93 replies to this topic

[James Cain]

EDIT: I posted an update with a new NMR LipoProfile from December 2013 (~1.5 years on a vegan diet) here.

 

EDIT: I posted another update with two new NMR LipoProfile results from August 2014 (2 years on a vegan diet) after 3 and 5 weeks experimenting with a very-low-fat diet (CFP 72/14/14%) at apoe4.info here, as well as posting my results in this thread here.

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Original post:

 

I thought I'd share my blood test results from a recent vegan experiment to possibly help others, and to stimulate further discussion on a sorely lacking topic. I have experimented with various paleo eating methods over the past two years, but decided to spend these past few months of summer cutting back on meat (and eating mostly chicken breast) and most dairy (eating some cheese and kefir). I guess this would be a sort of plant-based "real food" diet.

Bio: Male, 27 years, 195 lbs, 6'3", BMI 24.4, ~7% body fat (via calipers, an confirmed with hydrostatic weighing in the past). I have been weight stable +/- 3 lbs for at least 6 months. I strength train 4-5 days per week and walk 4-8 miles per day (usually at a treadmill desk), but am otherwise sedentary. I am homozygous E4/E4.

Previous diet staples: Meats, veggies, fruits, potatoes, beans, rice, olive oil, nuts (walnuts, almonds, chia), limited dairy (some cheese and kefir), pea and rice protein powders, 100% cocoa baking chocolate, spices, coffee and wine.

Current experiment: Over the past 3-4 months I had severely limited dairy (basically 1-2 servings per week) and ate 100g meat only 5-8 meals per week (instead of 150-200g basically every meal, plus eggs for breakfast). I very rarely eat added sugars (I eat fruit) or packaged food products. My digestion is usually such that I get bloated eating a lot of foods, so while I adequately digest my food the bloating limits the intake volume, so I have limited vegetable intake in order get in enough calories. Caloric staples included potatoes, rice, olive oil, nuts, and bananas. 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 decided to push this to full vegan for a month and get blood work. I consumed no animal products (except supplement capsules), kept weight stable and maintained all of my lifestyle parameters (supplements, workout, sleep, meal timing, caffeine, alcohol, etc.).
 

My combinations of various paleo eating methods over the past two years have yielded three times over 15 months (I'm really surprised at the consistency!):

Date -- 4/2010, 10/2010, 7/2011
Cholesterol (mg/dl) -- 201, 201, 200
HDL-C (mg/dl) -- 50, 50, 56
LDL-C (mg/dl) -- 131, 128, 129
Tryglycerides (mg/dl) -- 99, 99, 74
Chol/HDL-C (ratio) -- 4.0, 3.8, 3.6

After 3-4 months of reduced meat and dairy, followed by 1 month of full vegan:

Date -- 8/2012
Cholesterol (mg/dl) -- 133
HDL-C (mg/dl) -- 46
LDL-C (mg/dl) -- 76
Triglycerides (mg/dl) -- 56
Chol/HDL-C (ratio) -- 2.9

LDL-P (nmol/l) -- 717
HDL-P (umol/l) -- 27.1
Small LDL-P (nmol/l) -- 297
Large VLDL-P (nmol/l) -- 1.1
Small LDL-P (nmol/l) -- 297
Large HDL-P (umol/l) -- 5.1
VLDL Size (nm) -- 42.6
LDL Size (nm) -- 21.1
HDL Size (nm) -- 9.1

 

Edited by James Cain, 26 June 2014 - 01:17 AM.

[Hebbeh]

I know you said you ate to maintain weight, but to clarify, your weight and body composition didn't change over the 4 month experiment? How were weight lifting workouts affected?

[James Cain]

I know you said you ate to maintain weight, but to clarify, your weight and body composition didn't change over the 4 month experiment? How were weight lifting workouts affected?

My weight and body composition didn't change. I know that hypocaloric diets and weight loss generally account for dietary interventional lipid changes, so I really tried to keep it consistent. Visually, it almost seemed as if I lost a few pounds of muscle and gained some extra water weight, staying the same weight, especially since my weight lifting workout performance and my recovery seemed to noticeably suffer the first two weeks. By the last week, and even now (week 5), I seem to recover just as well and have maintained or improved most of my lifts.

While I kept my protein intake consistent from my baseline diet, I think the plant-based protein being less bioavailable meant I was consuming less complete protein. I'd imagine I would have noticed the same effects, and time to adaptation, if I were to simply cut my baseline (animal) protein intake back by 25%.

[Hebbeh]

Those are some impressive improvements....thanks for sharing.

