34 replies to this topic

[sthira]

Here's how I practiced CR over one recent three-day period. My efforts are loaded into COM.

I aim for 1800/kcal per day in a vegan CR practice. I weigh food (at home) with a scale, and load the values in right away to minimize errors. The three-day example doesn't include supplements. This is just an example of how I ate over three days. I do change things up, especially with the seasons; I'm flexible yet try to stay under the vegan umbrella. Your comments are welcomed.


SUNDAY, March 13, 2011
_____________________________
**7:20 am**
Collard greens, boiled: 362/g: 94/kcal
Flax seed oil: 9/g: 79/kcal
Mustard greens, boiled: 348/g: 90/kcal
Almonds, raw: 10/g: 57/kcal
Kale, boiled: 205/g: 57/kcal
Olive oil: 7/g: 61/kcal
Green tea: 20/oz: 0/kcal
Raspberries, raw: 186/g: 96/kcal
Blueberries, raw: 179/g: 102/kcal
Spinach, boiled: 454/g: 104/kcal
Strawberries, raw: 234/g: 74/kcal
Hazelnuts, raw: 10/g: 62/kcal

**10:30 am**
Green tea: 20/oz: 0/kcal

**12:30 pm**
Grapefruit, raw: 3 whole: ±135/kcal
Pear, raw: 1 whole: ±124/kcal
Apple, raw: 1 whole: ±87/kcal
Green tea: 20/oz: 0/kcal

**4:00 pm**
Oranges, raw: 2 whole: ±130/kcal
Green tea: 20/oz: 0/kcal

**7:00 pm**
Beet greens, boiled: 661/g: 178/kcal
Strawberries, raw: 454/g: 145/kcal
Blueberries, , raw, cultivated: 169/g: 97/kcal

Total calories: ±1778
Height: 6' 2"
Weight: 130.2 lbs

MONDAY, March 14, 2011
_____________________________
**6.15 am**
Cabbage, red, boiled: 429/g: 124/kcal
Collard greens, boiled: 384/g: 100/cal
Flax seed oil: 9/g: 79/kcal
Walnuts, raw: 10/g: 65/kcal
Almonds, raw: 8/g: 46/kcal
Chard, boiled: 254/g: 50/kcal
Pecans, raw: 12/g: 82/kcal
Pumpkin seeds, raw: 8/g: 44/kcal
Grapefruit, raw: 166/g: 50/kcal
Brussels sprouts, steamed: 372/g: 134/kcal
Tomatoes, steamed: 534/g: 96/kcal
Mushrooms, shiitake, steamed: 204/g: 114/cal
Olive oil: 8/g: 71/kcal
Tumeric, spice: 3/g: 0/kcal
Black pepper, spice: <1/g: 0/kcal

**11.30 am**
Orange, raw: 128/g: 59/kcal
Green tea: 20/oz: 0/kcal

**2:30 pm**
Blackberries, raw: 279/g: 120/kcal
Cocoa powder, unsweetend: 11/g: 25/kcal
Green tea: 20/oz: 0/kcal
Okra, steamed: 318/g: 70/kcal
Spinach, boiled: 722/g: 166/kcal
Green tea: 20/oz: 0/kcal

**4.20 pm**
Raspberries, raw: 337/g: 175/kcal
Cocoa powder, unsweetend: 12/g: 27/kcal

Total calories: ±1701
Weight: 130.4 lbs

TUESDAY, March 15, 2011
_____________________________
**5:45 am**
Collard greens, boiled: 331/g: 86/kcal
Flaxseed oil: 6/g: 53/kcal
Asparagus, steamed: 441/g: 97/kcal
Olive oil: 7/g: 62/kcal
Kale, boiled: 254/g: 71/kcal
Almonds, raw: 9/g: 52/kcal
Walnuts, raw: 5/g: 32/kcal
Mustard greens, boiled: 291/g: 44/kcal
Pecans, raw: 4/g: 27/kcal
Pumpkin seeds, raw: 10/g: 56/kcal
Hazelnuts, raw: 7/g: 44/kcal

**7:45 am**
Strawberries, raw: 222/g: 71/kcal
Blueberries, raw: 181/g: 103/kcal

**10:50 am**
Nectarine, raw: 113/g: 50/kcal
Cabbage, red, steamed: 221/g: 64/kcal
Cauliflower, steamed: 389/g: 90/kcal
Olive oil: 10/g: 88/kcal
Tumeric: 7/g: 0/kcal
Black pepper, spice: <1/g: 0/kcal
Grapefruit, raw: 158/g: 47/kcal
Green tea: 20/oz

