10

votes

Potential hacks resolve heart/brain dilemma for APOE4?

Answered on September 12, 2014
Created December 01, 2011 at 12:21 AM

Looking for some suggestions on hacks to resolve what appears to be a heart/brain dilemma associated with apoE4 allele?

Experimenting on myself as safer/quick guinea pig for my father. He has been lifelong sufferer of minor Essential Tremor, but neurodegeneration accelerated rapidly following heart bypass surgery nearly 4 years ago. ET got bad enough that he chose to have a Deep Brain Stimulation implant ~12 months after heart surgery. Neurodegeneration continued resulting in falls, muscle weakness, etc. and a likely diagnosis of a 'Parkinsonism' called Progressive Supranuclear Palsy.

Long journey since <12 mos ago my father's supposedly positive blood work with 'great' LDL = 27 mg/dL just sounded like an anomalous clue when I learned that he started Lipitor for the first time following heart surgery. Found my way through all the statin skeptic literature (e.g. Graveline, Seneff, Deans) where it became very clear to me that cholesterol depletion was a very plausible cause of the overall rapid neurodegeneration. Should probably note here that I also stopped Lipitor immediately upon realizing this about 9 months ago.

About 9 months ago, due to serendipity alone (sequenced family genes as 'gift' for son studying biochemistry undergrad), we discovered that both my father and myself are carriers of a single apoE4 allele, which many of you here know has a large impact on lipid transport and metabolism. This gave me understanding of not only the potential cause of the problem, but led me to believe that by hacking my own health I can come up with recommendations for my dad (to at least arrest the decline). I've finally convinced him to get off the g****mn Lipitor so save his brain and not worry about his heart.

Following clues from books, scientific papers, and web sluthing (thanks esp AHS for bringing so many clues to one place!), I've been drifting to paleo diet for ~ 6months and presently largely paleo plus some 'safe' carbs (a-la Jaminet). Especially since cutting out wheat totally about 3 months ago (thanks Dr. Davis), I quickly lost 15 unnecessary lbs (although never heavy), and frankly feel much better than I have in decades (age 50).

I managed to find cholesterol numbers for both myself and my father from just prior to beginning Lipitor at a time where we were both likely eating a fairly typical American diet. Baseline numbers were very similar...

Self: TC=205, LDL=125, HDL=37, TriG=216

Father: TC = 196, LDL=118, HDL=30, TriG=240

FWIW, 2 other number sets maybe have clues...

Father on on 40 mg/d Lipitor: TC=129, LDL=27, HDL=45, TriG=258

Self on Pritikin (mid 90's): TC=184, LDL=127, HDL=36, TriG=106

From all of my reading, I had formed a hypothesis that my low-carb/high fat diet should have a large effect on my own cholesterol profile: (a) LDL likely up in count, (b) HDL up, (c) TriG's down, and (d) presence of LDL pattern A (i.e. large and fluffy). I also hypothesized e) low CRP. Got VAP test results yesterday from samples taken last Friday (some risk of Thanksgiving cheats?), but indeed I got positive confirmation of a, b, and c, but d (most important) is mixed, and e (CRP) not clear as follows:

Total LDL = 194

LDL4 = 34.6

LDL3 = 100.7

LDL2 = 22.7

LDL1 = 21.9

LP(a) = 5

IDL = 9

Pattern = A/B

Total HDL = 47

HDL2 = 8

HDL3 = 39

Total VLDL = 21

VLDL1+2 = 9.3

VLDL3 = 11

Total Cholesterol = 262

TriG = 97

Remnant Lipoproteins = 20

apoB = 136

apoA1 = 146

CRP = .78 mg/L

So overall, positive news of impact of diet on HDL (except maybe not enough HDL2?) and TriG (clear benefit of low carb), but mixed results in the A/B news on LDL particle size (with full caveats re Masterjohn's warnings on VAP size accuracy).

Although I feel great, my sense is that this profile is not super-healthy yet. From both prior Pritikin diet and Paleo today clear that cutting carbs cuts TriG's. But referencing the banter between Dr's Kruse and Davis in Trackyourplaque comments in August, simply cutting out fats doesn't seem right either. I tend to agree with dr. Kruse because the logic of Seneff that high absolute cholesterol is actually neuroprotective for APOE4's makes sense (i.e. because by body sucks at transporting lipids across BBB, I need more lipid in my blood). But for best heart health, feels like I need to increase the size of those LDL particles?

Finally, maybe worth noting that am already on a men's multivitamin and Vitamin K2 (Mk-7) (Masterjohn inspired).

So, I think my question to the Paleohack community is... as APOE4, since I want plenty of cholesterol in my blood for brain health, but I want that cholesterol to have a heart-healthy profile, what other hacks should I try to improve my own cholesterol profile? ...such that if I achieve success I can give clear and simple recommendations to help my Dad.

Thanks hackers for any suggestions!

Cbdc8318738324492f2d5918868ce4c9

(1211)

on August 31, 2012
at 11:39 PM

Russ, I agree completely. It seemed odd to me their healthy example had overweight BMI and high trigs. I think I have a similar dilemma as you where my TC=400 on 50% fat (mostly SF) and TC=225 on low fat.

A1081af52b61372dbb3ed572d88968f4

(425)

on August 31, 2012
at 07:20 PM

MarkES, Read the linked "Omega-3..." reference. Good support for keeping oxidation potential low, but following the link to abstract (20) on APOE4 on Native Americans eating their natural food was unconvincing (at least for me). Conclusion seemed predicated on cholesterol status, not actual risk reduction. I ate Pritikin-style years ago and indeed found I was able to drop my LDL significantly, but not clear that is necessarily best for health. Still, very good thread on merits of oxidation status, which is good food for further thought.

A1081af52b61372dbb3ed572d88968f4

(425)

on August 31, 2012
at 04:54 PM

MarkES - Checked back randomly on this old question today, and very cool to see a new and such well thought out answer. Thanks! Will do some additional reading and maybe come back for discussion. My Dad recently lost his battle against the disease which I believe is rooted in this issue, so I have a renewed sense of commitment to keep learning so as to avoid the same fate.

A1081af52b61372dbb3ed572d88968f4

(425)

on February 24, 2012
at 04:40 PM

Jeff, Thanks. Indeed interesting. Just completed a month of moderate HIIT weight lifting plus dairy elimination, and drew blood for workup this morning. So will be interesting to see if it moved the needle on my HDL as in this paper. One thing that has me intrigued is that this paper seems to indicate net time in high intensity training is the driving variable, but not clear the study was clearly designed to look for 'more' vs 'optimum.' In any case, one thing I might play with myself is increasing the time in the gym during the week. Gives me another variable to play with - Thanks!