[Chupo]

Your numbers look fantastic for ApoE4!

[niner]

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.

[James Cain]

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?

The low triglycerides really surprised me because I drink two glasses of wine every evening, and eat a good amount of "sugar" from berries, bananas, and sweet potatoes. I guess not overeating really helps, my liberal use of olive oil, and probably my muscle mass. I'm debating on being mostly-vegan or full-vegan for the next few months and retesting. I don't really mind foregoing meat, but excluding all animal products makes it a huge pain in the ass when eating socially. It's nice to have a bit of cheese in a dish (for ease of ordering, not necessarily taste) instead of trying to find full-vegan fare at restaurants or parties. I was mostly limited to a few vegetable side dishes, various chips and dips, and bean tacos. I could see that getting really annoying long-term, hence my consideration of 95% vegan. I'm just wondering if there would be a significant trade off in benefits would be for that 5%.

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.

This was not a low-fat diet. I was eating 30-40% calories from fat each day, mostly from olive oil, nuts, and chia, with a bit of 100% cocoa chocolate. I could palatably eat less fat, around 20% with no feeling of deprivation, but then my blood sugar tends to be a bit higher after meals, and the volume of food got to be too much for my preference.

[niner]

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.

This was not a low-fat diet. I was eating 30-40% calories from fat each day, mostly from olive oil, nuts, and chia, with a bit of 100% cocoa chocolate. I could palatably eat less fat, around 20% with no feeling of deprivation, but then my blood sugar tends to be a bit higher after meals, and the volume of food got to be too much for my preference.

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?

[TheFountain]

Hmm. Maybe fat's not so much the point as is reducing the amount of animal products?

Arachidonic acid maybe?

[TheFountain]

To the OP, have you considered a pescetarian diet experiment? I have been doing lacto-ovo pescetarian for a while now and my last blood work numbers were pretty good. For dairy I mainly do low or non-fat to try and keep AA consumption low. But sometimes I splurge on cheese and full fat dairy. Most of my regular fat intake comes from olive oil, nuts, seeds and occasional coconut milk.

[James Cain]

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?

It is pretty convincing that ApoE4 responds poorly to saturated fats compared to E3 or E2, and E4/E4 even more so than E3/E4. Likewise with cholesterol, as ApoE4 has much more efficient intestinal cholesterol absorption with much lower hepatic production. This is one of them main reasons ApoE4 subjects have greater diet-induced lipid changes, but poorer statin responses, compared to E3 or E2. Low fat may indeed be more beneficial in general, or more specifically for ApoE4, but then we'd have to figure out how low to go in order to maximize benefit. We'd also have to determine to what extent the benefit is reduced cholesterol and saturated fat, or total fat. There is evidence to suggest ApoE4 don't just have poor lipid markers, but actually do have a greater pathogenic response. IMO, If ever the lipid hypothesis were true, it would be most evident in ApoE4. I follow a lot of Michael Rae's reasoning and his wealth of posted references regarding diet and lipids. In this regard I believe *quality* olive oil is beneficial for it's ability to reduce in vivo lipid oxidation, and there's enough epidemiology and other trials to suggest it's either positive or neutral per se. Then again, some stuff by Rudel has me thinking that excess MUFA isn't completely neutral. For example:

Arterioscler Thromb Vasc Biol.

1995 Dec;15(12):2101-10.

Compared with dietary monounsaturated and saturated fat, polyunsaturated fat protects African green monkeys from coronary artery atherosclerosis.

Rudel LL, Parks JS, Sawyer JK.

Source

Department of Comparative Medicine, Bowman Gray School of Medicine of Wake Forest University, Winston-Salem, NC 27157-1040, USA.