**5:40 pm**
Raspberries, raw: 178/g: 93/kcal
Blackberries, raw: 346/g: 149/kcal
Plum, raw: 121/g: 56/kcal

**7:30 pm**
Tomatoes, raw: 454/g: 82/kcal
Tomatoes, steamed: 311/g: 56/kcal
Brussels sprouts, steamed: 281/g: 101/kcal
Broccoli, steamed: 412/g: 144/kcal

Total calories: 1818
Weight: 131.8

This is CoM's Nutrition Report over the three days listed above.

General (92%)
------------------------
Energy: 1746.3 kcal: 94%

Protein: 79.0/g: 65%
Carbs: 311.3/g: 124%
Fiber: 117.0/g: 308%
Starch: 0.4/g:
Sugars: 123.7/g: 247%
Fat: 50.3/g: 87%

Alcohol: 0.0/g
Caffeine: 17.6/mg
Water: 3968.4/g: 107%
Ash: 36.5/g

Vitamins (84%)
-----------------------
Vitamin A: 136838.5 IU: 4561%
Retinol: 0
Alpha-carotene: 575.5
Beta-carotene: 81267.4
Beta-cryptoxanthin: 289.3
Lycopene: 12533.8
Lutein+Zeaxanthin: 133364.8

Folate: 2113.2: 528%
B1 (Thiamine): 2.7/mg: 227%
B2 (Riboflavin): 3.8/mg: 296%
B3 (Niacin): 23.9/mg: 149%
B5 (Pantothenic Acid): 11.9/mg: 237%
B6 (Pyridoxine): 5.1/mg: 392%
B12 (Cyanocobalamin): 0: 0%
Vitamin C: 1228.0: 1364%
Vitamin D: 21.1 IU: 11%
Vitamin E: 42.5: 283%
Beta Tocopherol: 0.4/mg
Delta Tocopherol: 4.6/mg
Gamma Tocopherol:13.2/mg
Vitamin K: 7618: 6349%
Biotin: 0: 0%
Choline: 671.4/mg: 122%

Minerals (99%)
---------------------
Calcium: 2352.9/mg: 235%
Chromium: 0/ 0%
Copper: 5.4/mg: 596%
Iron: 44.7/mg: 559%
Magnesium: 1238.3/mg: 295%
Manganese: 16.8/mg: 730%
Phosphorus: 1649.5: 236%
Selenium: 61.5: 112%
Sodium: 1346.9/mg: 90%
Zinc: 15.9/mg: 144%

Amino Acids (93%)
------------------
ALA: 2.9/g
ARG: 4.5/g
ASP: 7.1/g
CYS: 0.8/g
GLU: 10.2/g
GLY: 2.5/g
HIS: 1.5/g: 104%
HYP: 0.0/g
ILE: 2.8/g: 146%
LEU: 4.1/g: 97%
LYS: 3.3/g: 88%
MET: 0.9/g: 48%
PHE: 2.8/g
PRO: 2.4/g
SER: 2.4/g
THR: 2.5/g: 126%
TRP: 0.9/g: 290%
TYR: 1.9/g: 120%
VAL: 3.3/g: 138%

Lipids
-----------------------------------
Saturated: 6.1/g: 30%
Monounsaturated: 20.2/g
Polyunsaturated: 18.4/g
Omega-3: 7.5/g: 467%
Omega-6: 10.9/g: 64%
Trans-Fats: 0
Cholesterol: 0
Phytosterol: 124.8/mg

Edited by Michael, 26 September 2011 - 07:49 PM.

[Skötkonung]

I stuck your Sunday diet in cron-o-meter and got the following:
- 1858 calories
- 69.7 g protein
- 368 g carbohydrate
- 38.5g fat

Just looking at your diet, cron-o-meter says you're getting 150~g from sugar. Don't you think that's a little high? Your fat intake is also very low (below 18% of total calories). I question if you are getting adequate fat to absorb most of the nutrients in your various greens and even fruit (fat is essential for carotenoid absorption). And given that flax doesn't convert well to longer chain omegas, I wonder if your omega 6 / 3 balance isn't that great. Plus your saturated fat intake is so low... it may be debateable about whether one should consume a lot of saturated fat, but there is also a lower limit. I would be concerned you're below that.

