Diet help. Please post what is working for you!

[mimik67]

Greetings all!

I know there is a lot of discussion here about what is best fore each person, based on tracking biomarkers. But are there any guidelines to follow? Upping plant foods (MIND Diet suggestions) and phytonutrients and lowering animal fat seems prudent. Avoiding processed and sugary foods does too. I would like to include more fish, but have histamine issues (I do recommend the new Umbrellux DAO enzyme! Really fantastic!). I am going to try to include wild caught fish frozen at sea,, similar to that found at Trader Joes) to reduce histamines.

I also try to follow a 12-16 hour daily fast.

I will have my baseline labs here to share soon, but wonder are things like avocado and nuts ok?

Thanks for posting dietary ideas here! (Like, what does your food day look like?)

[SusanJ]

Both avocado and nuts are fine. I have found avocado on some histamine "foods to avoid" lists. I can eat it just fine, even during seasonal allergy flares. YMMV.

[mimik67]

Thanks Susan!

Good to know. I can sneak in avocado too. I also posted on another thread that using Umbrellux DAO enzyme (the only DAO available in the US at this time) has really allowed me to eat some higher histamine meals (cooked tomato sauce, etc...) so that is exciting. I think it helps me get away with avocado on a nearly daily basis.

[TheresaB]

Mimik67

My husband (ApoE3/4 and a mother who died with dementia) and I (ApoE4/4) follow the dietary guidance of Dr Steven Gundry. If you use the advanced search function, you’ll see LOTS of posts on him (not everybody adheres to everything he says). We chose him because about 17 years ago, when Dr G switched career paths from cutting on people as a cardiothoracic surgeon to helping people restore their health through diet and supplements, he started testing for the ApoE4 gene (among many other tests) and he’s observed/followed this gene in thousands of patients. He’s aggregated his blood test observations to his medical training and to undergraduate research in human dietary evolution to develop the dietary advice he espouses today.

He’s written two books, “Diet Evolution” in 2009 and “Plant Paradox” published earlier this year (2017). He addresses diet in general in those books, not specifically ApoE4. He does address ApoE4 diet in this video from last year, “AHS16 - Steven Gundry - Dietary Management of the Apo E 4” https://www.youtube.com/watch?v=Bfr9RPq0HFg&t=36s

The diet has worked for us, our insulin sensitivity is high, our inflammation markers are low, our good cholesterol is up, triglycerides are down, organ function markers are good, etc. We still have areas we’re working on tweaking, but we feel we are on the dietary path that is right for us.

[mimik67]

Theresa thanks for posting.

I will look more closely. I cant take his products because my gut (and indirectly, Bladder-have Interstitial Cystitis) are both damaged from SIBO and CIRS/lyme. So those powerful antioxidant pills he sells are likely a no go for me. But I can look at his diet again.

[mimik67]

Theresa!
Thanks I watched the Gundry talk. What does a typical day look like for you? Is there a diet list anywhere? Do you eat oysters, clams, crab on a daily basis?? if so where do you get it? Also what is your source of protein if no dairy allowed and only 4 ounces of animal protein per day? Thanks! Also the resistant starch, good grief. Cant touch that stuff with my gut issues.

[swampf0etus]

It's worth noting that large LDLs are still atherogenic and probably more so in healthy individuals without metabolic syndrome.

Don't let anyone tell you that 'large and fluffy' LDLs are harmless, they are not. FH sufferers, who suffer heart attacks earlier in life because of their extremely high LDL levels, tend to have large LDLs.

For anyone interested, I can link an excellent talk on this subject with some excellent evidence to back it up.

[Julie G]

It's worth noting that large LDLs are still atherogenic and probably more so in healthy individuals without metabolic syndrome.

Yes, please show us your evidence, Swamp.

Mimi, here's a power point with a description of my current diet with pics. It also has a lot of superfluous information you can skip over .

March Immersion.pdf

[P45VA]

Juliegee, thank you for sharing your protocol. It seems a bit overwhelming at this point. I found out that I am APOE4/4 the week of my 72nd birthday and while I hate the thought, I may have to be as strict as you, given my age. I knew I as at risk for CVD as evidenced by my family history, so since retiring 6 yrs ago, I have been exercising 5 days a week, dropped 15 lbs and am watching my diet. My eldest sister has AD but I had attributed that to the fact that she was alcoholic, smoked since she was 13, never exercised and had a terrible diet. Now I suspect that it was more than that. No one else in the family with AD since they all died much younger.