Abstract

Atherogenic diets enriched in saturated, n-6 polyunsaturated, and monounsaturated fatty acids were fed to African green monkeys for 5 years to define effects on plasma lipoproteins and coronary artery atherosclerosis. The monkeys fed polyunsaturated and monounsaturated fat had similar plasma concentrations of LDL cholesterol, and these values were significantly lower than for LDL in the animals fed saturated fat. Plasma HDL cholesterol concentrations were comparable in animals fed saturated and monounsaturated fat and were significantly higher than in animals fed polyunsaturated fat. Thus, the monounsaturated fat group had the lowest LDL/HDL ratio. LDL particle size was largest in the saturated and monounsaturated fat groups, significantly larger than in the polyunsaturated fat group. LDL particle enrichment with cholesteryl oleate was the greatest in the animals fed monounsaturated fat, next greatest in the saturated fat-fed animals, and was least in the polyunsaturated fat-fed animals. Coronary artery atherosclerosis as measured by intimal area was less in the polyunsaturated fat compared with the saturated fat groups, was less in the animals fed polyunsaturated fat compared with the monounsaturated fat-fed animals, but did not differ between the monounsaturated and saturated fat groups. Cholesteryl ester, particularly cholesteryl oleate, accumulation in the coronary arteries was also similar between groups fed monounsaturated and saturated fat but was minimal in the animals fed polyunsaturated fat. In sum, the monkeys fed monounsaturated fat developed equivalent amounts of coronary artery atherosclerosis as those fed saturated fat, but monkeys fed polyunsaturated fat developed less. The beneficial effects of the lower LDL and higher HDL in the animals fed monounsaturated fat apparently were offset by the atherogenic shifts in LDL particle composition. Dietary polyunsaturated fat appears to result in the least amount of coronary artery atherosclerosis because it prevents cholesteryl oleate accumulation in LDL and the coronary arteries in these primates.

PMID: 7489230

Curr Atheroscler Rep.

2010 Nov;12(6):391-6.

Dietary monounsaturated fatty acids appear not to provide cardioprotection.

Degirolamo C, Rudel LL.

Source

Department of Translational Pharmacology, Consorzio Mario Negri Sud, via Nazionale 8/A, 66030, S. Maria Imbaro, CH, Italy. degirolamo@negrisud.it

Abstract

Dietary interventions have been consistently proposed as a part of a comprehensive strategy to lower the incidence and severity of coronary heart disease (CHD), in the process providing long-term cardioprotection. Replacement of dietary saturated fatty acids (SFA) with higher intakes of monounsaturated fatty acids (MUFA) and polyunsaturated fatty acids (PUFA) has been reported to be inversely associated with risk of CHD. The observed lower incidence of CHD among populations consuming a Mediterranean-type diet, mainly enriched in MUFA from olive oil, has long supported the belief that MUFA are an optimal substitution for SFA. However, both epidemiologic and interventional studies suggest that although substituting MUFA-rich foods for SFA-rich foods in the diet can potentially lower total plasma cholesterol concentrations, this substitution does not lower the extent of coronary artery atherosclerosis. In addition, although recent evidence suggests that the source of MUFA (animal fat vs vegetable oils) may differentially influence the correlation between MUFA intake and CHD mortality, animal studies suggest that neither source is cardioprotective.

PMID: 20725810

I figure that I need to get enough fat to buffer my postprandial glucose, to enhance nutrient absorption, enhance palatability, and primarily (for me) to reduce overall meal volume. I eat 30g almonds, 30g walnuts, and 10g chia with breakfast, and then have olive oil with lunch and dinner. Any more nuts and my digestion is impaired and I become concerned with fatty acid profiles. Given the evidence, I believe olive oil is a better choice for me than coconut, palm, soy, canola, and other oils. There's also this and similar studies (keep in mind that there are always studies to show the converse):

Arteriosclerosis.

1987 Mar-Apr;7(2):125-34.

Regression of experimental atherosclerotic lesions in rhesus monkeys consuming a high saturated fat diet.

Eggen DA, Strong JP, Newman WP, Malcom GT, Restrepo C.

Abstract

Atherosclerotic lesions were induced in rhesus monkeys by feeding them a high-fat, high-cholesterol diet for 2 years. Arteries were examined after autopsy of a subgroup of animals (group P) and cholesterol was removed from the diet of the remaining animals. Lesions were examined in other subgroups after 30 weeks (group R1) and after 52 weeks (group R2). A control group (group C) was fed the diet without cholesterol throughout the study. The mean total serum cholesterol concentration before, during, and after lesion induction was 151, 390, and 157 mg/dl, respectively. The mean percent of surface area with fatty streak or fibrous plaque and the free and esterified cholesterol content of the artery increased in all six arterial segments examined in group P. The means for percent of surface with fatty streak and for arterial cholesterol content or concentration (but not for extent of surface with fibrous plaque) were consistently less in groups R1 and R2 than in group P, although they remained greater in groups R1 and R2 than in group C. The mean intimal thickness for coronary arteries was 10-fold greater in group P than in group C and 60 percent less in groups R1 and R2 than in group P; there was, however, much variability among animals and these differences among groups were not statistically significant. By using several measures in several arterial systems, we have shown that there was regression of diet-induced atherosclerotic lesions in rhesus monkeys while they were fed a diet high in saturated fat but without cholesterol for 30 or 52 weeks.

