-splendoured thing) #40

Interestingly, Paul Mason is now maintaining that recent data show that blood clots (not LDL) actually cause atherosclerosis—in addition to doing damage by blocking narrowed arteries, of course. I want to learn more before I accept this blindly, but it’s an interesting take on the situation. Ravnskov and Diamond are on record as suggesting that if we can keep the rate of arterial damage low enough, it will heal before it becomes necessary to form a plaque on site. They, too, have suggested hypercoagulability of the blood as the proximate cause of cardiovascular disease.

(Robin) #41

That’s what I got from his video you shared, and since it would be good news for me, I am gonna run with that theory!

#42

Hi mugwump, I don’t know if I’m in the same boat, as I don’t know my current cholesterol levels (haven’t checked them since Oct 2022 - back then they were within normal range) and don’t know whether I could be a hyper responder or not. But my mom recently made me aware her cholesterol levels are higher than normal, her Serum cholesterol being 5.0 mmol/L, and she told me her mother were on medication for high cholesterol. Now she fears if her cholesterol doesn’t come down, she’ll be requiring heart surgery in the future, so she’s quite stressed, due to her doctors also having discovered calcification of an artery in her heart recently. Admittedly she’s less concerned about that than her higher than normal cholesterol.

So, to try and alleviate my mom’s concerns I’ve been, for the last few days, pouring over articles, studies, both on english sites and norwegian, Dave Feldman’s and Siobhan Huggins’ the cholesterol code, Dr. Nadolsky’s guestpost mirroring a lot of other articles I’d read, and it would be most tempting to just go with Dave Feldman’s (perhaps overly simplified) cautiously optimistic views and Siobhan Huggins’ views which mirror Dave’s, but 1) They are both avid advocates for the HF/LC WOE and not doctors, and 2) There is much opposing data to their optimistic views.

So in light of all this, of what I’ve read, and in light of what my mom has told me, I am doing a bit of a U-turn, from carnivore to how my ketogenic WOE was when I started. So … Replacing half the saturated fats (and more if needed) with polyunsaturated fats and foods rich in DHA. So green vegetables, and other keto friendly vegetables, berries, fruits (avocado, bell peppers, cucumber, cherry tomatoes, etc) nuts and seeds. This is basically how I was eating when I first started keto, before I fell in love with the simplicity of carnivore, and became addicted to whipped cream. I will be cutting down on the latter, whilst still having some in my morning coffee, as I’ve been consuming about 340-350ml cream daily.

Weight issues were never my troubles, as I was slim on my HC/LF WOE, and slim now on HF/LC WOE, so that matters not to me, but I have experienced streamlining, or a better word for it is body recomposition, so that is an added incentive for me, as well as the clear reduction in inflammation. So, like you, I would really like to continue my WOE long term, for my health.

I am sorry you attempted to adjust your WOE and this didn’t work, but could you share a bit more information about how you adjusted your WOE? On the cholesterol code you can read Dr. Nadolsky’s guest post which might be helpful to you. Sorry I can’t post the link now as I’m only on my phone.

(Bob M) #43

That’s a good take, I think. I’m just wondering that if you have atherosclerosis whether that provides a point at which a coagulation/clot could cause more of an issue than, say, in an area where there’s no atherosclerosis?

I’m fairly convinced that LDL is not that big of an operator in all of this. At least not nearly as big to fear it.

(Bacon is a many-splendoured thing) #44

I should think so, absolutely!

(Bob M) #45

It just has me wondering if there are two mechanisms going on in parallel: atherosclerosis; and coagulation/clotting. Even someone like myself, with low atherosclerosis as indicated by CAC scan, isn’t free because of clotting (which also concerns me about my high Lp(a), which might cause clotting). And everyone looks at atherosclerosis, but no one is looking at clotting. (Though, along with Paul Mason, I remember Dr. Kendrick discussing someone looking into this, a long time ago.)