3864f9a2af09b1b447c7963058650a34

(3703)

on February 20, 2012
at 05:00 AM

Very N I C E !!! Thanks!!!!! I've been wondering the link betw low hdls and cortisol... The authors said simething really helpful for me ' High-intensity prolonged exercise has been shown to increase plasma adrenocorticotropin53,54 and, hence, cortisol. HDL cholesterol may be the preferred lipoprotein as a source for adrenocorticosteroid synthesis.55 Indeed, although glucocorticoid therapy often has adverse effects on the cardiovascular system, including dyslipidemia,56 corticotropin seems to contribute to the increase in HDL cholesterol level.57'

Cdb9e467dac06a12c515ddfd18a4cdda

(140)

on December 08, 2011
at 01:17 AM

Thank you guys also for the discussion. We all have our own opinion and without DEFINITIVE evidence we all speculate as best we can, hopefully discussions like this help us bring us closer to our goals. My goal is longevity.

A1081af52b61372dbb3ed572d88968f4

(425)

on December 07, 2011
at 12:01 PM

Hans and Grace - just want to go on record that you guys are amazing! I have so much to learn and am thankful for your engagement!

Cdb9e467dac06a12c515ddfd18a4cdda

(140)

on December 07, 2011
at 03:53 AM

....athletes and their high carbohydrate diet. While in the short-term it is great for performance in the long-term (as we would probably all agree) a high carbohydrate diet (especially with caloric excess, regardless of activity level) is bad. This is my spiel for now, after exams I'll come back and look over the various posts you guys have provided. Thanks.

Cdb9e467dac06a12c515ddfd18a4cdda

(140)

on December 07, 2011
at 03:52 AM

...antagonistic pleitropy and disoposable soma theory we should be keeping these down in the long-run to prevent ourselves from experience the pleiotropic effects of these factors in old age, esp middle age where most of these chronic illnesses manifest. It is quite possible that in the short term a high-fat diet with 50/50 MUFA/SAFA could be beneficial but my main focus in what will happen to me when I'm 70 or 80 and to be healthy at that age (and hopefully live to 100 or more) the body needs to be maintained in good condition. If we take an even shorter term outlook, we could look at....

Cdb9e467dac06a12c515ddfd18a4cdda

(140)

on December 07, 2011
at 03:50 AM

Thanks for all the wishes of good luck. There does seem to be a Antagonstic Pleiotropy theory with regards to ApoE (http://hanswuhealth.blogspot.com/2011/11/antagonistic-pleiotropy.html) however the is still tentative but not without evidence. If this application of the theory applies to E4 then keeping cholesterol levels for those with E4 may be beneficial in the long-run. E.g. with testosterone supplementation in the elderly they experience increased risk of CVD/stroke while those of younger age supplemented to physiological levels experience benefit. However if we are to glean anything from

3864f9a2af09b1b447c7963058650a34

(3703)

on December 07, 2011
at 03:24 AM

Hans, I've been very curious about the J-curves in epidemiological studies. What you see may be the high carb consequences. Have you read these: (1) http://www.carbohydratescankill.com/3248/jcurve-hypotheses-hyperglycemia-culprit-2-of-2?utm_source=feedburner&utm_medium=feed&utm_campaign=Feed%3A+CarbohydratesCanKill+%28Carbohydrates+Can+Kill%29 and (2) http://healthydietsandscience.blogspot.com/2011/04/high-cholesterol-levels-boost-memory.html [esp Apo E4]

3864f9a2af09b1b447c7963058650a34

(3703)

on December 07, 2011
at 03:22 AM

which we know in nearly all RCTs extend life (unless the study used inferior omega-3 containing pesticides,mercury, POPs, PCBs, other environmental contaminant). Animal fats would also contain stigamesterol (plant sterol), vitamin A, retinoids, carotenoids, tocopherols and CoQ10/ubiquinone and menaquinones. This mimics the cholesterol rich and omega-3 abundant sources from the ocean and the littoral.

3864f9a2af09b1b447c7963058650a34

(3703)

on December 07, 2011
at 03:17 AM

Also I think the biggest causes of death were: predators, parasites, climate, drought, hunger (and partners -- fighting, jealousy, property, etc). SFAs may have helped boost immunity to fight infections as well stay strong against predators... Monounsaturated fats just do not improve the function of HDLs and the immunity the identical way that SFAs do. The MCT oil trials prove this to me, even with high carb (cupcake) vehicles for the SFA (coconut oil is predominantly MCT, medium chained). SFA in animal fats -- ghee, butter, cream, yolks, brain, fat, marrow -- also come with the omega-3s

3864f9a2af09b1b447c7963058650a34

(3703)

on December 07, 2011
at 03:12 AM

Russ, It is ALL VERY FASCINATING!! Animal fat is 50/50 mono v. saturated. When I think about humans migrating beyond the marine shores toward the steppes and inland areas, basically the sources of cholesterol, omega-3 fats and minerals dramatically decline... to survive these had to be upregulated in both production and retention, as well as decreased metabolism and elimination... this is like drugs too. I do concur -- I think in E3/E4s there may be a preference for the SFAs because the animal fats are more nutrient dense.

A1081af52b61372dbb3ed572d88968f4

(425)

on December 06, 2011
at 01:13 PM

Grace, Read the 2004 Moreno paper you linked on LDL Size, Diet, and APOE. Quite good - thanks. Once again clear that carbs are particularly bad for APOE4's. I am somewhat intrigued by Table 5 that shows avg LDL size is higher for APOE3/4's compared to 3/3's and 3/2's regardless of diet? Wonder if there is meaning? Also appears that 3/4's had slight preference for Sat Fat (SFA) vs Mon Unsat Fats (MUFA)? Interesting to note that regardless of alleles, either SFA or MUFA generates significantly more 'Pattern A' profiles than carbohydrate diet. May dig deeper yet into the data.

3864f9a2af09b1b447c7963058650a34

(3703)

on December 06, 2011
at 11:42 AM

1 million upvotes

3864f9a2af09b1b447c7963058650a34

(3703)

on December 06, 2011
at 11:11 AM

thanks so much for your question and for Hans honest reply. It is a much needed discussion with all the evidence presented and differrent spectrum of hypotheses... we're all different and have diff Achille's heels!

A1081af52b61372dbb3ed572d88968f4

(425)

on December 06, 2011
at 01:16 AM

Hans. Read the abstract as the full paper is behind a pay wall. However, hard to see how they go to the stated conclusion. Abstract says study was ex-vivo oxidation test, not atherosclerosis test. My understanding of the small particle theory is that it takes both oxidation and small particles to induce athersclerosis, as the small particle size is required for penetrating the pores/cracks in the inflamed endothelial lining. Perhaps I understand wrong (or the theory itself is wrong?)?

A1081af52b61372dbb3ed572d88968f4

(425)

on December 06, 2011
at 12:44 AM

Still lots of learning for me, but just want to say what a spectacular discussion you're having with me and each other, Hans and Grace. Thanks for taking the time. We'll see where this goes, and deeply appreciate you're sharing. Han's, good luck with med school exams!