PMID: 3579722

It's really difficult to figure out what's what with so many conflicting, overlapping, poorly designed, and misinterpreted studies. I try to read as much as I can, but in the end I need to follow a diet that I can maintain long-term, and I think the diet I outlined above meets those criteria, at least at this stage in my life, physically and mentally. Another reason I kept my fat intake high is to make a more appropriate comparison with my prior diets, so it was more beneficial to change only dietary lipid intake, rather than to change both the type and amount. I was expecting improvement, but not to this degree, so I plan on continuing with a full-vegan diet to the best of my ability and retest in a few months.

[James Cain]

To the OP, have you considered a pescetarian diet experiment? I have been doing lacto-ovo pescetarian for a while now and my last blood work numbers were pretty good. For dairy I mainly do low or non-fat to try and keep AA consumption low. But sometimes I splurge on cheese and full fat dairy. Most of my regular fat intake comes from olive oil, nuts, seeds and occasional coconut milk.

ApoE4 carriers tend to accumulate heavy metals and contaminants, so I've largely avoided fish for quite some time. I have a long history of taking fish oil, but between my own reading and the information posted by Michael Rae, I don't think there is any benefit it can offer me over an adequate intake of ALA or other short-chain omega-3. There is also some evidence that fish oil is not a good idea for ApoE4 lipid profiles. The Berkeley HeartLab has a good primer with references.

Apolipoprotein E (apoE) Genotype for Cardiovascular Disease Management
http://www.bhlinc.co...anual/chapter19




This is also why I've considered heavily reducing or eliminating my daily 10oz (two glasses) of wine. They have good info there, but if you pursue the subject in PubMed you'll find that the almost every study study shows even moderate alcohol consumption to be detrimental to ApoE4 lipid profiles, and furthermore to be neurotoxic independent of lipids. ApoE4 have much reduced neural regenerative/remodeling, so this has weighed heavily on me while considering an appropriate lifestyle. I didn't change my alcohol consumption during this current dietary experiment to get an adequate comparison to my older diet lipid profiles, and because I wanted to see how far dietary lipid modifications could go even with alcohol. I may reduce or eliminate alcohol before my retest in a few months, but there are the very real mental and social benefits of drinking that may offset some of the negative effects, though for this to be worth it I would probably still need to cut back my average intake.

[maxwatt]

wrt sugars: I suspect that in fruits they are much less detrimental, as fruits tend to contain polyphenols and such that greatly reduce their impact. Berries especially. For instance, apples, especially the peels, are rich in phloridzin, which slows or blocks intestinal uptake of sugars.

[scottknl]

Glad to see that you found the vegan diet agreeable. I've also found very similar stats/changes in my own case, with very similar macro-nutrients, but also reducing portion size in my near vegan CRON diet. I'm E3/E4. Now that you've removed the risk of heart attack and stroke, all you have to do is tackle cancer! Vegan diets carefully implemented with real foods are found to be really good at cancer too.

I lost lots of strength in bench etc, but gained in running, balance and joint health. Also my sore back is cured. BMI 25 ---> 19.9. An added benefit I found over the longer run is that I never get sick from colds or flu anymore. 3 yrs and no days away from work due to sickness.

[brianmdelaney]

Hey,

I just stumbled upon this thread via a link in the CR Society archives in a post by James. I'm doing research about what ε4 carriers (hetero- or homozygotes) can do to maintain their health and have been looking into the question of dietary fat composition. Yall have talked about the effects on cholesterol and lipids, which seem important, but a lot of people in the "ε4 community" are trying to improve brain health via the induction of ketogenesis. (Many are using coconut oil, for example, which seems to have very little research to support it.) I wonder whether anyone here has looked into that. My preliminary research indicates it would not help ε4s.

A representative study:

Conclusions

In conclusion, despite the relatively small size of this study, genetic influences on cognitive scores in response to induced ketosis were noted. The main modulator of induced ketosis appears to be the carriage status of APOE4. It may not be a coincidence that APOE4 is also the major genetic risk factor for late onset AD. The failure of APOE4 carriers to respond to ketosis may indicate a more insidious metabolic problem. APOE4 carriers may be overly reliant on glucose and hence, over a lifetime, cerebral neurons are deprived of the metabolic advantages conferred by ketone body metabolism and this may be crucial to etiology of AD [36]. Importantly, this type of pharmacogenomic profiling not only offers insights into the disease process, it also allows targeting of patients who are most likely to respond to therapy. In this way, better and more effective therapeutics can be developed.

http://www.ncbi.nlm....les/PMC3213220/

The more I look into this, the more I realize that there isn't much ε4s can do aside from CR and regular, though probably non-intense, exercise. Turmeric might also help (and is very unlikely to hurt). It's amazing how mixed research results are on everything else!

