82 replies to this topic

[mikeinnaples]

Also, for what it is worth.... I feel more mentally sharp and even keeled through the day in keto than I do with a non keto healthy diet. The only issue I have is that once I got down to very low body fat, when I run out of fuel to burn it is like a car running out of gas. I am done until I get more in my body. Wasn't like that though until I was down to very low body fat %.


Sorry for the somewhat disjointed replies, but this isn't playing nice on my tablet.

[sthira]

I'm on a vegan diet-- whole foods only, nothing processed, no junk vegan garbage, no alcohol -- I eat veggies, fruits, legumes, nuts, evoo, coffee, cream in the coffee (which I reckon dethrones my veganitude...)

Here are my recent cholesterol numbers, for what it's worth:

Recent Selected Results

Body Mass Index
20.1 kg/m2 (Normal)

Cholesterol Level Total:
176 mg/dL (Normal)

Triglyceride:
25 mg/dL (Normal)

HDL Cholesterol:
71 mg/dL (Normal)

Non-HDL Cholesterol:
105 mg/dL (Normal)

LDL Cholesterol:
100 mg/dL (High)

Hemoglobin A1C:
4.5 %(Normal)

[Darryl]

OP: I did it with a low-added fats whole plant based diet, daily almonds (for add'l phytosterols) and 1000 mg nicotinic acid daily.

 

Judging by total cholesterol reports from bimonthly blood donations, I was only able to reduce total cholesterol to ~ 170 mg/dL (4.39 mmol/L) through the low fat diet alone. Its not unusual for progress to stall around here. It required an addition of the daily almonds and niacin to achieve my < 150 mg/dL (3.88 mg/dL) goal with regularity. My most recent annual blood lipids test was somewhat dissappointing to me, but not bad: Total 170 mg/dl, HDL 62 mg/dl, LDL 75 mg/dl, I attribute this to discovering inexpensive, but saturated fat laden, frozen Indian entrees at a local import grocer in the weeks prior.

 

Another person pointed out the growing evidence that longer saturated fats increase risk via inflammatory signalling independent of their effects on LDL. I thought this was an excellent recent review of the field:

 

Fritsche, Kevin L. "The Science of Fatty Acids and Inflammation." Advances in Nutrition: An International Review Journal 6, no. 3 (2015): 293S-301S.

 

It's available at LibGen, but there's been a publisher clampdown on access from the U.S. & Europe. A VPN (I use Hola Better Internet wtih chrome) can facilitate access. 

 

 

 

 

[pamojja]

I was planning to increase the intake of healthy saturated fats (such as butter from grass-fed cows). Would that lead to a further spike in the LDLC?

 

A plant based diet (vegan or not, your choice) will lower your LDL drastically.

 

I asked this question cause the LDL-C went up in the period when I switched from a bread-based breakfast to one with vegetables, 2 eggs and tuna/salmon (more paleo compatible sort of). It might have been a coincidence and the higher LDL-C is caused by something else.

 

First I would definitely retest, because LDL can fluctuate widely and by many unrelated factors in my experience (inflammation, infections, liver enzymes...)

 

 

When I was diagnoses a 85% stenosis at my abdominal aorta bifurcation with worse lipids I had been low-fat and vegetarian almost my whole life!

 

Just eliminating any Sugar (along with the other Pauling's Therapy recommendation) improved my pain-free walking distance (due to my severe PAD) from mere 3-400 meter to 1 hr within 1 year - LDL, HDL and Trigs together improved around 30%. Following the additional recommendations of Cardiologist William Davis from the second year onward (esp. grain free) improved walking distance up to 2 hrs, and since then my Lipids fluctuated between 40-50% improvement.

 

From my 1st year, with sugar already eliminated, my macro intake changed the following, compared to the initial, with relatively less improvement:

Fat from 41 to 68 %.