3864f9a2af09b1b447c7963058650a34

(3703)

on December 05, 2011
at 12:12 AM

E4 is very important. It is rare in the general population except northern Europe and aboriginal subpops (Native Americans, etc). However, for heart disease it can be a large percentage of victims... imho E4 is more adapted to HG lifestyles -- more exercise, more low-GI foods, more protein/meat/organs/marrow.

3864f9a2af09b1b447c7963058650a34

(3703)

on December 05, 2011
at 12:07 AM

Hans, Good luck with your med school exams!!! You are going to make a wonderful physician in the future I believe because you leave no rocks unturned and you critically evaluate the evidence. That is a wonderful new website (like the daily food/supp log) -- awesome evolution... I'll have to update my bloglist...

3864f9a2af09b1b447c7963058650a34

(3703)

on December 05, 2011
at 12:04 AM

My hypothesis is that E4 was 'selected' in mountainous and inland terrain (eg northern europe/china) which were less saturated with marine minerals essential for brain development and reproductive function (iodine, zinc, magnesium, etc). pubmed studies support this line of reasoning. Some of the studies for metal toxic accumulation and apoE4, I listed on this thread: http://paleohacks.com/questions/69109/autism-and-paleo-tips-and-links-do-you-have-a-favorite-resource-not-an-a/69493#69493

3864f9a2af09b1b447c7963058650a34

(3703)

on December 05, 2011
at 12:04 AM

I agree too that the ApoE4 pathogenesis in AD is beyond cholesterol. E4 functions as a 'chelator' of metals -- iron, zinc, magnesiu, lead, mercury, etc. E4 has less of this function compared with E2 and E3.

3864f9a2af09b1b447c7963058650a34

(3703)

on December 04, 2011
at 11:59 PM

For FH -- on NMR lipoprotein analysis, the 'death band' is for the smallest, densest LDL particle LDL-IVb. The larger the band, the larger the incidence for coronary mortality. Yes FH have predominance of lbLDL but they still have sdLDL and the absolute and relative quantity define their risk. Google 'animal pharm death band'.

3864f9a2af09b1b447c7963058650a34

(3703)

on December 04, 2011
at 11:57 PM

Hans, Yes I think your right -- sometimes lower LDL overall concomitantly with low TG (and high HDL) is a good bioindicator. LDL goes up also with hypometabolic pathogenic states like hypothyroidism. I think fiber that feeds the good gut flora also help to control LDL in multiple ways, studies indicate. Did you read the Dreon Krauss et al study in apoE4? http://jn.nutrition.org/content/134/10/2517.full.pdf

Cdb9e467dac06a12c515ddfd18a4cdda

(140)

on December 04, 2011
at 09:34 PM

Hi Russ, While the mechanistic reasoning makes sense with regards to Seneff and Masterjohn I am inclined to disagree. ApoE4 plays a larger role in AD pathogenesis then just cholesterol. When I have time I'll expand on it (studying for exams right now).

Cdb9e467dac06a12c515ddfd18a4cdda

(140)

on December 04, 2011
at 09:29 PM

Hi Grace, yes I am. My blog is currently http://hanswuhealth.blogspot.com/ I have read many of Krauss' work for me both the pathogenesis and outcome research coincide so I find it very very hard to accept it all comes down to particle size. I know I am referring to a pathologic state here, however in FH they have large particles: http://www.ncbi.nlm.nih.gov/pubmed/11718692 If the argument is that large LDL is good and small is bad (which I am inclined to agree with), then wouldn't having less LDL overall with low TG lead to less overall sdLDL as compared to higher LDL levels?

A1081af52b61372dbb3ed572d88968f4

(425)

on December 03, 2011
at 03:26 PM

Hans, Read the paper. Great to see that they actually did track by APOE4. May be noteworthy that APOE4's was almost twice as high as the general population (28% vs 15%). Too bad they didn't measure TC/LDL during stay, nor whether statins started after admin. It certainly confirms that APOE4 is associated with AD (but less so with other dementia's), but at face value, doesn't seem like the data tell us much about causal direction. Data seem consistent with Seneff where higher TC in APOE4 is an attempted protection mechanism for the brain, and Masterjohn's note APOE4 prefer to carry LDL.

A1081af52b61372dbb3ed572d88968f4

(425)

on December 03, 2011
at 01:28 PM

Hans, Grace, Thanks - good discussion. I'm off to read the DCGD 2009 paper and will revert with further thoughts or questions.

3864f9a2af09b1b447c7963058650a34

(3703)

on December 03, 2011
at 08:13 AM

Russ (or anyone with E4): you need to clear the excess metals out of the body that have accumulated from modern, neolithic exposures over time. Don't be like me, my children or BA88 at this thread -- http://paleohacks.com/questions/80393/what-sort-of-damage-will-30-days-of-anti-biotics-do/80586#80586

3864f9a2af09b1b447c7963058650a34

(3703)

on December 03, 2011
at 08:04 AM

Keep digging. Read all the work of Ronald Krauss at CHORI. The LDL is high in the studies you cite due to elevated LDL particles which are mostly comprised of sdLDL, not lbLDL (large buoyant). You'll know because the TG/HDL ratio will be >> 1.0. Low HDL is a screaming indicator of pattern 'B' sizing and oxidation/inflammation. I hope that helps.

3864f9a2af09b1b447c7963058650a34

(3703)

on December 03, 2011
at 08:03 AM

HDL is a more 'honest' marker because most pharmaceuticals at this time cannot statistically modify (except Niaspan, fish oil and vitamin D). TGs go down with statins esp the potent ones Crestor and Lipitor, but besides the multitude of downstream problems with statins, these potent statins also raise the incidence of frank T2DM. Bad.

3864f9a2af09b1b447c7963058650a34

(3703)

on December 03, 2011
at 08:01 AM

I apologize for the flaming.

3864f9a2af09b1b447c7963058650a34

(3703)

on December 03, 2011
at 08:01 AM

Keep digging. Read all the work of Ronald Krauss at CHORI. The LDL is high in the studies you cite due to elevated LDL particles which are mostly comprised of sdLDL, not lbLDL (large buoyant). You'll know because the TG/HDL ratio will be >> 1.0. Low HDL is a screaming indicator of pattern 'B' sizing and oxidation/inflammation. I hope that helps.

3864f9a2af09b1b447c7963058650a34

(3703)

on December 03, 2011
at 07:58 AM

Are you hans wu of specific strength??????!

