93 replies to this topic

[Elus]

Thanks for that report, James. I agree that these are impressive markers. Interesting that trigs went down so much with meat reduction. I wonder how much of this is the move from high meat to low meat versus the last month of mostly Vegan diet? Do you think you'll stick with the Vegan diet for a while, or go back to the low meat version? It's nice to see something that looks like it's working well for ApoE4. Low fat diets are supposed to be the bomb for ApoE4, and this seems to back that up.

hmmm... from today...

http://www.wired.com...d: Top Stories)

[Chupo]

hmmm... from today...

http://www.wired.com...d: Top Stories)

That contradicts the RCTs that show benefits of carnitine on CVD.

http://www.ncbi.nlm....les/PMC2398308/
http://www.ncbi.nlm....pubmed/10650325
http://www.ncbi.nlm..../pubmed/1292918

Edited by Chupo, 08 April 2013 - 09:40 PM.

[rwac]

I would think TMAO is generated from a combination of gut dysbiosis and carnitine (also choline!).

I think that focusing on gut dysbiosis is the more important aspect.

[niner]

http://www.wired.com...d: Top Stories)

That contradicts the RCTs that show benefits of carnitine on CVD.

http://www.ncbi.nlm....les/PMC2398308/
http://www.ncbi.nlm....pubmed/10650325
http://www.ncbi.nlm..../pubmed/1292918

I'm not sure it's a contradiction- the first and third of these were looking at carnitine as therapy post-MI, and the second was as therapy in heart failure. Carnitine is clearly good in all three cases, but that doesn't mean that it couldn't also be bad as a long term supplement. This is not to say that I'm convinced that supplemental carnitines are a problem, I don't have enough information to say that.

[tunt01]

Thx for this thread.

Any thoughts on dealing with the accumulation of heavy metals (as a preventive measure) in Apoe4 allele (hetero or homo) status individuals? I've read a bit about cilantro and other items which facilitate the excretion of heavy metals. Just wondering if anyone else had an obvious idea that I am missing (maybe chelation?).

Thx

[tunt01]

Looking for this article if anyone can help:

http://link.springer...0044-011-9595-3

Structure-based drug discovery of ApoE4 inhibitors from the plant compounds

Apolipoprotein E4 (ApoE4) is a potential target for developing new therapeutics for Alzheimer’s disease (AD). Till now there is no drug available to inhibit this protein and cholinesterase inhibitor was given for almost all the AD patients. In this study, we have approached to identify the potential ApoE4 inhibitor from the plant compounds. Rigid docking study was performed for 18 plant compounds and 11 cholinesterase inhibitors. Based on the docking score, binding energy and number of hydrogen bonding curcumin posses the best scoring function. For further validation induce fit docking was performed and it also shows that curcumin binds to the same binding pocket of ApoE4 protein. Biological activity prediction reveals that curcumin has a potential therapeutic activity against AD. Pharmacokinetic properties of this compound are under the acceptable range. From the results we concluded that the plant compound curcumin could be a potential inhibitor of ApoE4 and it can control the AD.

[niner]

Any thoughts on dealing with the accumulation of heavy metals (as a preventive measure) in Apoe4 allele (hetero or homo) status individuals? I've read a bit about cilantro and other items which facilitate the excretion of heavy metals. Just wondering if anyone else had an obvious idea that I am missing (maybe chelation?).

Do ApoE4 people accumulate heavy metals at a higher rate than other ApoE genotypes? This thread is the first I've heard of it- a quick search in pubmed didn't come up with anything that clearly showed this, but it wasn't a particularly extensive search. Assuming that's the case, or even if it's not, older adults can have a significant lead burden in their large bones, and the half time for lead loss is about 30 years. If you were alive in the leaded gasoline era, you could be carrying around a fair amount of lead. It's possible to get a measurement of your tibial lead burden by an x-ray method that's similar to a DEXA Scan. I don't know how hard it is to find a place that does this, or what it would cost.

I don't have any particular insight into methods for reducing metal burden, other than chelation. Before embarking on a therapeutic regimen, I'd want to look for analytical methods that could tell me if I had a problem or not.

[tunt01]

Do ApoE4 people accumulate heavy metals at a higher rate than other ApoE genotypes? This thread is the first I've heard of it- a quick search in pubmed didn't come up with anything that clearly showed this, but it wasn't a particularly extensive search.