I'm assuming you're supplementing B12 and D3, but you're also very low on Selenium. Something to consider...

Also, you're quite low on a bunch of essential amino acids, so I'm wondering if the protein reading from cron-o-meter is accurate. Hydroxyproline, for instance, was completely missing from your diet. Others are extremely low. You may want to practice some form of protein combining as well as better food choices to get enough of these essential amino acids.

Not to pick on you.. but your diet is a good example of how just eating "superfoods" really doesn't provide adequate nutrition. It may be even hurting you depending on your view of polyphenols and hormesis. And avoiding animal foods may also be damaging to your health. Have you ever had a serum vitamin A test done? I'd be curious if you're vitamin A deficient.

Edited by Skötkonung, 17 March 2011 - 12:27 AM.

[Application]

I stuck your Sunday diet in cron-o-meter and got the following:
- 1858 calories
- 69.7 g protein
- 368 g carbohydrate
- 38.5g fat

[...] Your fat intake is also very low (below 18% of total calories). [...] Plus your saturated fat intake is so low... it may be debateable about whether one should consume a lot of saturated fat, but there is also a lower limit. I would be concerned you're below that. [...]

Also, you're quite low on a bunch of essential amino acids, so I'm wondering if the protein reading from cron-o-meter is accurate. Hydroxyproline, for instance, was completely missing from your diet. Others are extremely low. You may want to practice some form of protein combining as well as better food choices to get enough of these essential amino acids. [...]

And avoiding animal foods may also be damaging to your health. Have you ever had a serum vitamin A test done? I'd be curious if you're vitamin A deficient.

I am not aware of any nutritional requirement for saturated fat (which is found in small amounts in almost all plant food). The mono fats and other vegetable oils serve the same purpose for carotenoid absorption, no? Also, hydroxyproline is not an essential amino acid. As has been posited here, it seems low protein could be a key part of the CR benefit.

I would be curious to see vitamin A levels too.

Edited by Michael, 17 March 2011 - 01:59 PM.

[sthira]

Thanks for commenting, Skot.

You wrote: "Just looking at your diet, cron-o-meter says you're getting 150~g from sugar. Don't you think that's a little high? "

I think you're probably correct: too much fruit. I love fruit; it's a difficult challenge for me to cut back. But I'm confused about how much is too much. I think Paul McGlothin aims for way less than I do.

You wrote: "Your fat intake is also very low (below 18% of total calories). I question if you are getting adequate fat to absorb most of the nutrients in your various greens and even fruit (fat is essential for carotenoid absorption)."

I do try to include some fat with many of the greens I eat: nuts, olives, olive oil, flax seed and oil. The trouble, of course, is these are extremely energy dense. So eating more fat quickly uses up my self-imposed calorie limits. You're suggesting eat more fat and fewer fruits.

You wrote: "And given that flax doesn't convert well to longer chain omegas, I wonder if your omega 6 / 3 balance isn't that great."

I've been debating within myself eating small amounts of sardines. Also oysters. And as you note, I'm supplementing B12 and D3. In the bigger picture, my selenium levels seem better. I would eat a few brazil nuts from time to time, but I don't trust them for several reasons.

You wrote: "Have you ever had a serum vitamin A test done? I'd be curious if you're vitamin A deficient."

Me, too, actually: retinol, in particular. I know you take cod liver oil.

[Skötkonung]

I am not aware of any nutritional requirement for saturated fat (which is found in small amounts in almost all plant food). The mono fats and other vegetable oils serve the same purpose for carotenoid absorption, no? Also, hydroxyproline is not an essential amino acid. As has been posited here, it seems low protein could be a key part of the CR benefit.

I would be curious to see vitamin A levels too.

Sure, the mono-fats probably help with nutrient absorption but even those are such a low proportion of the diet that I would be concerned about actual nutrient uptake. If I were determined to keep my fat intake very low, I would want to make sure my serum levels of the pertinent nutrients aren't deficient. My comment relating to saturated fat pertains mostly to HDL cholesterol. I've seen some people on a almost fat free diet have dangerously low HDL cholesterol. Some fat, particularly saturated fat, is great at raising HDL. I'd be interested to see what Sthira's lipid profile looks like?