Cdb9e467dac06a12c515ddfd18a4cdda

(140)

on December 03, 2011
at 03:38 AM

Dement Geriatr Cogn Disord. 2009;27(1):42-9. Epub 2009 Jan 8. Serum lipids are related to Alzheimer's pathology in nursing home residents. Lesser GT, Haroutunian V, Purohit DP, Schnaider Beeri M, Schmeidler J, Honkanen L, Neufeld R, Libow LS. (briefly disccused here: http://hanswuhealth.blogspot.com/2011/11/cholesterol-targets.html) You talk about the brain, but as studies like the one I quote here and others, they show that high cholesterol is detrimental, regardless of ApoE genotype. These studies go back 10 years thus avoid reverse causation.

3864f9a2af09b1b447c7963058650a34

(3703)

on December 03, 2011
at 01:55 AM

Same research also discussed by DR. Larry McCleary, a neurosurgeon, in 'Brain Trust'

3864f9a2af09b1b447c7963058650a34

(3703)

on December 03, 2011
at 01:54 AM

This is one of the presentations on the evidence for preserving and optimizing the brain-gut-body axis and neurologic function, Dr.Datis Kharazzian. http://www.slideshare.net/CyFairLIFE/renewing-the-aging-brain

3864f9a2af09b1b447c7963058650a34

(3703)

on December 03, 2011
at 01:07 AM

Conventional 'wisdom' is killing us. Good luck Russ.

A1081af52b61372dbb3ed572d88968f4

(425)

on December 02, 2011
at 01:50 PM

But my point previously was that Dr. Davis' logic doesn't make biochemical sense unless you address the heart issue in isolation. In other words, the key issue for APOE4 in the dilemma is that the brain needs the extra cholesterol - i.e. reducing it may improve heart health, but seems almost guaranteed to kill the brain. As noted, the big clue for me was the incredibly low LDL number for my father. There may be still better ways, but the first hypothesis seems to be to keep cholesterol high, but increase LDL size (and HDL fraction)?

Cdb9e467dac06a12c515ddfd18a4cdda

(140)

on December 02, 2011
at 05:15 AM

This is also my interpretation with regards to Alzheimer's. Heck even with Dr Davis (TrackYourPlaque) has been changing his mind with regards to E4:http://www.trackyourplaque.com/blog/2011/07/the-exception-to-low-carb.html While before he advocated the same diet for all genotypes. Based on my understanding of ApoE4 metabolism and function SAFA should be limited.

Cdb9e467dac06a12c515ddfd18a4cdda

(140)

on December 02, 2011
at 05:10 AM

Well my interpretation of the evidence is that a lot of short-term (<5 years, heck maybe even 20 years) results are due to reverse causation. For e.g. [Epidemiology. 1997 Mar;8(2):132-6.Time trends in serum cholesterol before cancer death.Sharp SJ, Pocock SJ. Am J Epidemiol. 1992 Jun 1;135(11):1251-8.Short- and long-term association of serum cholesterol with mortality. The 25-year follow-up of the Finnish cohorts of the seven countries study.Pekkanen J, Nissinen A, Punsar S, Karvonen MJ.] Thus in terms of cancer, latent cells may be causing decreased cholesterol.

A1081af52b61372dbb3ed572d88968f4

(425)

on December 02, 2011
at 02:02 AM

Just finished the QJM paper. Although abstract was promising re APOE4, paper is more indirect and ambiguous - i.e. observationally proposing that rising Alzheimer's in APOE4's on statins is simply due to fact that they're not dying younger from heart disease. Maybe is irresolvable, but seems to be that there is a biochemical optimum that is good for both?

A1081af52b61372dbb3ed572d88968f4

(425)

on December 02, 2011
at 12:47 AM

Hans, I truly appreciate the pushback, but having read, it doesn't make wholistic sense. Whereas I appreciate the negative impact of APOE4 cholesterol profile on heart health, lowering cholesterol seems exactly the wrong thing to do for the brain. This link does not seem to address that issue. I note that I had a great additional find yesterday in a new paper in the Oxford Journal QJM just published online entitled "Cardiovascular Disease prevention and the rise in dementia" that seems to be now providing solid evidence of the problem in following this strategy in APOE4's.

A1081af52b61372dbb3ed572d88968f4

(425)

on December 02, 2011
at 12:43 AM

Thanks. Will check out Jonathan. Grace - Agree Seneff is key here. She's the one that started connecting the dots that led me in this direction.

A1081af52b61372dbb3ed572d88968f4

(425)

on December 02, 2011
at 12:41 AM

Dex. Thanks. Clear steer. Glad you agree the high cholesterol itself is a good thing - seems pretty clear based on biochemistry. Now just need to change the size distribution. Will read and try the reset protocol and keep watching numbers. Yep - got my Mom to start my Dad on coconut oil yesterday and my wife and I are going up next week to begin their new life on paleo diet :-) Will provide updates as available.

3864f9a2af09b1b447c7963058650a34

(3703)

on December 01, 2011
at 08:37 AM

Add'l trackyourplaque is heavy into lowering LDL to brain damaging and testosterone depleting levels of 60 and below. this is insane. Use of statins and other pharmaceuticals are highly supported to reach the LDL goal and this is dubious as well as unsupported by medical literature. Seneff has great resources and also has been interviewed by Jimmy Moore, check out her potcast; smart chick!!

3864f9a2af09b1b447c7963058650a34

(3703)

on December 01, 2011
at 08:21 AM

Pritikin died of suicide, depression and had cancer... Hhhhhmmmhhhh...

3864f9a2af09b1b447c7963058650a34

(3703)

on December 01, 2011
at 08:20 AM

Right on Dex!!!

3864f9a2af09b1b447c7963058650a34

(3703)

on December 01, 2011
at 08:19 AM

1 million downvotes. They data does not support this. This is why parkinsons, heart disease, western civilization diseaeses and dementia/alzheimers are epidemic.

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7 Answers

4
3864f9a2af09b1b447c7963058650a34

(3703)

on December 03, 2011
at 01:29 AM

To Hans,

It is not that DR.Davis is incorrect but the litmus is that it is VERY RARE at TrackYourPlaque for heart plaque regression. One has to ask WHY?????!! wtf why???

http://blog.sethroberts.net/2011/08/04/how-rare-my-heart-scan-improvement/

Clearly the low chol, low sat fat, high canola/n-6 PUFA and high doses of pharmaceuticals at the website and advocated by the cardiologist have factors in this. I was 2 yrs at the site and case after sad, pathetic case of PROGRESSION every year is evidence to me that low chol, low sat, high canola/n-6 and pharmaceuticals are not recipes for success. For apoE4, FHC, or anybody with a risk factor for heart disease (which is nearly everyone since it is either #1 or #2 killer in the world).

Seth on the other hand consumes an insane amount of butter (pastured, high in K2, cholesterol and sat fat), low carb, pork belly and fermented foods and flaxseed/oil.