There is a theory out there that Apoe4 is worse at binding to heavy metals and removing them from the body as compared to Apoe2/Apoe4. I'm not sure if it's quackery or supported by the evidence.

Some suggest there is a straight line to be drawn between mercury exposure and Alzheimer's, with Apoe4 being a complicit party in causation due to its inability to mitigate mercury damage. My hunch is that it is quackery and that the underlying issue is still Apoe4, not mercury itself. With a poorly behaving apoe4, you could still get ALZ even without mercury exposure.

Examples:

• Google: apoe4 mercury
  
• A few minor pubmed comments: http://www.ncbi.nlm....pubmed/15580166

3. This paper is inconclusive, but sort of says the hypothesis might have legs or at least be a contributor.

According to Saunders, the underlying reason for the
apo-E-associated differences in AD susceptibility remains a mystery [40]. However, a logical biochemical
explanation has been proposed by Pendergrass and Haley, based on the different amino-acid configurations of
the three apo-E isomers and their potential relevance to mercury elimination [33]. Only ε2 (with two cysteine
-SH groups), and to a lesser extent ε3 (with one -SH
group), are able to bind and remove mercury from the
brain and cerebrospinal fluid. This would oppose accumulation of mercury which is reported to be causal
for the unique brain lesions that typify the AD brain
including neuro-fibrillary tangles [22,32,34]. We did
not find any evidence of higher post-DMPS mercury
excretion in those carrying the ε4 allele when compared to the other groups. However, this would not be
unexpected if mercury from amalgam has direct access
to the brain [4,19,31]. Mercury excretion after DMPS
challenge reflects a general body burden and especially
a renal loading [2,3]. Therefore, a DMPS challenge
would not necessarily be a quantitative indicator of
brain mercury levels.

Another aspect of AD pathology is the evidence that
enhanced mitochondrial damage occurs in AD and ε4
genotype [16]. Mercury is very destructive at the mitochondrial level where catalase can demethylate organic
mercury species into highly reactive inorganic mercury.
Inorganic mercury is also an extremely potent enzyme
inactivator [47]. Furthermore, chronic micro-mercurial
toxicity specifically from dental amalgam has been documented [14,23,31,36,45] and successfully treated by
removal of amalgam and medical detoxification in 796
patients [23].

Still, not all research results agree with mercury’s
causal role in AD. Elevated mercury was not found
in seven different regions of AD brains compared to
controls [15]. However, the “controls” had possessed
three amalgam surfaces whereas the AD subjects had
six, likely obscuring any differences. Saxe et al. [41]
reporting on the mental health of 129 nuns, found no
difference between those with amalgam and controls.
However, 72% of the controls had no posterior teeth,
and the remainder had a mean of only three teeth. All
129 could, therefore, have had a similar previous amalgam history and the half-life of mercury in the brain is
measured in decades. This paper’s conclusions, published in a dental trade journal, are at variance with
those of another paper in the same journal on risk
factors affecting dentists’ health. The authors identi-
fied 3 factors with equally high statistical values (i.e.
p < 0.001), namely, a mercury spill in the dental office,
manual amalgamation, and the dentists’ own amalgam
status [24].

Therefore, based on the suggestion that mercury is
causal for AD-like lesions due to its unique neurotoxicity, and that ε2 is potentially protective due to the
cysteine amino-acids, it could be contended that: (i)
those individuals who have inherited the ε4 allele and

who are exposed to mercury, including from numerous dental amalgam fillings, would be at greater risk
of developing AD at an earlier age than those with the
ε2 configuration; and (ii) those with ε4/4 would potentially be at the greatest risk of accumulating mercury
and developing symptoms. Consistent with this, are
our findings that short-term memory loss was common
among our patients in the ε4 groups with only one of
those possessing ε4/4 not listing this as a complaint.
Two patients (both ε3/4) were already suffering from
AD and there was a family history of some members
having had senile dementia in 20% of the ε3/4, 4/4
cohorts.

Edited by prophets, 03 May 2013 - 05:25 PM.