Protein: 18 → 19 %

Carb: 41 → 13 %

 

In my case I went from none to added eggs, fish and loads of fats (especially from nuts) and my numbers only improved. The more encouraging: increasing my handicapping little walking-distance to where I can have a life again.

 

The point I want to make: We are all different, and to know which life-style change really brings benefits you have to test repeatedly. (Unless you feel it too, like I did with the lack of walking pain)

 

 

PS: never mind, my stenosis remained exactly at 85% blockage the 6 years since.

Angiogenesis seem to have been my friend and I can hope it doesn't turn around, especially with the lower lipids, to make me have to fight cancer too one day...

Edited by pamojja, 21 June 2015 - 10:01 PM.

[HaloTeK]

So, has anyone really shown reversal of heart disease at fat percentage over 45%.  Looks like the above guy improved his numbers, but didn't lower his stenosis.  I'm starting to believe that only CR people can be at 40% fat or so and normal people need to keep it below 30% to keep the heart healthy.

[pamojja]

So, has anyone really shown reversal of heart disease at fat percentage over 45%.  Looks like the above guy improved his numbers, but didn't lower his stenosis.  I'm starting to believe that only CR people can be at 40% fat or so and normal people need to keep it below 30% to keep the heart healthy.

 

Did you read it?

 

When I was diagnoses a 85% stenosis at my abdominal aorta bifurcation with worse lipids I had been low-fat and vegetarian almost my whole life!

 

That's was one of the main preconditions for developing a 85% stenosis!. Been vegetarian since 10 years of age and hated eggs, fish or anything like butter.

 

Pathological coronary calcium score usually increases exponentially by about 30% annually. In my case this devastating progression even halted, once I quit low-fat and a purely vegetarian diet.

Edited by pamojja, 22 June 2015 - 09:25 PM.

[HaloTeK]

Why did you say PS no reversal still at 85% then?  Anyway, ultra low fat diets have been documented to reversal heart disease so you could be doing better than you are doing.

[ta5]

Pantethine 300mg x 4/day lowered my cholesterol from 174 to 148.

Grapeseed and chromium may help too.

Though, I'm not sure 148 is good since according to Chris Masterjohn and this study, stroke mortality is lowest between 180 and 200.

Edited by ta5, 23 June 2015 - 02:33 AM.

[misterE]

 

2. I'm not arguing that carbs that low are healthy, that is a very low carb diet, not low carb diet.

3. They evidently did well enough to survive, and if they are anywhere close to current hunter gatherers then their carbs would have varied considerably. There is also something i read about a certain hunter gatherer group only working for four hours a day, i swear i read it the other day yet i cant find it anywhere -.-. Also while they couldnt preserve the meat, they usually wouldnt have to. An animal would feed a tribe pretty well.

4. Apparently epilepsy, and i've heard positive things about a few others. http://www.epilepsyq...-ketogenic-diet

 

 

{2} This makes no sense at all, you are contradicting yourself here... please clarify.

 

{3} Sure they could survive, thankfully there are glucocorticoids, like cortisol, GH, and glucagon, that will keep you alive if you restrict carbohydrate intake or undergo starvation/famine

[misterE]

 

5. Ketosis is something diabetics experience? Really, that is a very misleading statement. Either you are confusing ketosis with ketoacidosis or you are way off base with your understanding of what being a diabetic is compared to someone who switches from glycolysis to ketosis through diet. For what it is worth, the only real way for a healthy person to get ketoacidosis through a ketogenic diet is from alcohol consumption either frequently or in large quantities.

I am under 30 grams net carbs per day mostly with a few days per month that I may go up to 50 or so. My latest number: LDL 89 HDL 64 Triglycerides 34, fasting glucose 78, BP 114/72, Pulse 52.... 40yo male.

I try to keep my fat intake on the healthy side, olives/oil, avocado, salmon, almonds, etc. I do eat eggs and will also have bacon once a week or so. Try to keep my protein down to what I need to maintain muscle and to recover from exercise. Coconut oil screwed up my cholesterol as well when I was using it, so I stopped.