By the way, I believe "essential" is misleading. Hydroxyproline is an essential amino acid in that the body must have it in the diet or have the constituent factors to produce it. Hydroxyproline is necessary for the construction of the body's major structural protein, collagen. Defects in collagen synthesis lead to easy bruising, internal bleeding, breakdown of connective tissue of the ligaments and tendons, and increased risk to blood vessel damage. The body produces hydroxyproline from proline, which is also in a very low in Sthira's diet. I agree that high protein may be a risk factor for premature aging, but adequate (or just below adequate) complete protein is necessary for proper functioning of the body. Since he is doing a CR diet, a protein intake at .8-1g/kg is already quite low by most standards. It's not just this one amino acid, though. His cysteine levels are also very low, which probably means his glutathione production is also fairly low since dietary cysteine (although a non-essential amino acid) helps raise this endogenous antioxidant. If not adequately supplied in the diet, cysteine is produced from serine (this is closer to adequate) and methionine (very low). Since he may want to keep methionine from getting too high, eating more cysteine containing foods could be advantageous.

Finally, Sthira's vitamin K2 intake is completely absent. K2 is proving to be more and more beneficial in terms of cardiovascular health.

Here are some ideas for Sthira's diet.. and I apologize if these are adressed with supplements:
- Eat humus, olive oil, and pita with your vegetables. This will improve the quality of your protein intake. Hummus, which is made from chickpeas, is comparatively low in methionine. Legumes and grains are complementary proteins.
- Consider having vitamin A levels tested and possibly supplementing small doses of the preformed vitamin A.
- Supplement vitamin D3. There is currently no vitamin D in diet.
- Supplement magnesium. This should be balanced with calcium intake. Currently calcium is almost double the magnesium intake. If you follow the inflammatory hypothesis, you'll want to make sure you have more than aequate amounts of dietary magnesium.
- Supplment vitamin K2 and / or eat more fermented foods. Natto, kimchi, tempeh... these are all good choices. Only natto contains K2 (MK7).
- Supplement long chain omega 3 fats in adequate amounts. There is evidence that too much omega 3 (or 6) can be detrimental or cause no benefit, but adequate amounts are important for cardiovascular health.
- Reduce sugar content in diet. Add more saturated fats. Maybe a tablespoon or two of red palm oil.. which has all kinds of good stuff in it like large amounts of vitamin E (mostly tocotrienols), vitamin K1, coenzyme Q10 and assorted other fat-soluble constituents. http://wholehealthso...s-palm-oil.html
- Dark chocolate could be another way of adding more fat to your diet.

Sthira, I know you're worried about calorie intake, but you're tall ( I believe above 6ft) so 1800 calories may be too little. Consider increasing that amount to 2000. That would still be adequate CR for someone of your height.

Edited by Skötkonung, 17 March 2011 - 05:47 PM.

[kismet]

What is the evidence for the SAFA claim? I would be interested to hear something on this (low fat diet ain't a good argument: carbs worsen the hdl/ldl ratio over almost ALL fats). And why do you support it with a link to Stephan's blog: one of the biggest opponents of reductionistic nutritionism. Some SAFA-rich foods may be healthy*, but this does not reduce to "SAFA is healthy".

*even on this front I tend to disagree: the olive oil - nuts - n3 source triad still seems best for fat

Edited by kismet, 17 March 2011 - 05:54 PM.

[Skötkonung]

What is the evidence for the SAFA claim? I would be interested to hear something on this (low fat diet ain't a good argument: carbs worsen the hdl/ldl ratio over almost ALL fats).

The way that dietary fat is tested remains largely questionable to me. I've seen some research using corn oil versus palm oil, but these laboratory diets rarely use real food and I question how they apply to actual free-living humans. Often the researchers fail to even account of trans-fats. I would also caution the tendency to lump all saturated fats together. Stearic acid comes to mind as a saturated fat that even the current literature recognizes as being beneficial for the lipid profile.

Intake of certain fatty acids may increase cholesterol levels, but again this is more consistent with greater cholesterol synthesis. For example the most powerful increaser of total cholesterol is probably lauric acid, but lauric acid is also the most powerful reducer of the LDL-to-HDL-cholesterol ratio -- this is consistent with lauric acid being burned for quick energy, thus increasing the energy state of the liver cell and allowing for greater cholesterol synthesis. Not "blocking" the LDL receptor or anything nefarious like that.