[DAMI]

Hmm. Maybe fat's not so much the point as is reducing the amount of animal products? "Low Fat" is the recommendation for ApoE4, even from guys like William Davis. This sounds like an amount of fat I could easily live with; I guess you go through a lot of olive oil. (If so, there's certainly good epidemiology on that.) Anyway, if it turns out that the real killer for ApoE4 is low animal products, that is a hell of a good discovery. One question I have that someone here may know the answer to is: Do conventional lipid markers mean the same thing if you are ApoE4? That is, would the typical ApoE4 person just have terrible markers, or be more likely to have CVD or Alzheimer's than someone who was ApoE3 with the same markers?

Did Bill Davis really say that? This is not the message I get from him: http://blog.trackyou...o-low-carb.html

Apo E4 people also typically have plenty of small LDL particles triggered by carbohydrates. Put fats and carbohydrates together and you get an explosion of small LDL particles. Remove fats, small LDL goes down a little bit, if at all. Remove carbohydrates, small LDL goes down but total LDL (mostly large) goes up. The large LDL in apo E4 does seem to be atherogenic (plaque-causing), though the data are fairly skimpy.
So apo E4 creates a nutritional rock and a hard place: To extract full advantage from diet, people with apo E4 have to 1) go wheat-free, low-carb, then 2) not overdo fats, especially saturated fat.

The way I see it both Carbs and SAFAs seem to be bad for ApoE4.

[James Cain]

I'm going to post a reply to a message I recently got about this thread. I think it applies to some other comments above too. This is copy+paste so may not make perfect sense given the context.
---------------------------

Regarding the Moreno, et. al study, (relevant data table here) "Carbohydrate intake of the CHO diet was based on the consumption of biscuits, jam, and bread. Butter and palm oil were used during the SFA dietary period." While both dietary choices are probably suboptimal, it's probably better for most people to eat butter and palm oil in place of those carb sources. Part of this comes back to the effect of dietary carb sources on hepatic lipogenesis and lipoprotein size, and you wouldn't see these effects if eating more "whole food" sources of carbs to balance the processed carbs. Sugar and processed carbs have been shown to be quite bad for you, hence the useless nature of most "high-fat" and "low-fat" studies that relied on these forms of carbs. "Low-fat" and even lower-carb diets relying on whole food sources of carbohydrate seem to level the playing field a bit.

My diet at the time of the NMR lipoprofile was about 30+% fat, largely from 100% cocoa, nuts, and olive oil. I got a decent amount of saturated fat. From what I've read, and what my own results seem to indicate, dietary cholesterol is going to be the most important contributor for those with ApoE4, with saturated and total fat playing a less crucial role.

These studies (I think three of them are from the same group of Rhesus monkeys) show that addition or removal of dietary cholesterol has the greatest effect on lipids, with saturated fats having a significant but lesser effect, but that together they have a synergistic effect. It also seems that total fat takes a back seat to the type of dietary lipids. I've taken this to mean that as long as I remove dietary cholesterol from my diet I gain most of the benefit, and that removing cholesterol coincidentally removes most of the saturated fat from my diet as well, and that any negative effect of remaining saturated or total fat is lessened by removal of cholesterol. My NMR lipoprofile seems excellent, so I'm sticking with this conclusions. These studies seem to be independent of ApoE4.


Quote

1. Eggen D a., Strong JP, Newman WP, Malcom GT, Restrepo C. Regression of experimental atherosclerotic lesions in rhesus monkeys consuming a high saturated fat diet. Arteriosclerosis 1987;7:125–34.
2. Zanni EE, Stephan ZF, Zannis VI, Breslow JL, Hayes KC. ApoE distribution among lipoproteins of rhesus monkeys is modulated by dietary fat and cholesterol. J Nutr 1986;116:1611–9.
3. Strong JP, Bhattacharyya a. K, Eggen D a., Malcom GT, Newman WP, Restrepo C. Long-term induction and regression of diet-induced atherosclerotic lesions in rhesus monkeys. I. Morphological and chemical evidence for regression of lesions in the aorta and carotid and peripheral arteries. Arterioscler Thromb 1994;14:958–65.
4. Strong JP, Bhattacharyya a. K, Eggen D a., et al. Long-term induction and regression of diet-induced atherosclerotic lesions in rhesus monkeys. II. Morphometric evaluation of lesions by light microscopy in coronary and carotid arteries. Arterioscler Thromb 1994;14:2007–16.
5. Zanni EE, Zannis VI, Blum CB, Herbert PN, Breslow JL. Effect of egg cholesterol and dietary fats on plasma lipids, lipoproteins, and apoproteins of normal women consuming natural diets. J Lipid Res 1987;28:518–27.