 

 

{5} Sure. Ketosis is the beginning stages of ketoacidosis. Severe diabetics are in ketoacidosis, don't you know this? Ketones help spare the glucose needs of the brain. Most diabetics are undergoing catabolic processes like gluconeogenesis, in order to make glucose to fuel the brain. This process stops as soon as you start consuming carbohydrates!

 

Much of those fats you consume for your primary fuel are mostly unsaturated and tend to produce lipid-peroxides! In you ate (and over ate) carbohydrates, you wouldn't have this problem.  

Edited by misterE, 23 June 2015 - 03:10 AM.

[misterE]

So, has anyone really shown reversal of heart disease at fat percentage over 45%.  Looks like the above guy improved his numbers, but didn't lower his stenosis.  I'm starting to believe that only CR people can be at 40% fat or so and normal people need to keep it below 30% to keep the heart healthy.

 

The only folks EVER able to report this, in the scientific-literature is Ornish and Esselstyn. They used a diet of 10% or less fat and <5mg cholesterol.

Edited by misterE, 23 June 2015 - 03:27 AM.

[Dolph]

As much as I support lowfat approaches to diet, but the "scientific" works of Esselstyn ans Ornish aren't worth the paper they are printed on, and I really hate to write that. Everybody with a minimum of knowladge about clinical science will be able to realize this and it's not exactly helping their point.

[mikeinnaples]

 

 

5. Ketosis is something diabetics experience? Really, that is a very misleading statement. Either you are confusing ketosis with ketoacidosis or you are way off base with your understanding of what being a diabetic is compared to someone who switches from glycolysis to ketosis through diet. For what it is worth, the only real way for a healthy person to get ketoacidosis through a ketogenic diet is from alcohol consumption either frequently or in large quantities.

I am under 30 grams net carbs per day mostly with a few days per month that I may go up to 50 or so. My latest number: LDL 89 HDL 64 Triglycerides 34, fasting glucose 78, BP 114/72, Pulse 52.... 40yo male.

I try to keep my fat intake on the healthy side, olives/oil, avocado, salmon, almonds, etc. I do eat eggs and will also have bacon once a week or so. Try to keep my protein down to what I need to maintain muscle and to recover from exercise. Coconut oil screwed up my cholesterol as well when I was using it, so I stopped.

 

 

{5} Sure. Ketosis is the beginning stages of ketoacidosis. Severe diabetics are in ketoacidosis, don't you know this? Ketones help spare the glucose needs of the brain. Most diabetics are undergoing catabolic processes like gluconeogenesis, in order to make glucose to fuel the brain. This process stops as soon as you start consuming carbohydrates!

 

Much of those fats you consume for your primary fuel are mostly unsaturated and tend to produce lipid-peroxides! In you ate (and over ate) carbohydrates, you wouldn't have this problem.  

 

 

Severe diabetics are are also not *in* ketoacidosis, perhaps you meant to say ketosis there? There is a huge difference between diabetic ketosis and nutritional ketosis. Anyways, ketoacidosis is a condition brought on by severe and uncontrolled ketosis. The key words here being severed and uncontrolled. a perfectly healthy person can shift to Keto and never go into ketoacidosis. The concentration of ketones in ketoacidosis are 5x or more higher than that in someone in ketosis via diet.  
 

 

 

On a side note, how was my post pointless and time wasting? FFS just use the disagree button if you don't agree with me.

 

 

 

Edit: Much of my fat comes from olive oil and avocado. Care to explain why I should be afraid of consuming that?

Edited by mikeinnaples, 23 June 2015 - 12:56 PM.

[aza]

 

 

2. I'm not arguing that carbs that low are healthy, that is a very low carb diet, not low carb diet.

 

 

{2} This makes no sense at all, you are contradicting yourself here... please clarify.