-G

3864f9a2af09b1b447c7963058650a34

(3703)

on December 03, 2011
at 01:54 AM

This is one of the presentations on the evidence for preserving and optimizing the brain-gut-body axis and neurologic function, Dr.Datis Kharazzian. http://www.slideshare.net/CyFairLIFE/renewing-the-aging-brain

3864f9a2af09b1b447c7963058650a34

(3703)

on December 03, 2011
at 01:55 AM

Same research also discussed by DR. Larry McCleary, a neurosurgeon, in 'Brain Trust'

3
Cbdc8318738324492f2d5918868ce4c9

(1211)

on August 25, 2012
at 03:45 PM

I've recently learned I'm APOE4/3 and so this is an interesting question for me.

Not really new in this forum, but maybe improved CRP is more critical for ApoE4 through better omega-6:omega-3 ratio, exercise, and stress management.

Chris Kresser suggests oxidation as common cause for heart/brain issues and ApoE4 variant is related to vitamin D and folate:

ApoE4 carriers have a higher risk of Alzheimer???s and dementia, and they have a higher risk of heart disease. And you know, the conventional view is that they have that higher risk because of higher levels of LDL, but actually the most recent research and our recent understanding of what causes both Alzheimer???s and heart disease suggests that the reason they have a higher risk is that ApoE4 carriers are more susceptible to oxidative damage and inflammation, and it???s the oxidation of the LDL particle that???s the common thread in both increased risk of heart disease and increased risk of Alzheimer???s and dementia. So this ApoE4 mutation that helps dark-skinned people produce vitamin D and also lighter-skinned people in northern latitudes produce enough vitamin D wouldn???t have been a problem in an environment where oxidative risk factors were low, like people weren???t smoking, they were getting plenty of exercise, their stress levels were managed, they weren???t eating a lot of omega-6 polyunsaturated fat that has the potential to oxidize. But in this modern world where the modern lifestyle is full of oxidative risk factors, then this ApoE4 mutation has a dark side. So I just find it fascinating. I mean, it???s like our genetic code is doing the best that it can to make us healthy and protect us from harm, but the lifestyle that we???re living keeps kind of throwing a monkey wrench in the plan.

This article had some interesting info, even though there was some convention wisdom to sift through. And I would have liked to see other healthy population examples than Pima Indians, which are not in my near ancestry. One interesting thing is Pima Indians had high trigs and overweight BMI: "Their age was 38+/-17 years and the BMI 25.7+/-4.5 kg/m2. Plasma cholesterol, triglycerides, LDL C and HDL C were 165+/-29.6, 126+/-83, 98+/-26 and 42+/-12.7 mg/dl respectively."

Omega-3s, ApoE Genotype and Cognitive Decline

Conclusion ??? A Healthy Redox Balance Should Allow Carriers of ApoE ??4 to Benefit from Omega-3s A number of studies have shown that the APOE ??4 allele does not promote cardiovascular disease or dementia progression in individuals in developing countries

The Moreno paper you and Grace discussed was pretty interesting, too. It was counter-intuitive that CHO had the best LDL-size at 26.47 vs. SFA 26.38, MUFA 26.26? Though lower HDL and small sample size.

Russ Dec 6 at 13:13:

Grace, Read the 2004 Moreno paper you linked on LDL Size, Diet, and APOE. Quite good - thanks. Once again clear that carbs are particularly bad for APOE4's. I am somewhat intrigued by Table 5 that shows avg LDL size is higher for APOE3/4's compared to 3/3's and 3/2's regardless of diet?

I wonder the significance to the decreased bile acid synthesis and if it's beneficial to improve that? Plus the faster LDL clearance for apoE4 seemed counter-intuitive, as well.

The apoE4 variant has been associated with increased LDL production from VLDL, increased uptake of postprandial lipoproteins, increased intestinal absorption of cholesterol, decreased bile acid synthesis, and faster LDL clearance from plasma compared with the apoE3 or apoE2 variants (6???8).

Thanks, Mark

A1081af52b61372dbb3ed572d88968f4

(425)

on August 31, 2012
at 07:20 PM

MarkES, Read the linked "Omega-3..." reference. Good support for keeping oxidation potential low, but following the link to abstract (20) on APOE4 on Native Americans eating their natural food was unconvincing (at least for me). Conclusion seemed predicated on cholesterol status, not actual risk reduction. I ate Pritikin-style years ago and indeed found I was able to drop my LDL significantly, but not clear that is necessarily best for health. Still, very good thread on merits of oxidation status, which is good food for further thought.

A1081af52b61372dbb3ed572d88968f4

(425)

on August 31, 2012
at 04:54 PM

MarkES - Checked back randomly on this old question today, and very cool to see a new and such well thought out answer. Thanks! Will do some additional reading and maybe come back for discussion. My Dad recently lost his battle against the disease which I believe is rooted in this issue, so I have a renewed sense of commitment to keep learning so as to avoid the same fate.

Cbdc8318738324492f2d5918868ce4c9

(1211)

on August 31, 2012
at 11:39 PM

Russ, I agree completely. It seemed odd to me their healthy example had overweight BMI and high trigs. I think I have a similar dilemma as you where my TC=400 on 50% fat (mostly SF) and TC=225 on low fat.

3
3864f9a2af09b1b447c7963058650a34

(3703)

on December 01, 2011
at 08:00 AM

I have a couple posts on apo E4 (google animal pharm apo e4) -- I entirely agree with Kruse. low carb, high fat are the way to go, esp if someone is a carrier for an E4 allele or both (!!) which is/are the least agriculture/carb tolerant folks.

Also please check out by my buddy Jonathon Carey Tripleyourhdl.com (he presented a poster at AHS) -- he is heteroxygous for FHC (familial hypercholesterolemia) with premature death all over his family tree. He is doing wonderfully and no evidence of heart disease on a low carb, high saturated fat + fiber diet. His blog reports his IBS is cured (guar gum).

if you cut saturated fat from diet, you are preventing the immune system and the brain from growing and being maintained at its optimum. The proble with trackyourplaque is that it is very heavy on things proven in medical literature that promote braing and heart degeneration:

-low cholesterol diet because cholesterol is the precursor of neurons, cell membrane and cell to cell communication, and all of our sex and vit D hormones and cortisol

-high canola oil (omega six) which causes rampant inflammatory disease

-low saturated fat because saturated fatty acids are necessary for PPAR and HDL2 and large buoyant pattern A

would love to hear your dad's progress in the future.

3864f9a2af09b1b447c7963058650a34

(3703)

on December 01, 2011
at 08:37 AM

Add'l trackyourplaque is heavy into lowering LDL to brain damaging and testosterone depleting levels of 60 and below. this is insane. Use of statins and other pharmaceuticals are highly supported to reach the LDL goal and this is dubious as well as unsupported by medical literature. Seneff has great resources and also has been interviewed by Jimmy Moore, check out her potcast; smart chick!!