That said, you wanted to see evidence supporting the consumption of saturdated fat. Here's something for you to review. Fat composition in the diet changes the composition / oxidation of the lipoprotein. PUFAs may lower LDL, but simply having a low LDL level may not be enough to be protective against CVD. Experimental evidence has shown in humans that saturated fats protect against in vivo LDL oxidation. You can see this by looking at the rightward most column in this graph: Dietary Fat and LDL Oxidation. This shows a graded increase in LDL oxidation occuring within the blood of live humans as the diet goes from 1) butter and palm oil to 2) olive oil to 3) sunflower oil and finally 4) sunflower oil and fatty fish, all diets being about 35% of calories from fat. The first two diets were statistically significant from the second two diets, but the increase between butter/palm and olive oil was not significant, nor was the increase between sunflower and sunflower/fatty fish. So what we can conclude here is that it is primarily dietary polyunsaturated fats from seed oils and excess amounts of fatty fish that contribute to LDL oxidation.

My diet is mostly saturated fat, I have a total cholesterol of 219.. but my HDL is 106 (it's been as high as 130) and LDL through direct measurement is 66. Calculated to be 75 or 104, depending on which formula you are using (Friedwald being the latter). Based on the peer reviewed research, one would expect me to be on death's door with as much saturated animal fat as I eat, but my lipids are excellent none the less. And while I haven't had it tested, I would speculate my LDL subtype to be low risk.

Honestly, I think fat isn't the demon people say it is and I think saturated fat is under-rated as a tool to positively modulate lipids. I speculate that Sthira has low cholesterol and probably a very low HDL. I have vegan friends consuming a similar diet with HDL cholesterol in the 20s and 30s and likely a LDL prone to oxidation. I'm not advocating he do the same borderline ketogenic diet as myself. He should have his lipids tested and modulate his diet to get it to an optimal level. Personalized nutrition trumps everything in my opinion.

Sthira asked for recommendations about his diet and I suggested more saturated fat based on these experiences.

Edited by Skötkonung, 17 March 2011 - 08:06 PM.

[scottknl]

Sthira, Do you balance your nutrition on a daily basis so that you get RDI of vitamins and minerals? or would you balance it out over a few days or a week so that on average you got RDI for each day?

I have to say chugging thru a whole pound of boiled spinach in addition to all those other greens that first morning musta been tough!.

[sthira]

Scottknl: I record what I eat on a daily basis, and I'm pretty solid at hitting RDA targets. I love food; I don't like supplements, but as I vegan I choke em down anyway.

With greens, I'm lucky because I crave them - just thinking about boiled collards, for example, makes my eyes cross and my knees quiver. I'm strange. I believe you have to be a little counter-culture to seriously practice this lifestyle. You mentioned spinach, and I try to moderate spinach because of the well-known concerns. Sometimes I don't moderate it, though, and will eat a pound or two. In fact, I just did - a few minutes ago.

I value Skot's erudite analysis and dietary suggestions. Some I will adopt, others are not yet for me. For example, I will further moderate my fruit intake; I may eat more beans, quinoa, barley, lentils. Skot suggests hummus: this is easy, who doesn't love hummus?! The pita bread isn't for me; I don't eat bread. Nor do I deliberately aim for much saturated fat. While I love coconut oil, for example, for me the downside risk seems steep. I do eat a lot of young coconuts, though, they're delicious. And what's the word on red palm oil? I thought it was poison. Justfuckinggoogleit.com???

Skot's retin comments have my attention - I need testing. But I don't need magnesium - my balance with calcium seems fine in my bigger dietary picture. Skot's right about K2 - I eat no natto and practically no fermented foods.

Skot suggests I lessen my CR when I'm actually going the other way and slowly intensifying. CR isn't easy but it works for me - I feel fantastic. I'm damned skinny, but I'm strong and my professional life as a television cameraman is important to me. I lug around a 30-pound camera and a bunch of heavy gear all day, and if CR made me weak, I wouldn't do CR. If anything, the CR has improved my work load - I have enormous amounts of energy and stamina and I haven't been sick in years.

I've been eating between 1700 to 1900 calories per day since 2007, and my weight has stayed steady at ~130 lbs - I'm 6'2". I may give up more fruit and drop down another 100 calories and see what happens. CR is an experiment - it's also interesting and can be trippy fun if you give it a chance.