[Dolph]

OK pals, I'm LATE. I know...
Just wanted to share the results of my part of the experiment!

What my labs looked before:
total C: 240mg/dl
ldl-C: 140mg/dl
hdl-C: 39mg/dl
Trigs: 72mg/dl
(all direct measurements)

What I did:
slight(!) CR
~1kg fruits and vegies /day
oats and or barlay ed
miniscule amounts of meat only for social reasons
oily fish 3 times a week
moderate amounts of canola and olive oil, some peanut butter now and then (total fat 30-60g max(!)/day)
2g niacin/day, later reduced to 1g

My lab results of today:
total C: 153mg/dl
ldl-C: 74mg/dl (damn, it's nearly HALF of the before result!)
hdl-c 62mg/dl
Trigs: 100mg/dl

Can't express how pleased I am! The only thing that surprises me are the "high" Trigs, the "highest" I ever had, despite lots of fish and niacin.(?) But I don't think there is lots of reason to be worried.

Edited by Dolph, 08 November 2013 - 03:16 PM.

[theconomist]

OK pals, I'm LATE. I know...
Just wanted to share the results of my part of the experiment!

What my labs looked before:
total C: 240mg/dl
ldl-C: 140mg/dl
hdl-C: 39mg/dl
Trigs: 72mg/dl
(all direct measurements)

What I did:
slight(!) CR
~1kg fruits and vegies /day
oats and or barlay ed
miniscule amounts of meat only for social reasons
oily fish 3 times a week
moderate amounts of canola and olive oil, some peanut butter now and then (total fat 30-60g max(!)/day)
2g niacin/day, later reduced to 1g

My lab results of today:
total C: 153mg/dl
ldl-C: 74mg/dl (damn, it's nearly HALF of the before result!)
hdl-c 62mg/dl
Trigs: 100mg/dl

Can't express how pleased I am! The only thing that surprises me are the "high" Trigs, the "highest" I ever had, despite lots of fish and niacin.(?) But I don't think there is lots of reason to be worried.

It might be the 1kg of fruit and vegies, depending on the vegie to fruit ratio the fructose might be raising your trigs. I have the same problem ; gotta limit your fruit intake :/

[Dolph]

Yes, I also thought about that. About half of that is fruit, almost entirely apples. I think I will keep these, cause I think they are partly responsible for the tremendous fall in LDL-C and non-HDL (over 50%...).
A confounder might be that three days before the blood was drawn I had a couple of Martinis at the birthday party of a friend. Three days should normally be enough to sort out the effect of alcohol, but I'm not entirely sure about that and will retest in a few months.
I think I'm more or less fine with the 100mg/dl as long as it doesn't get more. My LDL-C should be at least halfway concordant nonetheless because of the niacin.

[niner]

Dolph, while the fruit may have something to do with the high trigs, another possibility is the niacin. It raises blood glucose.

[Dolph]

I of course checked for this regularly and my blood glucose, also postprandial, is rather lower than before the change. I'm almost never above 100 at the spike one hour after a meal and always(!) under 90 at the usual two hour postprandial mark. My fasting BG is ~75.
Niacin is also regularly used to reduce triglycerides! It does so normally in the range of 25-50% and is almost as effective as the fibrates, even in diabetics.

My current suspicion is that the reason could simply be the general shift from fat/protein to carbs. You can observe this rising of triglycerides almost always in the Esselstyn and Ornish croud, although of course even more pronounced than in my case. First thing I will try is to slightly increase the fatfree protein content and reduce the grains a little.

I also suspect, that my VLDL before the experiment was pretty much depleted of triglycerides and very cholesterol rich. Mind the huge and strange gap between triglycerides (72 mg/dl) and the non-LDL part of the non-HDL (61mg/dl). Normaly 72 mg/dl triglycerides should give roughly ~15 mg/dl VLDL only. Something obviously was strange there.

Edited by Dolph, 10 November 2013 - 10:17 AM.