Brian

[James Cain]

Hi Brian. It'd be great to have someone with your experience and knowledge weight in on the issue. But as you seem to have found yourself, most treatments benefit only non-ApoE4 carriers, or the results are highly inconclusive. The only things that seem to work, which also work for all ApoE genotypes, are calorie restriction, physical activity, low stress and blood pressure, and avoidance of pollution and toxins. The only actual treatment that's shown very impressive results is adenoviral treatment (gene transfer) with ApoE3 (or even E2, though that comes with other problems).

Even though ketones don't provide an cognitive benefit for treating ApoE4 cognitive impairment, the ability of ketones to provide cellular protection (e.g., suppression of oxidative stress, as discussed in this recent CRS thread) may provide preventative benefits. Even using certain spices as you've mentioned may help, but only in the preventive stage of the disease. Prevention is pretty much the only viable option at this point for those with E4, until gene therapy becomes mainstream and "safe." Of course, prevention is the best option for any disease, which is why CR is so effective across the board.

[niner]

If I were ApoE4, I would get some C60 on board, in the form of C60-olive oil.

[brianmdelaney]

Niner- I'd like to see a repeat or two of those amazing C60 results. Even failing that, it seems mighty tempting to start now, to be sure.

James- I'm heading to Colombia in a few days, more when I'm settled. One quick response now. Gene therapy probably is the real solution, agreed: ApoE4 is simply a bad protein (though not in every way, as I'm sure you've read -- but nearly every way), and ε4 carriers need to stop making it. But there's another solution that will probably be available sooner: "small molecule correctors":

http://www.ncbi.nlm....pubmed/23013167

http://gladstoneinst...ression-of-alzh

These are chemicals that basically unstick the arm of the E4 form that gets bent in towards the rest of the molecule and lets it stick back out, which makes ApoE4 functionally -- it is thought -- like ApoE3. Check out the Mahley and Huang paper. It's amazingly hopeful, though the approach is still very new.

Edited by brianmdelaney, 30 December 2012 - 06:10 PM.

[HaloTeK]

James, here is an interesting wrinkle on your desire to lower saturated fat intake. Do you know your rs5082 gene status. If you are GG, there has been a study that shows weight gain from saturated fat intake. Here is the interesting part though, the reason why GG people are gaining weight is because they "suffer" from a lower postprandial rise in blood fat from a meal containing saturated fats. Now, we know that if you allow yourself to gain weight in most situations, your insulin handling and disease potential might get worse as you gain weight. I say might, because there are some studies that actually show that some fat people maintain insulin sensitivity in the face of weight gain! Also, because rs5082 GG people have a lower postprandial response, researchers seem to suggest this has beneficial cardio benefits in the long term. They also suggest that these people keep fat at lower than 30% and saturated fat extremely low (in order to curb weight gain). It does seem a little bit odd to me that they come to that conclusion when these are the exact people who do not seem to suffer the high postprandial rise in blood fat and therefore the possibility of increasing damage to their cardiovascular system! Now, I'm not a big fan of high fat intake, but I feel a little better about consuming sat fats as long as I am keeping a watch on my weight. (I happen to be rs5082 GG, remember I am ever cognizant that other genes have interplay)

Anyone else have a different take on this or comments?

[James Cain]

James- I'm heading to Colombia in a few days, more when I'm settled. One quick response now. Gene therapy probably is the real solution, agreed: ApoE4 is simply a bad protein (though not in every way, as I'm sure you've read -- but nearly every way), and ε4 carriers need to stop making it. But there's another solution that will probably be available sooner: "small molecule correctors":

Wow, thanks Brian! I use PubCrawler to find new articles, so I'm surprised I missed this. It is very exciting knowing the research is shifting focus and serious treatments may be available, and fairly soon at that!

James, here is an interesting wrinkle on your desire to lower saturated fat intake. Do you know your rs5082 gene status. If you are GG, there has been a study that shows weight gain from saturated fat intake. Here is the interesting part though, the reason why GG people are gaining weight is because they "suffer" from a lower postprandial rise in blood fat from a meal containing saturated fats.