3864f9a2af09b1b447c7963058650a34

(3703)

on December 03, 2011
at 01:07 AM

Conventional 'wisdom' is killing us. Good luck Russ.

A1081af52b61372dbb3ed572d88968f4

(425)

on December 02, 2011
at 12:43 AM

Thanks. Will check out Jonathan. Grace - Agree Seneff is key here. She's the one that started connecting the dots that led me in this direction.

2
64433a05384cd9717c1aa6bf7e98b661

(15236)

on February 19, 2012
at 10:37 PM

Have you seen this?

http://atvb.ahajournals.org/content/22/1/133.long

Looks like exercise is especially useful for E4s

3864f9a2af09b1b447c7963058650a34

(3703)

on February 20, 2012
at 05:00 AM

Very N I C E !!! Thanks!!!!! I've been wondering the link betw low hdls and cortisol... The authors said simething really helpful for me ' High-intensity prolonged exercise has been shown to increase plasma adrenocorticotropin53,54 and, hence, cortisol. HDL cholesterol may be the preferred lipoprotein as a source for adrenocorticosteroid synthesis.55 Indeed, although glucocorticoid therapy often has adverse effects on the cardiovascular system, including dyslipidemia,56 corticotropin seems to contribute to the increase in HDL cholesterol level.57'

A1081af52b61372dbb3ed572d88968f4

(425)

on February 24, 2012
at 04:40 PM

Jeff, Thanks. Indeed interesting. Just completed a month of moderate HIIT weight lifting plus dairy elimination, and drew blood for workup this morning. So will be interesting to see if it moved the needle on my HDL as in this paper. One thing that has me intrigued is that this paper seems to indicate net time in high intensity training is the driving variable, but not clear the study was clearly designed to look for 'more' vs 'optimum.' In any case, one thing I might play with myself is increasing the time in the gym during the week. Gives me another variable to play with - Thanks!

2
3a567c1637db69f1455ce35e78201a2c

(1054)

on December 01, 2011
at 03:47 AM

I hope you know that folks with higher than CW total cholesterol live longer than those with low cholesterol. 262 is great. Lowering total cholesterol starves the brain of vital cholesterol since the brain is made up of around 63% cholesterol. It is insanity to take statins.

Your Triglycerides are too high...down under 60 acceptable, but lower is better.
Your HDL at 47 is low. Should be above 60 and higher is better.

You have about 50/50 large bouyant to small dense LDL which is headed in the right direction.

Continue on with paleo/primal. If you follow Dr Kruse's Leptin Reset Protocol you will change your LDL particle size to mostly large bouyant pattern A and you will raise your HDL and lower your Triglycerides. Use copious amounts of coconut oil for you and your dad. Lots of animal protein. 70% fat, 20% animal protein, 10% tubers and green veggies without nightshades with coconut oil is a heart healthy, artery and vein strengthen protocol that will heal the leaky gut syndrome that most everyone has that is not paleo.

You do the Reset Protocol and you will feel very well very soon.

A1081af52b61372dbb3ed572d88968f4

(425)

on December 02, 2011
at 12:41 AM

Dex. Thanks. Clear steer. Glad you agree the high cholesterol itself is a good thing - seems pretty clear based on biochemistry. Now just need to change the size distribution. Will read and try the reset protocol and keep watching numbers. Yep - got my Mom to start my Dad on coconut oil yesterday and my wife and I are going up next week to begin their new life on paleo diet :-) Will provide updates as available.

3864f9a2af09b1b447c7963058650a34

(3703)

on December 01, 2011
at 08:20 AM

Right on Dex!!!

1
Da3d4a6835c0f5256b2ef829b3ba3393

on December 01, 2011
at 01:16 AM

I don't have an answer for you, Russ, but I appreciate your question and hope to see the braintrust here pitch in and give you some good info. This is simply my way of bringing your question back up to the top of the board.

0
Cdb9e467dac06a12c515ddfd18a4cdda

(140)

on December 01, 2011
at 06:16 AM

http://www.bhlinc.com/cirm.php?chapter=19

Adopt a lower fat diet please and remove all cholesterol and SAFA from the diet.

A1081af52b61372dbb3ed572d88968f4

(425)

on December 02, 2011
at 02:02 AM

Just finished the QJM paper. Although abstract was promising re APOE4, paper is more indirect and ambiguous - i.e. observationally proposing that rising Alzheimer's in APOE4's on statins is simply due to fact that they're not dying younger from heart disease. Maybe is irresolvable, but seems to be that there is a biochemical optimum that is good for both?

3864f9a2af09b1b447c7963058650a34

(3703)

on December 01, 2011
at 08:19 AM

1 million downvotes. They data does not support this. This is why parkinsons, heart disease, western civilization diseaeses and dementia/alzheimers are epidemic.

Cdb9e467dac06a12c515ddfd18a4cdda

(140)

on December 02, 2011
at 05:10 AM

Well my interpretation of the evidence is that a lot of short-term (<5 years, heck maybe even 20 years) results are due to reverse causation. For e.g. [Epidemiology. 1997 Mar;8(2):132-6.Time trends in serum cholesterol before cancer death.Sharp SJ, Pocock SJ. Am J Epidemiol. 1992 Jun 1;135(11):1251-8.Short- and long-term association of serum cholesterol with mortality. The 25-year follow-up of the Finnish cohorts of the seven countries study.Pekkanen J, Nissinen A, Punsar S, Karvonen MJ.] Thus in terms of cancer, latent cells may be causing decreased cholesterol.

A1081af52b61372dbb3ed572d88968f4

(425)

on December 02, 2011
at 12:47 AM

Hans, I truly appreciate the pushback, but having read, it doesn't make wholistic sense. Whereas I appreciate the negative impact of APOE4 cholesterol profile on heart health, lowering cholesterol seems exactly the wrong thing to do for the brain. This link does not seem to address that issue. I note that I had a great additional find yesterday in a new paper in the Oxford Journal QJM just published online entitled "Cardiovascular Disease prevention and the rise in dementia" that seems to be now providing solid evidence of the problem in following this strategy in APOE4's.

Cdb9e467dac06a12c515ddfd18a4cdda

(140)

on December 03, 2011
at 03:38 AM

Dement Geriatr Cogn Disord. 2009;27(1):42-9. Epub 2009 Jan 8. Serum lipids are related to Alzheimer's pathology in nursing home residents. Lesser GT, Haroutunian V, Purohit DP, Schnaider Beeri M, Schmeidler J, Honkanen L, Neufeld R, Libow LS. (briefly disccused here: http://hanswuhealth.blogspot.com/2011/11/cholesterol-targets.html) You talk about the brain, but as studies like the one I quote here and others, they show that high cholesterol is detrimental, regardless of ApoE genotype. These studies go back 10 years thus avoid reverse causation.