[James Cain]

For those interested in my and other people's diet experiments in this thread, a guy recently created the Five Diets website to do what I did here but with five different diets. It's very interesting and he's part way through the diets now, posting results as he goes.

[Dolph]

This is very interesting indeed, but I have my doubts if it's wise to do the experimental periods "back to back" in such a short cadence. I would think that especially some "washout" periods inbetween would give more meaningful information.(?)
I realize the "Potato Monodiet" and the PSMF somewhat serve this purpose.
I'm really curious how bad/good he will do on the Mediterranean Diet.

[James Cain]

This is very interesting indeed, but I have my doubts if it's wise to do the experimental periods "back to back" in such a short cadence. I would think that especially some "washout" periods inbetween would give more meaningful information.(?)
I realize the "Potato Monodiet" and the PSMF somewhat serve this purpose.

If you read the guidelines:

• UPDATE 10/19/13: Will include a break period between each diet (shorter before the Med and Vegan diets, longer before the fast diets), during which I will return to the pre-experiment diet, in order to provide a consistent preexisting condition for each diet, and int he case of the fast diets, get spiritually and mentally prepared. Also once I decided to take the breaks, I has to do some juggling to get the testing days to fall on days that the labs would be open.

[James Cain]

Update: New NMR Lipoprofile results

It's been about a year and a half and I'm still going strong with the vegan diet. I ensured weight stability for the first test but I aimed for ~ 1 lb/mo weight loss for the following test, so mildly calorie restricted. I also made a few changes to my diet.

Initial test: 27 years, 195 lbs, 6'3", BMI 24.4, ~7% body fat
Staples: veggies, fruits (mostly bananas, blueberries, and apples), potatoes, beans, rice, olive oil, nuts (walnuts, almonds, chia), pea and rice protein powders, 100% cocoa baking chocolate, spices, coffee and wine. I generally ate between 3000 kcal/day (20% protein, 30% fat, 50% carbohydrate) to maintain my weight, depending on activity level, not including my 10oz wine each day.

Current test: 29 years, 183 lbs, 6'3", BMI 22.9, ~7% body fat
Staples: veggies, fruits (mostly bananas, blueberries, and apples), potatoes, squash, beans, lentils, rice, corn tortillas, oats, olive oil, nuts (walnuts, almonds, chia, flaxseed), pea and rice protein powders, 100% cocoa baking chocolate, spices, coffee and wine. I generally ate between 3000 kcal/day (20% protein, 30% fat, 50% carbohydrate) to maintain my weight, depending on activity level, not including my 10oz wine each day I track my intake in Cronometer and consistently eat the same foods. I ate ~2400 kcal/day (13% protein, 22% fat, 65% carbohydrate (I've attached the reports below). I've been eating more vegetables and fiber (~85 g/day) since my first test, I cut out the chocolate and what little coconut oil I had been using (so very low saturated fat), and I cut back my wine intake to a single 5oz serving a few days per week and actually didn't drink for the month prior to the blood draw.

NMR Lipoprofile
Date -- 08/2012, 12/2013
Cholesterol (mg/dl) -- 133, 119
HDL-C (mg/dl) -- 46, 41
LDL-C (mg/dl) -- 76, 65
Triglycerides (mg/dl) -- 56, 63
Chol/HDL-C (ratio) -- 2.9, 2.9

LDL-P (nmol/l) -- 717, 923
HDL-P (umol/l) -- 27.1, 28.2
Small LDL-P (nmol/l) -- 297, 517
Large VLDL-P (nmol/l) -- 1.1, 0.9
Large HDL-P (umol/l) -- 5.1, 4.3
VLDL Size (nm) -- 42.6, 46.4
LDL Size (nm) -- 21.1, 20.6
HDL Size (nm) -- 9.1, 8.8

The initial test is essentially a whole-foods vegan diet with liberal wine, coffee, and saturated fat intake. The second test is probably closer to a stereotypical whole-foods vegan diet with no alcohol, less saturated fat, more fiber, and mild CR. The results are basically the same, so I'm further convinced that the focus on whole-foods and zero cholesterol intake drive most of the changes. I'd attribute most of the subtle changes to be normal testing variability, but it's interesting that the LDL-P and small LDL-P increased as much as they did, while total and LDL cholesterol dropped. The former could be due to eating more carbs and less total and saturated fat, and the latter could be due to reduced calories, saturated fat, and alcohol. These are obvious trade-offs, but the results are similar enough, and all under risk thresholds, so I figure as long as I focus on a whole-foods vegan diet and at least maintain my weight it probably doesn't much matter what else I do.