I am rs5082 AG (or TC). The studies you mentioned were listed on the SNPedia rs5082 page, which I'm sure you know about. The study you're referring to says "carriers of the minor allele for Apo A-II -265T/C (CC/TC) have a lower postprandial response compared with TT homozygotes," so I guess that means I'm more likely to better handle dietary (saturated) fats. The other study you mentioned showed "individuals carrying the 'CC' genotype for the APOAII rs5082 polymorphism had significantly lower risk of CAD than the 'T' allele carriers (OR=0.57, 95% CI 0.39-0.84, p=0.004)," so I guess having one 'G' allele helps reduce postprandial lipemia, but not as much as 'GG' and maybe not enough to be statistically beneficial.

This study mentioned the greater obesity in 'CC' individuals, but they also noted that they had significantly greater intakes of total energy, fat, and protein (though lower carb intake), so it seems that their high BMI are due to overeating. I don't see anything supporting that they gained weight due to lower postprandial lipemia as you suggested.

[MarkES]

Hi James,

This is fascinating and very timely for me, as well, thanks for sharing your experiment.

I'm ApoE4/3 and just considering low meat/vegetarian type diets to lower serum cholesterol. I've been eating closer to a Paleo type diet (no grains, legumes), but more starch (potatoes, sweet potatoes, white rice), dairy, and less fat.

What foods replaced the animal foods and still maintain same calories? Macronutrient ratios probably changed a little?

Have you decided if there's a trade-off or maybe lower limit for cholesterol levels? I've seen info that lower cholesterol (~150) can result in depression and violence/suicide.

I've also seen <200 being suggested as impaired immune function.

It makes it confusing as to what cholesterol level to target, since the evidence seems a little conflicting.

Note that I would normally include links to references, but I guess I have to wait until I have 10 posts under my belt.

Thanks,
Mark

[James Cain]

What foods replaced the animal foods and still maintain same calories? Macronutrient ratios probably changed a little?

I gave a description of my diet in my original post. Typically a whole-foods plant-based diet would be lower in protein and potentially fat compared to a mixed diet, but I was able to maintain my mixed diet macro ratios by using pea or rice protein powders and making an effort to eat more nuts, avocados, and olive oil. This would also keep calories up a bit higher than basing the diet on whole plant foods alone.

Having been on a vegan diet about six months now, so beyond trying to emulate my original macros for comparative purposes, I've decided to not track my food intake and I've allowed my palate and hunger to dictate food choices. My preference for fat intake has declined so I don't use much olive oil anymore, though I do eat chia and walnuts every day, with occasional avocados if they're in stores. I do make sure to add some fat source to each meal to aid in nutrient absorption and improve satiation, though I don't have as much of a palate for it anymore. I typically add a scoop of protein powder to some meal to ensure adequate protein intake, and again to increase satiation, though there are days and weeks (if traveling) where I don't do this, and much as with fat I don't seem to have as high of a palatable preference for protein foods. I've also lost about 1/2 lb per month, so about 3-4 pounds total.

Have you decided if there's a trade-off or maybe lower limit for cholesterol levels? I've seen info that lower cholesterol (~150) can result in depression and violence/suicide.

I've also seen <200 being suggested as impaired immune function.

It makes it confusing as to what cholesterol level to target, since the evidence seems a little conflicting.

I have considered the trade-offs you mentioned. However, much of that research is misrepresented by the paleo community who at times endorse high cholesterol levels, despite concurrently saying cholesterol levels are meaningless. While there are a few higher quality studies that make me consider including a source of cholesterol say once each week (to minimally raise plasma cholesterol), most of the research suggests that lower plasma cholesterol is associated with or due to various diseases or conditions that lower cholesterol. In such cases the disease itself is likely responsible for the increased mortality and psychological symptoms rather than the lower cholesterol.

Or course there are individual differences and anecdotal reports of dietary cholesterol helping people. Then again a lot of these people could be B12, D, protein, fat, or another nutrient deficient, so it might not be the cholesterol per se that is beneficial. In my own experience I haven't noticed anything substantially different with regards to sleep, energy, mood, sexual function, etc., other than just feeling slightly better in general. I chalk this up to a greater intake of nutrient-dense foods, what seems like better body fluid regulation, improved digestion probably due to more consistent food choice, and what appears to be a mild calorie restriction. I plug my diet into Cronometer every so often to measure nutrient intake, so I know I'm not deficient in anything, but I'll probably get blood work this week to measure my 6 month progress to have outcome measures.

[MarkES]

I gave a description of my diet in my original post. Typically a whole-foods plant-based diet would be lower in protein and potentially fat compared to a mixed diet, but I was able to maintain my mixed diet macro ratios by using pea or rice protein powders and making an effort to eat more nuts, avocados, and olive oil. This would also keep calories up a bit higher than basing the diet on whole plant foods alone.