 

 

 

Yes, i realised that i was contradicting myself a little. My bad. When i generally refer to low carb i mean low but not ketogenic. Which is considered VLCARB (very low carb) The inuit are close to no carbs, so they arnt particularly representative of the health of someone who eats 90g a day for example.  I suppose what i mean to say is all ketogenic diets are low carb, but not all low carb diets are ketogenic. I don't think this conversation is going anywhere, so i'll stop replying for now.

Edited by aza, 23 June 2015 - 02:31 PM.

[pamojja]

That's was one of the main preconditions for developing a 85% stenosis!. Been vegetarian since 10 years of age and hated eggs, fish or anything like butter.

 

Why did you say PS no reversal still at 85% then?  Anyway, ultra low fat diets have been documented to reversal heart disease so you could be doing better than you are doing.

 

Reminds me of the quote of Albert Einstein for Insanity: doing the same thing over and over again and expecting different results.

 

Please show me the link to only one documented case where a 85% stenosis at the abdominal aorta (about 2 cm in diameter) bifurcation was reversed by a ultra low fat diet - which was the diet which preconditioned it in my case.

[misterE]

As much as I support lowfat approaches to diet, but the "scientific" works of Esselstyn ans Ornish aren't worth the paper they are printed on, and I really hate to write that. Everybody with a minimum of knowladge about clinical science will be able to realize this and it's not exactly helping their point.

 

I don't see how you come to this conclusion Dolph. Take their work and compare it to the Okinawans and Tarahumarah-Indians, the migration studies and the dietary-change that is happing in Asia... and I think the science and literature paints a very clear picture. Why isn't Ornish and Esselstyn "worth the paper"?  

[misterE]

{1} a perfectly healthy person can shift to Keto and never go into ketoacidosis.

 

 

 

 

 

 

{2} Much of my fat comes from olive oil and avocado. Care to explain why I should be afraid of consuming that?

 

 

{1} That very well may be, but ketones are damaging and deplete your endogenous antioxidants, and release inflammatory, insulin-desensitizing free-fatty-acids... Diabetics are low in antioxidants, inflamed and have elevated FFAs; the hallmark of diabetes. I said it many times before and I guess I will say it again: Low-carb diets mimic type-1-diabetes. One of the symptoms of type-1-diabetes is weight-loss.

 

{2} These are neutral-fats [1]. Human-body-fat has a composition of 0.13, whereas olive and avocado fat have compositions of 0.15 and 0.12. So as you can see these fats are basically reflective of human body-fat, which is good. Soybean-oil, which is the most used fat-source in America has a composition of 1.5; a difference of 1054%!

 

Walnuts have a composition of 3.1 (2285% difference)

Trout (fish) has a composition of 0.54 (315% difference)

Turkey-fat has a composition of 0.31 (138% difference)

Chicken-fat has a composition of 0.27 (108% difference)

Pig-fat has a composition of 0.13 (0% difference)

Beef-fat has a composition of 0.04 (69% difference)

 

 

The only problem I see with eating olives and avocadoes shamelessly is that they have terrible omega-3 to omega-6 ratios.

 

Cottonseed: 1:292

Olives: 1:12

Avocado: 1:15

Butter: 1:11

Soybean: 1:7

Beef Tallow: 1:5

White-rice: 1:3

Pinto-bean: 1:1

Broccoli: 2:1

Spinach: 6:1

Oysters: 15:1

 

 

I hope this helps!!

 

 

 

 

 

[1] http://www.longecity...f-common-foods/

 

 

Edited by misterE, 23 June 2015 - 09:43 PM.

[Dolph]

Really, we had this discussion roughly a dozen times over here and you seem to "forget" it again and again. I don't understand it. Cerebral sclerosis maybe? 