3864f9a2af09b1b447c7963058650a34

(3703)

on December 01, 2011
at 08:21 AM

Pritikin died of suicide, depression and had cancer... Hhhhhmmmhhhh...

A1081af52b61372dbb3ed572d88968f4

(425)

on December 02, 2011
at 01:50 PM

But my point previously was that Dr. Davis' logic doesn't make biochemical sense unless you address the heart issue in isolation. In other words, the key issue for APOE4 in the dilemma is that the brain needs the extra cholesterol - i.e. reducing it may improve heart health, but seems almost guaranteed to kill the brain. As noted, the big clue for me was the incredibly low LDL number for my father. There may be still better ways, but the first hypothesis seems to be to keep cholesterol high, but increase LDL size (and HDL fraction)?

3864f9a2af09b1b447c7963058650a34

(3703)

on December 03, 2011
at 07:58 AM

Are you hans wu of specific strength??????!

A1081af52b61372dbb3ed572d88968f4

(425)

on December 03, 2011
at 01:28 PM

Hans, Grace, Thanks - good discussion. I'm off to read the DCGD 2009 paper and will revert with further thoughts or questions.

3864f9a2af09b1b447c7963058650a34

(3703)

on December 03, 2011
at 08:01 AM

I apologize for the flaming.

Cdb9e467dac06a12c515ddfd18a4cdda

(140)

on December 02, 2011
at 05:15 AM

This is also my interpretation with regards to Alzheimer's. Heck even with Dr Davis (TrackYourPlaque) has been changing his mind with regards to E4:http://www.trackyourplaque.com/blog/2011/07/the-exception-to-low-carb.html While before he advocated the same diet for all genotypes. Based on my understanding of ApoE4 metabolism and function SAFA should be limited.

3864f9a2af09b1b447c7963058650a34

(3703)

on December 03, 2011
at 08:03 AM

HDL is a more 'honest' marker because most pharmaceuticals at this time cannot statistically modify (except Niaspan, fish oil and vitamin D). TGs go down with statins esp the potent ones Crestor and Lipitor, but besides the multitude of downstream problems with statins, these potent statins also raise the incidence of frank T2DM. Bad.

3864f9a2af09b1b447c7963058650a34

(3703)

on December 05, 2011
at 12:07 AM

Hans, Good luck with your med school exams!!! You are going to make a wonderful physician in the future I believe because you leave no rocks unturned and you critically evaluate the evidence. That is a wonderful new website (like the daily food/supp log) -- awesome evolution... I'll have to update my bloglist...

3864f9a2af09b1b447c7963058650a34

(3703)

on December 05, 2011
at 12:04 AM

My hypothesis is that E4 was 'selected' in mountainous and inland terrain (eg northern europe/china) which were less saturated with marine minerals essential for brain development and reproductive function (iodine, zinc, magnesium, etc). pubmed studies support this line of reasoning. Some of the studies for metal toxic accumulation and apoE4, I listed on this thread: http://paleohacks.com/questions/69109/autism-and-paleo-tips-and-links-do-you-have-a-favorite-resource-not-an-a/69493#69493

3864f9a2af09b1b447c7963058650a34

(3703)

on December 03, 2011
at 08:04 AM

Keep digging. Read all the work of Ronald Krauss at CHORI. The LDL is high in the studies you cite due to elevated LDL particles which are mostly comprised of sdLDL, not lbLDL (large buoyant). You'll know because the TG/HDL ratio will be >> 1.0. Low HDL is a screaming indicator of pattern 'B' sizing and oxidation/inflammation. I hope that helps.

3864f9a2af09b1b447c7963058650a34

(3703)

on December 03, 2011
at 08:01 AM

Keep digging. Read all the work of Ronald Krauss at CHORI. The LDL is high in the studies you cite due to elevated LDL particles which are mostly comprised of sdLDL, not lbLDL (large buoyant). You'll know because the TG/HDL ratio will be >> 1.0. Low HDL is a screaming indicator of pattern 'B' sizing and oxidation/inflammation. I hope that helps.

A1081af52b61372dbb3ed572d88968f4

(425)

on December 03, 2011
at 03:26 PM

Hans, Read the paper. Great to see that they actually did track by APOE4. May be noteworthy that APOE4's was almost twice as high as the general population (28% vs 15%). Too bad they didn't measure TC/LDL during stay, nor whether statins started after admin. It certainly confirms that APOE4 is associated with AD (but less so with other dementia's), but at face value, doesn't seem like the data tell us much about causal direction. Data seem consistent with Seneff where higher TC in APOE4 is an attempted protection mechanism for the brain, and Masterjohn's note APOE4 prefer to carry LDL.

3864f9a2af09b1b447c7963058650a34

(3703)

on December 05, 2011
at 12:04 AM

I agree too that the ApoE4 pathogenesis in AD is beyond cholesterol. E4 functions as a 'chelator' of metals -- iron, zinc, magnesiu, lead, mercury, etc. E4 has less of this function compared with E2 and E3.

3864f9a2af09b1b447c7963058650a34

(3703)

on December 04, 2011
at 11:59 PM

For FH -- on NMR lipoprotein analysis, the 'death band' is for the smallest, densest LDL particle LDL-IVb. The larger the band, the larger the incidence for coronary mortality. Yes FH have predominance of lbLDL but they still have sdLDL and the absolute and relative quantity define their risk. Google 'animal pharm death band'.

3864f9a2af09b1b447c7963058650a34

(3703)

on December 06, 2011
at 11:42 AM

1 million upvotes

3864f9a2af09b1b447c7963058650a34

(3703)

on December 05, 2011
at 12:12 AM

E4 is very important. It is rare in the general population except northern Europe and aboriginal subpops (Native Americans, etc). However, for heart disease it can be a large percentage of victims... imho E4 is more adapted to HG lifestyles -- more exercise, more low-GI foods, more protein/meat/organs/marrow.

A1081af52b61372dbb3ed572d88968f4

(425)

on December 06, 2011
at 01:16 AM

Hans. Read the abstract as the full paper is behind a pay wall. However, hard to see how they go to the stated conclusion. Abstract says study was ex-vivo oxidation test, not atherosclerosis test. My understanding of the small particle theory is that it takes both oxidation and small particles to induce athersclerosis, as the small particle size is required for penetrating the pores/cracks in the inflamed endothelial lining. Perhaps I understand wrong (or the theory itself is wrong?)?