Having been on a vegan diet about six months now, so beyond trying to emulate my original macros for comparative purposes, I've decided to not track my food intake and I've allowed my palate and hunger to dictate food choices. My preference for fat intake has declined so I don't use much olive oil anymore, though I do eat chia and walnuts every day, with occasional avocados if they're in stores. I do make sure to add some fat source to each meal to aid in nutrient absorption and improve satiation, though I don't have as much of a palate for it anymore. I typically add a scoop of protein powder to some meal to ensure adequate protein intake, and again to increase satiation, though there are days and weeks (if traveling) where I don't do this, and much as with fat I don't seem to have as high of a palatable preference for protein foods. I've also lost about 1/2 lb per month, so about 3-4 pounds total.

Sounds like you're really getting this dialed in - I'm envious. I just started reading "Vegan for Life" to learn more and it seems a little less strict than some other vegan diets I've read about that recommend avoiding all fat (no oil, nuts, avocados). I can relate to palate adjusting over time. Do you have any favorite vegan books/references?

I have considered the trade-offs you mentioned. However, much of that research is misrepresented by the paleo community who at times endorse high cholesterol levels, despite concurrently saying cholesterol levels are meaningless. While there are a few higher quality studies that make me consider including a source of cholesterol say once each week (to minimally raise plasma cholesterol), most of the research suggests that lower plasma cholesterol is associated with or due to various diseases or conditions that lower cholesterol. In such cases the disease itself is likely responsible for the increased mortality and psychological symptoms rather than the lower cholesterol.

Or course there are individual differences and anecdotal reports of dietary cholesterol helping people. Then again a lot of these people could be B12, D, protein, fat, or another nutrient deficient, so it might not be the cholesterol per se that is beneficial. In my own experience I haven't noticed anything substantially different with regards to sleep, energy, mood, sexual function, etc., other than just feeling slightly better in general. I chalk this up to a greater intake of nutrient-dense foods, what seems like better body fluid regulation, improved digestion probably due to more consistent food choice, and what appears to be a mild calorie restriction. I plug my diet into Cronometer every so often to measure nutrient intake, so I know I'm not deficient in anything, but I'll probably get blood work this week to measure my 6 month progress to have outcome measures.

Good points.

I've just been reading about this recently and Dr. Greenblatt wrote this "Low Cholesterol and Its Psychological Effects" article on Psychology Today:
http://www.psycholog...logical-effects

He admits that while low cholesterol is linked to depression, suicide, and violence, the cause is unknown.

Anyhow, I guess I'm currently more interested in lowering serum cholesterol.

I'm looking forward to seeing your 6 month update. I'm curious what your vitamin D levels are and if low serum cholesterol affects it.

Edited by MarkES, 04 January 2013 - 03:38 PM.

[Elus]

I have considered the trade-offs you mentioned. However, much of that research is misrepresented by the paleo community who at times endorse high cholesterol levels, despite concurrently saying cholesterol levels are meaningless. While there are a few higher quality studies that make me consider including a source of cholesterol say once each week (to minimally raise plasma cholesterol), most of the research suggests that lower plasma cholesterol is associated with or due to various diseases or conditions that lower cholesterol. In such cases the disease itself is likely responsible for the increased mortality and psychological symptoms rather than the lower cholesterol.

Or course there are individual differences and anecdotal reports of dietary cholesterol helping people. Then again a lot of these people could be B12, D, protein, fat, or another nutrient deficient, so it might not be the cholesterol per se that is beneficial. In my own experience I haven't noticed anything substantially different with regards to sleep, energy, mood, sexual function, etc., other than just feeling slightly better in general. I chalk this up to a greater intake of nutrient-dense foods, what seems like better body fluid regulation, improved digestion probably due to more consistent food choice, and what appears to be a mild calorie restriction. I plug my diet into Cronometer every so often to measure nutrient intake, so I know I'm not deficient in anything, but I'll probably get blood work this week to measure my 6 month progress to have outcome measures.

James, I have a few questions for you:

1. What is your rationale for avoiding cholesterol? Is it because you believe that high cholesterol is the cause of atherosclerosis (Which I believe is the current consensus in scientific community, or am I wrong?)? Or is there another reason you are avoiding cholesterol?

2. Are you avoiding animal products in your diet as a way to reduce your cholesterol or are there other reasons as well?

[James Cain]

James, I have a few questions for you:

1. What is your rationale for avoiding cholesterol? Is it because you believe that high cholesterol is the cause of atherosclerosis (Which I believe is the current consensus in scientific community, or am I wrong?)? Or is there another reason you are avoiding cholesterol?