 

I say again that I more or less agree with a plant based low fat diet, but Esselstyn and Ornish have done nothing, I repeat, nothing to add scientific credibility to their hypothesis. And no, trials with 12(!) patients (sometimes also 15 or 16, depending on what Esselstyn thinks is offering a more convincing theme...) comedicated with lipid lowering drugs and without a control group are not what I or anybody else considers to be scientific.

 

I will now unfollow this thread. It really makes my head ache. Feel like trapped in some kind of time loop... 

[misterE]

Really, we had this discussion roughly a dozen times over here and you seem to "forget" it again and again. I don't understand it. Cerebral sclerosis maybe? 

 

I say again that I more or less agree with a plant based low fat diet, but Esselstyn and Ornish have done nothing, I repeat, nothing to add scientific credibility to their hypothesis. And no, trials with 12(!) patients (sometimes also 15 or 16, depending on what Esselstyn thinks is offering a more convincing theme...) comedicated with lipid lowering drugs and without a control group are not what I or anybody else considers to be scientific.

 

I will now unfollow this thread. It really makes my head ache. Feel like trapped in some kind of time loop... 

 

Ornish had a control group.

[mikeinnaples]

 

{1} a perfectly healthy person can shift to Keto and never go into ketoacidosis.

 

 

 

 

 

 

{2} Much of my fat comes from olive oil and avocado. Care to explain why I should be afraid of consuming that?

 

 

{1} That very well may be, but ketones are damaging and deplete your endogenous antioxidants, and release inflammatory, insulin-desensitizing free-fatty-acids... Diabetics are low in antioxidants, inflamed and have elevated FFAs; the hallmark of diabetes. I said it many times before and I guess I will say it again: Low-carb diets mimic type-1-diabetes. One of the symptoms of type-1-diabetes is weight-loss.

 

Honestly, you can say it again and again, but it doesn't change anything. Part of your reasoning that you detailed in the other thread comes from a flawed understanding of cortisol metabolism and making a blanket statement that ketogenic diets mimic type-1 diabetes in a healthy person is grossly misleading.

[niner]

 

If you are really homozygous for ApoE4 (indeed the worst variant for lipid metabolism and Alzheimer's disease risk), those dietary changes are likely very detrimental to your long-term health and you should be much more concerned about the saturated fat content of your diet than about the glycemic load. I would urge you to cut back on butter and coconut oil, go back to olive/canola oil and to limit your intake of saturated fat from animal food (e.g. by choosing lean meats and low-fat dairy). Also, forget my advice about moderate alcohol consumption, as the HDL-boosting effect alcohol doesn't seem to work for ApoE4.

 

Indeed, you can be happy to have such a decent lipid profile as an E4/E4 carrier. Don't ruin it by falling for the LC/Paleo hype!

 

Btw. pasta, if cooked al dente, is not a particularly high-GL food. Nor is white rice if allowed to cool down (and reheated) before consumption. In Asian cultures, it is customary to cook large amounts of white rice in a rice pot and eat it troughout the day. Therefore, much of the rice will be enriched in resistant starch. I think this is an often neglected fact that (besides the fiber-rich, low protein dietarry pattern) may help to explain the beneficial outcomes of white rice in those cultures.

 

Chris_T_Malta, this is very good advice.  ApoE4/4 people are the specific population that should really be eating low fat.  We have some good apoe4 threads here, and there are apoe4 forums on the internet.  I'd look into these things, as it might well be the best way to maintain / improve your long term health.  You're lucky that you know your genotype, because there are things you can do to reduce your risk.