Attached Files

•  CRON-O-Meter - 4 weeks - 131212.pdf   273.84KB   19 downloads
•  CRON-O-Meter - 8 weeks - 131212.pdf   274.07KB   22 downloads

[Dolph]

but it's interesting that the LDL-P and small LDL-P increased as much as they did, while total and LDL cholesterol dropped. The former could be due to eating more carbs and less total and saturated fat, and the latter could be due to reduced calories, saturated fat, and alcohol.

Hm, I really don't think that eating less saturated fat should give you a higher LDL-P.(?) At least that's not how I understand the interaction between the consumption of saturated fats and the expression of LDL-receptors in the liver. Maybe I have to change my mind about that.

Isn't the change in mean LDL particle size the sole culprit for the fall in LDL-C? I think your lab results are a rather benign but good example for the frequent discordance between LDL-P and LDL-C.
More carbs indeed may play a role and explain the reduced LDL particle size, but I'm really somewhat surprised the LDL-P did rise, given your weight reduction, too.

Did you already decide if you will change anything soon? And if yes, what will it be? This is still the most inspiring thread on this forum for me by far, so I'm eager to know what are your conclusions and plans for the future.
If I interpret the results correctly you should feel a little more relaxed know about a somewhat more liberal use of saturated and monounsaturated vegetable fats and oils? Does that matter to you anyway in the way you enjoy food?

[James Cain]

Hm, I really don't think that eating less saturated fat should give you a higher LDL-P.(?) At least that's not how I understand the interaction between the consumption of saturated fats and the expression of LDL-receptors in the liver. Maybe I have to change my mind about that.

Reducing saturated fat, or increasing unsaturated, generally leads to increased LDL receptor activity and reduced LDL-C. This seemed to be the case for me, however minor the changes were. It's hard to find information about how this directly effects LDL-P, and I don't know how much of a role this had in the context of my diet. I'm mostly speculating, albeit in an educated fashion.

Isn't the change in mean LDL particle size the sole culprit for the fall in LDL-C? I think your lab results are a rather benign but good example for the frequent discordance between LDL-P and LDL-C.
More carbs indeed may play a role and explain the reduced LDL particle size, but I'm really somewhat surprised the LDL-P did rise, given your weight reduction, too.

My LDL-C dropped while I had an increase in total and small LDL-P. This means less total and LDL cholesterol but more smaller particles. Though the changes were minimal and possibly testing variability, it would otherwise be textbook LDL-C/LDL-P discordance as you said. I'd say the relationship between LDL-P, LDL-C, and particle size can't be separated such that you can predict one value without knowing the other two, so I'm not sure you can say that the change in LDL particle size is responsible for the fall in LDL-C. Here's a sort of chart of what I'm trying to say:

[LDL-P] [LDL-C] [LDL particle size]
[no change] [increase] [increase]
[no change] [decrease] [decrease]
[increase] [increase] [decrease]
[decrease] [decrease] [increase]

I agree about carbs and calories. I do eat 4-8 tortillas on most days, and a lot of fruit (mostly bananas, calorically).

Did you already decide if you will change anything soon? And if yes, what will it be? This is still the most inspiring thread on this forum for me by far, so I'm eager to know what are your conclusions and plans for the future.
If I interpret the results correctly you should feel a little more relaxed know about a somewhat more liberal use of saturated and monounsaturated vegetable fats and oils? Does that matter to you anyway in the way you enjoy food?

Someone in the newer ApoE4 forum posted about a $75 NMR Lipoprofile test through LabCorp without a doctor's order. With this I'll probably test a few changes, and possibly just retest for validity. My total intake of sugar is fairly high at ~ 100 g/d. This comes from fruit, sweet potatoes, and vegetables (especially things like tomato paste). I'm seriously considering cutting back on my fruit consumption in place of more starches, and possibly bumping my fat back up to 30%. 22% fat is quite palatable to me, but 30% is nice sometimes as it helps the food seem more rich, and especially since higher fat intake seems to help reduce my appetite. The appetite is only a problem under 15-20% fat, and seems to be maxed out at 30-35% fat.