Some questions: Bredesen says he recommends a "modified Ketogenic diet" but it looks like you are doing the full Keto. Is that the recommendation for most 4/4s.??
I was told that I could stay in Ketosis if I drank a cup of Bullet Proof Coffee before exercising. Is this true?
Can you please define some of the abbreviations in your Protocol:
SFA ; PCOS; NAC; NAD; SIRT1; ApoB; oil pulling?

Thank you so much!

[swampf0etus]

Yes, please show us your evidence, Swamp.

Hi Juliegee,

Here are a few studies/review papers with quotes;

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Clinical implications of discordance between low-density lipoprotein cholesterol and particle number

http://www.sciencedirect.com/science/article/pii/S1933287411000274

‘Although the ability to form strong inferences regarding biological mechanisms from epidemiologic studies may be questioned by some, it is evident that to the extent LDL-C does not provide a full accounting for LDL-related risk, incorrect conclusions may have been drawn regarding the potential importance of certain “novel” risk factors. One example is small LDL size, which is associated with atherosclerotic risk independently of LDL-C, but not LDL-P. The former observation led to the belief that small LDL particles are inherently more atherogenic than large ones, a conclusion not supported by recent analyses.’


Comparability of methods for LDL subfraction determination: A systematic review

http://www.sciencedirect.com/science/article/pii/S0021915008008976

‘In summary, the currently available literature does not provide adequate data about comparability in terms of test performance to choose one or another method to serve as a standard nor are data on comparability in terms of predicting CVD outcomes.’



Increased Small Low-Density Lipoprotein Particle Number
A Prominent Feature of the Metabolic Syndrome in the Framingham Heart Study

http://circ.ahajournals.org/content/113/1/20.short

‘Conclusions— Small LDL particle number is elevated in the MetSyn, increases with the number of MetSyn components, and most prominently is correlated with triglycerides and HDL-C. Whereas increased small LDL particle number identified the MetSyn with high sensitivity, a higher small LDL particle number was not associated with greater CVD event rates in people with the MetSyn.’


LDL particle subclasses, LDL particle size, and carotid atherosclerosis in the Multi-Ethnic Study of Atherosclerosis (MESA)

https://www.researchgate.net/publication/7017381_LDL_particle_subclasses_LDL_particle_size_and_carotid_atherosclerosis_in_the_Multi-Ethnic_Study_of_Atherosclerosis_MESA

‘However, after accounting for their inverse correlation, both LDL subclasses showed highly significant and independent associations with IMT, with a greater difference in IMT per large LDL particle compared with small LDL. Smaller LDL size was no longer significant after taking into account the particle concentrations of the two LDL subclasses and risk factors. Thus, small LDL was a strong confounder of the association of large LDL with subclinical atherosclerosis, which may explain the widely-held view that larger LDL size is less atherogenic. ‘

‘Moreover, both large and small LDL were significantly associated with carotid atherosclerosis in our study participants, whether or not they had diabetes mellitus. Our findings regarding the atherogenicity of both LDL subclasses have been confirmed in the VA-HIT trial, where both subclasses were significantly associated with coronary events once their correlation was taken into account.’

‘There are several mechanisms that may underlie the atherosclerotic effect of both large and small LDL. At both extremes of LDL size, there is decreased receptor-binding affinity for LDL receptors. Small LDL may be oxidized more rapidly and have been associated with endothelial dysfunction and metabolic dyslipidemia. In comparison, large LDL predominate in patients with familial hypercholesterolemia and those consuming high saturated fat diets. Large LDL have higher core cholesterol ester content, potentially delivering more cholesterol per particle to arterial walls, a speculation supported by our finding a greater IMT difference for large compared to small LDL on a per particle basis.’


Low-density lipoprotein size, pravastatin treatment, and coronary events.

https://www.ncbi.nlm.nih.gov/pubmed/11572739

‘RESULTS: Overall, the mean LDL size was identical in cases and controls (25.6 nm). In patients in the placebo group, large LDL predicted coronary events in models adjusted only for age.’