[Michael]

So, to start, I strongly endorse Sköt's suggestions that you cut down your fruit intake, and get some legumes into you. I also agree that you need to eat more fat, tho' not SAFA (more on this below); can you please post your macronutrient ratios from the COM pie graph? Either post or PM or email me, and I'll edit them into your post.

I'm also a bit concerned about the specific PATTERN of your fruit intake (almost always alone, in large quantities): all that sugar with no protein or fat really isn't a good thing for your liver and postprandial insulin and lipids.

I agree that you (and, really, everyone who isn't eating a huge amount of liver or a variety of fatty fish, and isn't a Damned Fool about sun exposure) need to supplement vitamin D, and get yourself tested. OTOH, I really don't think you need to worry about your vitamin A levels: sure, you get no preformed retinol, but you're getting 45 times the RDA, for chrissake! Your conversion rate can't possibly be that poor, or you'd be long since have gone blind.

Also, the widespread notion, often repeated even in the scientific literature, that we need to get dietary EPA & DHA because ALA conversion rates are 'poor.' This is a mechanistically-based, make-the-case petitio principii, which assumes that some higher rate is necessary, finds that it's lower, and gets worried, despite the overwhelming evidence that ALA conversion to EPA and DHA is adequate to ensure cardiovascular and other health outcomes. And, you (Sthira) are getting lots of ALA. As well, there's good reason to think that people on CR should minimize dietary EPA, DHA, & fish oil.

Similarly, the belief that dietary saturated fat is 'necessary' based on its better support of HDL levels is also mechanistically backward, and again rebutted by the evidence from actual health outcomes. There are now several meta-analyses of prospective epidemiology and clinical trials (1-3) all showing that substitution of saturated with polyunsaturated fat (but not, importantly, with carbohydrate) leads to better cardiovascular health outcomes. This conclusion actually very likely underestimates the strength of the effect, in part because in many of the included studies, the 'low' SaFA diets still contained way too damned much saturated fat (should be ≤7% of energy), and the high intake of carbohydrate (esp. high-GI carb (see eg. (4)) and prevalence of overweight and obesity and ensuing insulin resistance (see studies by Volek and by others), and other reasons to think that the evidence that saturated fat really is bad for you probably underestimate the true strength of their effect.

I think the evidence on this is clear, and have no intention of re-litigating this subject, NB. However, I will (with some trepidation) address some of Sköt's specific issues.

First, the easy one: HDL. Plenty of mono fats -- combined with cutting back the sugar -- should, IAC, deal with low HDL cholesterol. But a better question would be: Sthira, I know you get tested; are you happy with your HDL levels? IF not, another good reason to get yourself some olive oil!

Now, the harder ones:

Intake of certain fatty acids may increase cholesterol levels, but again this is more consistent with greater cholesterol synthesis. For example the most powerful increaser of total cholesterol is probably lauric acid, but lauric acid is also the most powerful reducer of the LDL-to-HDL-cholesterol ratio -- this is consistent with lauric acid being burned for quick energy, thus increasing the energy state of the liver cell and allowing for greater cholesterol synthesis. Not "blocking" the LDL receptor or anything nefarious like that.

This is, again, a mechanistically-based argument. It is unfortunately difficult to do proper, prospective epidemiological studies on actual health outcomes associated with consumption of individual fatty acids, and esp lauric acid, because it's such a minor contributor to total SFA intake and in most populations is too strongly correlated with same; however, (5) did indeed find a small increase in CHD risk with each SaFA individually from lauric (12:0) to stearic (18:0). Notably, these subjects were free of not only atherosclerosis, but even hypercholesterolemia, when the study began.

For mechanism addicts can indulge their habits with (6-10), and here andhere; but really, this is all speculative, vs. the well-supported generalized evidence that lowering SaFA as a class in favor of PUFA is protective against negative cardiovascular outcomes.

Fat composition in the diet changes the composition / oxidation of the lipoprotein. PUFAs may lower LDL, but simply having a low LDL level may not be enough to be protective against CVD. Experimental evidence has shown in humans that saturated fats protect against in vivo LDL oxidation. You can see this by looking at the rightward most column in this graph: Dietary Fat and LDL Oxidation. This shows a graded increase in LDL oxidation occuring within the blood of live humans as the diet goes from 1) butter and palm oil to 2) olive oil to 3) sunflower oil and finally 4) sunflower oil and fatty fish, all diets being about 35% of calories from fat.