I don't consciously try to eat lower saturated fat, I just chose not to restock my coconut oil and chocolate seemed to be giving me headaches. While it was neat for this experiment for it to be lower, I don't otherwise worry about their intake. I think I posted some research earlier in this thread about how the effects on lipids and atherosclerosis seem to be in the order of dietary cholesterol > saturated fat > total fat.

[Dolph]

Reducing saturated fat, or increasing unsaturated, generally leads to increased LDL receptor activity and reduced LDL-C. This seemed to be the case for me, however minor the changes were. It's hard to find information about how this directly effects LDL-P,

True, that's the problem. As I understood it the LDL-receptor doesn't delipidate the LDL-particle but literally "absorbs" it. But I'm not sure if this is a fact or just speculation, too.

Someone in the newer ApoE4 forum posted about a $75 NMR Lipoprofile test through LabCorp without a doctor's order.

That's a decent offer indeed. I wishd I could find something like that in Germany. All I could find was a LDL subtype (particle size) analysis for almost 100€... Not very useful.

I think I posted some research earlier in this thread about how the effects on lipids and atherosclerosis seem to be in the order of dietary cholesterol > saturated fat > total fat.

Yes, and that seems to be the way it is. I'm still stunned that it's possible to achieve these "dream"-values so relatively easy. I could be well wrong but it even seems it is easier for ApoE4s in the end than for the other ApoE genotypes.

By the way... Do you think the alcohol or the lack of it could be responsible for some of the changes? It seems to be a fact that it raises LDL-C(!) for ApoE4s but I couldn't find anything about changes in particle size/number in relation to ethanol consumption.

[scottknl]

I'd make a couple of dietary changes to see if I could get the HDL numbers up a bit. Reduce or eliminate banana and apple in favor of more nutritionally dense frozen berries like blueberries, blackberries, raspberries and strawberries taken with some nuts and seeds to increase nutrient absorption. Hopefully the reduction of carbs will help with the HDL numbers. You may also want to consider raising your saturated fat intake slightly and see if that also helps with the HDL. RDA is < 10g per day IIRC. Mine used to be 23 - 24 and went up to 56 by going right to 10 g per day sat fats and reducing simple carbs. Also reduce omega-3 fatty acid consumption to 3.5 g per day or less. Higher consumption of omega-3 fatty acids has been linked to bleeding problems. Otherwise, looks like a great job in improving the numbers.


http://en.wikipedia....id#Daily_values

The FDA has advised that adults can safely consume a total of 3 grams per day of combined DHA and EPA, with no more than 2 g per day coming from dietary supplements.

Edited by scottknl, 05 January 2014 - 09:22 PM.

[Chupo]

I think I posted some research earlier in this thread about how the effects on lipids and atherosclerosis seem to be in the order of dietary cholesterol > saturated fat > total fat.

Yes, and that seems to be the way it is. I'm still stunned that it's possible to achieve these "dream"-values so relatively easy. I could be well wrong but it even seems it is easier for ApoE4s in the end than for the other ApoE genotypes.

E4s tend to be able to change their TC and LDL quite drastically with diet. As an E2 carrier, my TC and LDL hardly changed at all going from high fat to low fat. It was my HDL and TG that changed drastically.

Edited by Chupo, 05 January 2014 - 10:25 PM.

[James Cain]

I think I posted some research earlier in this thread about how the effects on lipids and atherosclerosis seem to be in the order of dietary cholesterol > saturated fat > total fat.

Yes, and that seems to be the way it is. I'm still stunned that it's possible to achieve these "dream"-values so relatively easy. I could be well wrong but it even seems it is easier for ApoE4s in the end than for the other ApoE genotypes.

E4s tend to be able to change their TC and LDL quite drastically with diet. As an E2 carrier, my TC and LDL hardly changed at all going from high fat to low fat. It was my HDL and TG that changed drastically.

In some ways I'm glad that I'm ApoE 4/4 (if I had to have E4 at all), assuming that's the major basis for this diet having such a dramatic effect. I doubt it would be as simple for 3/4, and especially not for 2/4.