3864f9a2af09b1b447c7963058650a34

(3703)

on December 07, 2011
at 03:17 AM

Also I think the biggest causes of death were: predators, parasites, climate, drought, hunger (and partners -- fighting, jealousy, property, etc). SFAs may have helped boost immunity to fight infections as well stay strong against predators... Monounsaturated fats just do not improve the function of HDLs and the immunity the identical way that SFAs do. The MCT oil trials prove this to me, even with high carb (cupcake) vehicles for the SFA (coconut oil is predominantly MCT, medium chained). SFA in animal fats -- ghee, butter, cream, yolks, brain, fat, marrow -- also come with the omega-3s

Cdb9e467dac06a12c515ddfd18a4cdda

(140)

on December 04, 2011
at 09:29 PM

Hi Grace, yes I am. My blog is currently http://hanswuhealth.blogspot.com/ I have read many of Krauss' work for me both the pathogenesis and outcome research coincide so I find it very very hard to accept it all comes down to particle size. I know I am referring to a pathologic state here, however in FH they have large particles: http://www.ncbi.nlm.nih.gov/pubmed/11718692 If the argument is that large LDL is good and small is bad (which I am inclined to agree with), then wouldn't having less LDL overall with low TG lead to less overall sdLDL as compared to higher LDL levels?

Cdb9e467dac06a12c515ddfd18a4cdda

(140)

on December 04, 2011
at 09:34 PM

Hi Russ, While the mechanistic reasoning makes sense with regards to Seneff and Masterjohn I am inclined to disagree. ApoE4 plays a larger role in AD pathogenesis then just cholesterol. When I have time I'll expand on it (studying for exams right now).

3864f9a2af09b1b447c7963058650a34

(3703)

on December 04, 2011
at 11:57 PM

Hans, Yes I think your right -- sometimes lower LDL overall concomitantly with low TG (and high HDL) is a good bioindicator. LDL goes up also with hypometabolic pathogenic states like hypothyroidism. I think fiber that feeds the good gut flora also help to control LDL in multiple ways, studies indicate. Did you read the Dreon Krauss et al study in apoE4? http://jn.nutrition.org/content/134/10/2517.full.pdf

3864f9a2af09b1b447c7963058650a34

(3703)

on December 07, 2011
at 03:22 AM

which we know in nearly all RCTs extend life (unless the study used inferior omega-3 containing pesticides,mercury, POPs, PCBs, other environmental contaminant). Animal fats would also contain stigamesterol (plant sterol), vitamin A, retinoids, carotenoids, tocopherols and CoQ10/ubiquinone and menaquinones. This mimics the cholesterol rich and omega-3 abundant sources from the ocean and the littoral.

3864f9a2af09b1b447c7963058650a34

(3703)

on December 07, 2011
at 03:12 AM

Russ, It is ALL VERY FASCINATING!! Animal fat is 50/50 mono v. saturated. When I think about humans migrating beyond the marine shores toward the steppes and inland areas, basically the sources of cholesterol, omega-3 fats and minerals dramatically decline... to survive these had to be upregulated in both production and retention, as well as decreased metabolism and elimination... this is like drugs too. I do concur -- I think in E3/E4s there may be a preference for the SFAs because the animal fats are more nutrient dense.

A1081af52b61372dbb3ed572d88968f4

(425)

on December 06, 2011
at 12:44 AM

Still lots of learning for me, but just want to say what a spectacular discussion you're having with me and each other, Hans and Grace. Thanks for taking the time. We'll see where this goes, and deeply appreciate you're sharing. Han's, good luck with med school exams!

A1081af52b61372dbb3ed572d88968f4

(425)

on December 06, 2011
at 01:13 PM

Grace, Read the 2004 Moreno paper you linked on LDL Size, Diet, and APOE. Quite good - thanks. Once again clear that carbs are particularly bad for APOE4's. I am somewhat intrigued by Table 5 that shows avg LDL size is higher for APOE3/4's compared to 3/3's and 3/2's regardless of diet? Wonder if there is meaning? Also appears that 3/4's had slight preference for Sat Fat (SFA) vs Mon Unsat Fats (MUFA)? Interesting to note that regardless of alleles, either SFA or MUFA generates significantly more 'Pattern A' profiles than carbohydrate diet. May dig deeper yet into the data.

3864f9a2af09b1b447c7963058650a34

(3703)

on December 07, 2011
at 03:24 AM

Hans, I've been very curious about the J-curves in epidemiological studies. What you see may be the high carb consequences. Have you read these: (1) http://www.carbohydratescankill.com/3248/jcurve-hypotheses-hyperglycemia-culprit-2-of-2?utm_source=feedburner&utm_medium=feed&utm_campaign=Feed%3A+CarbohydratesCanKill+%28Carbohydrates+Can+Kill%29 and (2) http://healthydietsandscience.blogspot.com/2011/04/high-cholesterol-levels-boost-memory.html [esp Apo E4]

Cdb9e467dac06a12c515ddfd18a4cdda

(140)

on December 07, 2011
at 03:50 AM

Thanks for all the wishes of good luck. There does seem to be a Antagonstic Pleiotropy theory with regards to ApoE (http://hanswuhealth.blogspot.com/2011/11/antagonistic-pleiotropy.html) however the is still tentative but not without evidence. If this application of the theory applies to E4 then keeping cholesterol levels for those with E4 may be beneficial in the long-run. E.g. with testosterone supplementation in the elderly they experience increased risk of CVD/stroke while those of younger age supplemented to physiological levels experience benefit. However if we are to glean anything from

3864f9a2af09b1b447c7963058650a34

(3703)

on December 06, 2011
at 11:11 AM

thanks so much for your question and for Hans honest reply. It is a much needed discussion with all the evidence presented and differrent spectrum of hypotheses... we're all different and have diff Achille's heels!

Cdb9e467dac06a12c515ddfd18a4cdda

(140)

on December 08, 2011
at 01:17 AM

Thank you guys also for the discussion. We all have our own opinion and without DEFINITIVE evidence we all speculate as best we can, hopefully discussions like this help us bring us closer to our goals. My goal is longevity.

Cdb9e467dac06a12c515ddfd18a4cdda

(140)

on December 07, 2011
at 03:53 AM

....athletes and their high carbohydrate diet. While in the short-term it is great for performance in the long-term (as we would probably all agree) a high carbohydrate diet (especially with caloric excess, regardless of activity level) is bad. This is my spiel for now, after exams I'll come back and look over the various posts you guys have provided. Thanks.

Cdb9e467dac06a12c515ddfd18a4cdda

(140)

on December 07, 2011
at 03:52 AM

...antagonistic pleitropy and disoposable soma theory we should be keeping these down in the long-run to prevent ourselves from experience the pleiotropic effects of these factors in old age, esp middle age where most of these chronic illnesses manifest. It is quite possible that in the short term a high-fat diet with 50/50 MUFA/SAFA could be beneficial but my main focus in what will happen to me when I'm 70 or 80 and to be healthy at that age (and hopefully live to 100 or more) the body needs to be maintained in good condition. If we take an even shorter term outlook, we could look at....

A1081af52b61372dbb3ed572d88968f4

(425)

on December 07, 2011
at 12:01 PM

Hans and Grace - just want to go on record that you guys are amazing! I have so much to learn and am thankful for your engagement!

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