You have to be really, really careful when you look at studies of LDL oxidation. Notably, this study does not show that dietary saturated fats protect against in vivo LDL oxidation: it shows that dietary saturated fats "protect" against ex vivo LDL peroxidizability. They are not the same thing, even tho' abstracts sometimes assert "LDL oxidation" without qualification. They did not measure actual, in vivo oxidized LDL levels: they extracted LDL out of the body, and then assessed "Lag time of Cu2+-oxidated LDL" and "Conjugated dienes in Cu2+-oxidated LDL." Ie, they soaked them in unphysiologic levels of copper ions, and induced the Fenton reaction. Surprise! You get lipid peroxidation. This doesn't reflect the in vivo situatioin at all, at all.

Unfortunately, while at least a few studies have confirmed that replacing carb with mono fat lowers in vivo LDL oxidation, only one study that I've been able to find tested a high-MUFA diet against a high-SaFA diet -- and it's a graduate thesis, still unpublished, and in Spanish, and in insulin-resistant subjects.(11) However, it did indeed find that a high-MUFA (mostly from olive oil) diet lowered in vivo postprandial oxidized LDL relative to a high-SaFA one (mixed sources, but a lot of butter). You'd likely need a longer time period to meaningfully assay typical basal oxLDL levels.

After the initial selection of volunteers and obtaining informed consent, the 11 participants, randomly and in a Latin square crossover design for Williams, followed by three dietary periods of 28 days duration: one rich in SAT fat to a composition of 47% CHO, 15% protein and 38% fat (23% SAT, 9% Mono, 6% poly), another low in fat and high in CHO consisting of 65% CHO, 15% protein and 20% fat (6% SAT, 8% and 6% POLY MONO) and a third rich in mono with 47% CHO, 15% protein and 38% fat (9% SAT, 23% and 6% POLY MONO), then all patients were treated, sequentially, the other two diets up to a total of 12 weeks. ... The design of the experimental diets was based on the replacement of fat SAT CHOC in low-fat diet while in the high-fat diet, the fat MONO replaced the SAT ...

The postprandial expression of messenger ribonucleic acid (mRNA) of UCP2 in the peripheral adipose tissue was higher after the CHO diet. Postprandial concentrations of glucose and insulin increased after the meal high in HC while free fatty acids (FFAs) increased after high-fat diets. The levels of total cholesterol, triglycerides and low density lipoprotein (LDL) did not change during the three phases of diet, whereas cholesterol high density lipoprotein (HDL) decreased after the diet high in CHO. Postprandial concentration of LDL-ox decreased after ingestion of the MONO diet and serum NT [nitrotyrosine] levels increased after ingestion of a diet rich in CHO.(11)

Figure 14. Representation of the mean values &#8203;&#8203;of LDL-ox baseline and at 60, 120 and 180 minutes of breakfast. ANOVA for repeated measures. *P <0.05, **p <0.01.


Figure 15. Representing the area under the curve (AUC) postprandial plasma concentrations of LDL-ox after ingestion of each of the diets. ANOVA for repeated measures. *P <0.05.

But, again, in evaluating the effect of diet on health outcomes, one should rely on the long-term, prospective epidemiology and clinical trials with health outcomes, not these make-the-case, mechanistically-based speculations.

Similarly, I have little concern about intake of nonessential amino acids, granted that you're getting well over the RDA for total protein, and at least the RDA for individual essential aminos. (Remember that you have to add Met + Cys to get the %RDA for S-containing aminos. More legumes should deal with your marginal lysine intake).

Again, similarly, I wouldn't arbitrarily conclude that any given Calorie intake may be too little. Just as it's impossible to define what is "enough" CR or the "%CR" of any given person, I don't think one can say a priori that someone is consuming 'too few' Calories -- esp just based on hir height, w/o knowing hir weight or anthropometry. The questions are: is his weight stable? Does he feel good? Is he subjectively healthy? Does his bloodwork look reassuring? If you hit all the checklists, an arbitrary idea of how many Calories one 'needs' (or how one should not go below some 'minimum' BMI) is not grounded in evidence.

References
1: Mozaffarian D, Micha R, Wallace S. Effects on coronary heart disease of increasing polyunsaturated fat in place of saturated fat: a systematic review and meta-analysis of randomized controlled trials. PLoS Med. 2010 Mar 23;7(3):e1000252. Review. PubMed PMID: 20351774; PubMed Central PMCID: PMC2843598.