 

After some back and forth on this with MisterE, I looked at the recent literature on ApoE4 diet interactions, and the data for ApoE4 heterozygotes is mixed regarding the effect of dietary lipids on LDL-C.  However, in a 2012 prospective analysis, a low fat diet x genotype effect was significant for the ApoE3/4 heterozygote group for C-reactive protein and for Trigs.  I think that the significant CRP effect is a pretty good reason to reduce fat.  More importantly for the OP, they pointed out that ApoE4/4 homozygotes appear to have a different response with LDL-C:

 

 

Although very underinvestigated [with only 6 of 42 studies in the Masson et al review having a separate APOE4/E4 group and only 1–15 per group (8)] and therefore somewhat speculative, it is likely that the effect of the APOE allele is dependent on heterozygosity (APOE3/E4, 20–25% whites) or homozygosity (APOE4/E4, 1–2% whites). In agreement with our observations, Tikkanen et al (22) observed no differences in responses between the APOE3/E4s and wild-type genotypes, with significantly greater cholesterol responses in the APOE4/E4 subgroup after the switch to a lower-fat, lower-SFA diet, which is consistent with the observations of Sarkkinen et al (23) in subjects with familial hypercholesterolemia (23).

 

It's also the case that as a group, ApoE3/4 people have moderately higher baseline LDL, which does respond to a lower fat diet, even if that change is similar in ApoE3/3.  Thus, for all ApoE4 carriers, and particularly for the ApoE4/4 homozygotes, I think a lower fat diet is still pretty good advice.
 

[blood]

... daily almonds and niacin ... 

 

What's your daily "dose" of almonds, Darryl?

[Darryl]

I buy 1.5 oz (42g) packets sold at a wholesale club, as its one of few ways I've found to ration my consumption. Its rather convenient as this is approximately the amount required to cover most vitamin E requirements (11.1 mg) and is a useful supplement for Ca (112 mg) and Mg (114 mg) intake.

 

I'm well aware that this is a fairly high dose, as 42 g carries a heavy 240 kcal, and there's no evidence of further benefit from more than 15 g nuts in a recent study:

 

van den Brandt, PA. & Schouten, LJ. 2015. Relationship of tree nut, peanut and peanut butter intake with total and cause-specific mortality: a cohort study and meta-analysis. International journal of epidemiology, dyv039.

 

Almond trials have been a pretty busy field of late:

 

Jenkins DJ  et al. 2002. Dose response of almonds on coronary heart disease risk factors: blood lipids, oxidized low-density lipoproteins, lipoprotein (a), homocysteine, and pulmonary nitric oxide a randomized, controlled, crossover trial. Circulation, 106(11), 1327-1332.

Chen CY et al. 2005. Flavonoids from almond skins are bioavailable and act synergistically with vitamins C and E to enhance hamster and human LDL resistance to oxidation. The Journal of nutrition, 135(6), 1366-1373.

Wien M et al. 2010. Almond consumption and cardiovascular risk factors in adults with prediabetes. Journal of the American College of Nutrition, 29(3), 189-197.

Li SC et al. 2011. Almond consumption improved glycemic control and lipid profiles in patients with type 2 diabetes mellitus. Metabolism, 60(4), 474-479.

Berryman CE et al. 2011. Effects of almond consumption on the reduction of LDL-cholesterol: a discussion of potential mechanisms and future research directions. Nutrition reviews, 69(4), 171-185.

Jaceldo-Siegl K et al. 2011. Influence of body mass index and serum lipids on the cholesterol-lowering effects of almonds in free-living individuals. Nutrition, Metabolism and Cardiovascular Diseases, 21, S7-S13.

Tan SY & Mattes RD 2013. Appetitive, dietary and health effects of almonds consumed with meals or as snacks: a randomized, controlled trial.European journal of clinical nutrition, 67(11), 1205-1214.

Liu,Z et al. 2014. Prebiotic effects of almonds and almond skins on intestinal microbiota in healthy adult humans. Anaerobe, 26, 1-6.

Jamshed H & Gilani AH. 2014. Almonds inhibit dyslipidemia and vascular dysfunction in rats through multiple pathways. The Journal of nutrition, 144(11), 1768-1774.

Berryman CE et al. 2015. Effects of daily almond consumption on cardiometabolic risk and abdominal adiposity in healthy adults with elevated LDL‐cholesterol: a randomized controlled trial. Journal of the American Heart Association, 4(1), e000993.