[James Cain]

I'd make a couple of dietary changes to see if I could get the HDL numbers up a bit. Reduce or eliminate banana and apple in favor of more nutritionally dense frozen berries like blueberries, blackberries, raspberries and strawberries taken with some nuts and seeds to increase nutrient absorption. Hopefully the reduction of carbs will help with the HDL numbers. You may also want to consider raising your saturated fat intake slightly and see if that also helps with the HDL. RDA is < 10g per day IIRC. Mine used to be 23 - 24 and went up to 56 by going right to 10 g per day sat fats and reducing simple carbs.

I already eat 100-200g blueberries and 20-60g nuts each day. I'm deciding between replacing some of my sugary foods (mostly bananas, apples only occasionally) with either olive oil or starchy carbs. I'm sure I'd be better off either way. I know a lot of the sugar comes from sweet potatoes and tomato products, but I'd make a big dent by cutting out the major fruit offenders.

I've cut out chocolate, so unless I use coconut oil I can't think of another way to increase my saturated fat intake. Chocolate was great, but coconut oil doesn't seem to have clinical and epidemiological benefits, and quite possibly could be negative.

Also reduce omega-3 fatty acid consumption to 3.5 g per day or less. Higher consumption of omega-3 fatty acids has been linked to bleeding problems. Otherwise, looks like a great job in improving the numbers.


http://en.wikipedia....id#Daily_values

The FDA has advised that adults can safely consume a total of 3 grams per day of combined DHA and EPA, with no more than 2 g per day coming from dietary supplements.

I don't take a fish oil supplement or eat fish, and my omega-3 intake is essentially all ALA. These same recommendations don't apply to ALA, and with the low conversion rate and an absence of bleeding problems (both subjectively and measured prothrombin and INR), I'm not concerned and see no benefit to lowering my intake. Do you think there's some benefit I'm missing? I do consume 20g flaxseed each day and I've considered lowering it to 10g, so that would be a sort of middle ground between our approaches.

I think I'll make some of these changes and retest in 6-8 weeks. Regardless, we're talking about a great lipid profile versus a slightly less great profile. I'm surprised the weight loss didn't have more of a impact, but really there isn't much room for obvious improvements.

[James Cain]

By the way... Do you think the alcohol or the lack of it could be responsible for some of the changes? It seems to be a fact that it raises LDL-C(!) for ApoE4s but I couldn't find anything about changes in particle size/number in relation to ethanol consumption.

Alcohol in E4 has been reported to increase LDL-C and decrease HDL-C. Alcohol in general has been reported to decrease LDL-P size. It's hard to say if the alcohol had any impact considering the other dietary changes and that my numbers couldn't really improve much more. I didn't expect much change in LDL-C, but I was hoping for an increase in HDL-C with the reduced alcohol and weight loss, but not such luck.

The only time I've gotten my HDL-C in to the 50s was in my paleo diet days mainlining meat and butter (also with my two servings of wine). It's also consistently tested in the 30s when I've been on an omnivore or vegetarian low fat diet, albeit with more processed "healthy" food products. It's most often been in the 40s and it just doesn't seem to want to budge regardless of what I do.

[scottknl]

I'd guess that 20 - 30 g of cashews would provide the saturated fats to get you close to 10 g per day. Of course it comes at the cost of a slightly worse Omega ratio, but I live with that and a high(er) HDL level.

I also eat no fish oil and get everything from ALA conversion. My 23 and me profile suggests that I may be extra sensitive to warfarin and other blood thinners and I find if I go over 4 g per day in my diet of Omega-3 fatty acid consumption, I get nose bleeds within a week or so. If I stay below 3.5g everything's good. While you probably don't have the same SNP's, I think it's validation enough about keeping a reasonable enough level of ALA in one's diet and thus following the recommendation I sited. What I worry about is that the first sign for you, or someone else reading this, is a bleeding on the brain issue instead of the early warning nose bleeds like I get.

Yah, You do already have a pretty good profile with little chance of stroke or heart disease by the numbers, so it's optional if you change to add more healthy fats in place of simple carbs. All the best in 2014. KS

Edited by scottknl, 06 January 2014 - 01:30 AM.

[DAMI]

James Cain, do think that eating a gluten-free diet is important for E4s?

[Dolph]

For what reason would anybody think it was??? There is no connection whatsoever.