2. Are you avoiding animal products in your diet as a way to reduce your cholesterol or are there other reasons as well?

Those with ApoE4 status have a greater than average absorption of intestinal cholesterol and less endogenous production. This explains why many statins show little therapeutic effect in ApoE4 individuals because they produce less cholesterol to start with, and conversely why they tend to respond more than other groups to dietary interventions. I've found that years of lipid tests showed as much.

Dietary cholesterol absolutely raises plasma cholesterol, and I subscribe to the lipid hypothesis in that cholesterol contributes to atherosclerosis. This is without a doubt proven, and even most of the cholesterol skeptics agree that cholesterol is bad if oxidized or in an inflammatory environment, they just seem to think that their high saturated fat and high cholesterol diets are inflammatory or provide some unique protection. I was once one of them, but education prevails. Based on the literature and my own experience, it is my understanding that plasma cholesterol levels (and to a lesser degree inflammation/oxidative stress) are improved by reducing, in order of magnitude of effect, dietary cholesterol > saturated fat > total fat. This of course leaves out other relevant factors such as trans fats, total calories, nutrient density of the diet, processed sources of foods, etc.

Assuming a real-food plant-based diet is in place then cholesterol and saturated fat seem to be the best ways to reduce risk factors (cholesterol, lipids) as well as hard endpoints (atherosclerosis, heart attacks, etc.). I say total fat only in that it isn't super high, as it seems there are perhaps more downsides than benefits to an intake over 35-40% of total calories and below perhaps 15%. Even at that, I've seen some evidence that a cholesterol-free (vegan) diet has virtually the same benefits regardless of having saturated fat lowered or not, though you're pretty much stick with coconut and palm oils at that point, so you'd almost have to go out of your way to get saturated fat high enough to be a problem on its own.

[Sillewater]

Hey those results look pretty impressive. I myself am Apoe3 homozygous and this has been my cholesterol journey:

https://robustbiolog...nd-cholesterol/
See figures 1 and 2. I haven't had one tested recently though but I suspect it is even lower now.

[MarkES]

Hi James,

What do you think of plant sterols being a possible concern for ApoE4?

My prediction: Despite the fact that sterols reduce LDL, they may, in certain genetically-susceptible people, such as those with apo E4, increase risk for heart disease: heart unhealthy.

Here are two studies that suggest that greater sterol absorption in people without sitosterolemia are at higher risk for heart disease:

Alterations in cholesterol absorption/synthesis markers characterize Framingham offspring study participants with CHD:
http://www.ncbi.nlm....pubmed/19436064

Plasma sitosterol elevations are associated with an increased incidence of coronary events in men: results of a nested case-control analysis of the Prospective Cardiovascular Münster (PROCAM) study:
http://www.ncbi.nlm....pubmed/16399487

→ source (external link)

Edited by MarkES, 23 February 2013 - 04:18 PM.

[Dolph]

This is one inspiring thread!

It's just coincidence that I have chosen to try a similar dietary change about three months ago. My "before" diet looked essentialy exactly as yours did, even down to the details.
My "after" diet is very similar too, yet including two to three small portions of fish (~2-5 ounces per portion) per week and small amounts of fat free quark now and then. No meat, no eggs. Judging by now I just can say that I feel very good and think I have a stronger feeling of energy through the day.

After reading your stunning results I'm really curious what this may do for my lipids. My last TC on my old diet was 240, with LDL-C being 140 and HDL-C 40. Quite depressing numbers to say the least...

[scottknl]

This is one inspiring thread!

It's just coincidence that I have chosen to try a similar dietary change about three months ago. My "before" diet looked essentialy exactly as yours did, even down to the details.
My "after" diet is very similar too, yet including two to three small portions of fish (~2-5 ounces per portion) per week and small amounts of fat free quark now and then. No meat, no eggs. Judging by now I just can say that I feel very good and think I have a stronger feeling of energy through the day.

After reading your stunning results I'm really curious what this may do for my lipids. My last TC on my old diet was 240, with LDL-C being 140 and HDL-C 40. Quite depressing numbers to say the least...

Do you know your Apolipoprotien type? E3/E4 or E4/E4 or other? It might be interesting to know if a little meat spoils the good results or not. I've found that it takes at least 8 wks to see the differences when I make a change.

[Dolph]

I'm E3/E4. I will post the results when I get my levels tested, but this will probably not be until summer, when I have my regular TSH check anyway.