‘CONCLUSIONS: Large LDL size was an independent predictor of coronary events in a typical population with myocardial infarction, but the adverse effect was not present among patients who were treated with pravastatin. Identifying patients on the basis of LDL size may not be useful clinically, since effective treatment for elevated LDL cholesterol concentrations also effectively treats risk associated with large LDL.’

Systematic review: association of low-density lipoprotein subfractions with cardiovascular outcomes.

https://www.ncbi.nlm.nih.gov/pubmed/19349632

‘CONCLUSION: Higher LDL particle number has been associated with cardiovascular disease incidence, but studies have not determined whether any measures of LDL subfractions add incremental benefit to traditional risk factor assessment. Routine use of clinically available LDL subfraction tests to estimate cardiovascular disease risk is premature.”

Low-Density Lipoprotein Size and Cardiovascular Disease: A Reappraisal

https://oup.silverchair-cdn.com/oup/backfile/Content_public/Journal/jcem/88/10/10.1210_jc.2003-030636/1/jcem4525.pdf?Expires=1498589223&Signature=MMupL6yjzrjLSHroW3J8C6Ikcs6ILRfRDQlBOSS--eRq654RecFKNfpmt~OtqdkL~c5xzPVwIM5AkVoVSNcnN2yJcVNFXmZOAo~pq5NIrPXf7PZqdnRrkuK8ypiZ1INSaR61cs-30Qlzt0GbliVFE5twvYkFpkeZHMPLqDqYvgKgTHTxXhkhAn-6cwCGuftjy9v4ZcG-mx7xB7Xl4HRlT3PwzYuUxKVkyLzsM2bCEO9QW65Uujts1li5EPQ3v8D8p4VgdV2DgRASgLVhjjsMQBIixn2dP0EqVttN7r80UEmO3TR4ouHskSJmpjQrPZg~xegEwWQ5EPyRRisIUaEsAw__&Key-Pair-Id=APKAIUCZBIA4LVPAVW3Q

‘Mechanistic support for small LDL having a special atherogenicity depends on atherogenic actions being greater for small than for intermediate or large LDL. This case has not been proven, however. Both large and small LDL compared with intermediate size LDL have reduced affinity for the LDL receptor which clears LDL from plasma. Decreased clearance of these forms of LDL by the liver and steroidogenic tissues is thought to lead to increased uptake by the arterial wall’

‘Thus, large and small LDL are atherogenic, and it is not possible to judge which if any is more harmful, overall.’

‘Although this was found in experiments in rabbits (34), a study of transvascular transport of LDL in vivo in humans did not find a correlation with LDL size. This finding suggests that for every unit of time, large LDL is just as likely as small LDL to enter the arterial intima. Because large LDL has more cholesterol ester than small LDL, a large LDL particle would deposit more cholesterol into plaque than small LDL… Thus, it appears that both large and small LDL share undesirable characteristics’

‘Interestingly, after adjusting for plasma triglyceride and HDL cholesterol levels, large not small LDL size trended toward predicting CHD along with low HDL levels. This observation in the Japanese cohort agrees with results in U.S. and Canadian patients who had had a MI. Large, not small LDL, was a strong predictor of CHD death and recurrent MI, significant in both multivariate and univariate analyses.’

‘Conclusions: The burden of proof for any newly proposed risk factor is that it must add significantly to risk assessment by existing measurements, or that it is equivalent but more economical. LDL subtyping does not meet either of these expectations. Metabolic studies demonstrate that large and small LDL subtypes are atherogenic. In as much as any type of LDL is contained in the plasma total LDL concentration, the standard clinical measurement of risk, all LDL types should be viewed as harmful. The best indicator of response to lipid therapy is a reduction in the plasma concentration of atherogenic lipoproteins, as conventionally measured by LDL and triglycerides, but alternatively by non-HDL cholesterol or apo B.’

******

Some of the above papers, and more besides, are covered in this video, which puts a lot of context around the small/large LDL argument. I highly recommend it, but you need to skip forward to around 10 minutes if you want to skip his initial destruction of Dr Lustig.

https://youtu.be/_wmidN8rYkU?list=PLv3Q ... 2oYyAFZDBA

I also recommend the other Cholesterol Confusion videos in that series.