2: Skeaff CM, Miller J. Dietary fat and coronary heart disease: summary of evidence from prospective cohort and randomised controlled trials. Ann Nutr Metab. 2009;55(1-3):173-201. Epub 2009 Sep 15. PubMed PMID: 19752542.

3: Jakobsen MU, O'Reilly EJ, Heitmann BL, Pereira MA, Bälter K, Fraser GE, Goldbourt U, Hallmans G, Knekt P, Liu S, Pietinen P, Spiegelman D, Stevens J, Virtamo J, Willett WC, Ascherio A. Major types of dietary fat and risk of coronary heart disease: a pooled analysis of 11 cohort studies. Am J Clin Nutr. 2009 May;89(5):1425-32. Epub 2009 Feb 11. PubMed PMID: 19211817; PubMed Central PMCID: PMC2676998.

4: Jakobsen MU, Dethlefsen C, Joensen AM, Stegger J, Tjønneland A, Schmidt EB, Overvad K. Intake of carbohydrates compared with intake of saturated fatty acids and risk of myocardial infarction: importance of the glycemic index. Am J Clin Nutr. 2010 Jun;91(6):1764-8. Epub 2010 Apr 7. PubMed PMID: 20375186.

5. Hu FB, Stampfer MJ, Manson JE, Ascherio A, Colditz GA, Speizer FE, Hennekens CH, Willett WC. Dietary saturated fats and their food sources in relation to the risk of coronary heart disease in women. Am J Clin Nutr. 1999 Dec;70(6):1001-8.
PMID: 10584044 [PubMed - indexed for MEDLINE]

6: Tholstrup T. Influence of stearic acid on hemostatic risk factors in humans. Lipids. 2005 Dec;40(12):1229-35. PubMed PMID: 16477807.

7: Fernandez ML, West KL. Mechanisms by which dietary fatty acids modulate plasma lipids. J Nutr. 2005 Sep;135(9):2075-8. Review. PubMed PMID: 16140878.

8: Mensink RP, Zock PL, Kester AD, Katan MB. Effects of dietary fatty acids and carbohydrates on the ratio of serum total to HDL cholesterol and on serum lipids and apolipoproteins: a meta-analysis of 60 controlled trials. Am J Clin Nutr. 2003 May;77(5):1146-55. PubMed PMID: 12716665.

9: Steer P, Vessby B, Lind L. Endothelial vasodilatory function is related to the proportions of saturated fatty acids and alpha-linolenic acid in young men, but not in women. Eur J Clin Invest. 2003 May;33(5):390-6. PubMed PMID: 12713452.

10: Temme EH, Mensink RP, Hornstra G. Effects of diets enriched in lauric, palmitic or oleic acids on blood coagulation and fibrinolysis. Thromb Haemost. 1999 Feb;81(2):259-63. PubMed PMID: 10064003.

11: Sánchez García, María Esther, Juan Antonio.Efectos de tres modelos de dieta sobre la expresión de UCP-2 en tejido adiposo periférico y marcadores de oxidación en pacientes con resistencia a la insulina. 2008; Universidad de Córdoba. Servicio de Publicaciones. http://helvia.uco.es...andle/10396/325

Edited by Michael, 15 December 2013 - 04:29 PM.

[sthira]

Word: less fruit, more beans, more olive oil. The macronutrient ratios from the COM pie graph are:

March 13: 70 carbs/ 11 protein/ 20 fat.
March 14: 59 carbs/ 13 protein/ 28 fat.
March 15: 60 carbs/ 12 protein/ 28 fat.

3-days: 63 carbs/ 12 protein/ 25 fat

[Sillewater]

Did the olive oil have polyphenols?

[Skötkonung]

...

I appreciate some of the points you have made, as always your critiques are very comprehensive.

I'm curious Michael, if saturated fats are so bad, why is my lipid profile not reflecting this reality? I've also had a heart scan recently done as part of some other non-related health issues (benign adrenal adenoma) and had no problems. Is it your opinion that saturated fats are ALWAYS bad or bad only within the context of most diets?

Also, if MUFA are healthy, do you support consumption of high-oleic sunflower and canola oils?

Did the olive oil have polyphenols?

Have you seen studies where they specify use of olive oil without polyphenols?

Edited by Skötkonung, 18 March 2011 - 11:58 PM.

[scottknl]

Sthira, I noticed that your Flax seed oil: 9/g: 79/kcal seems a bit high to me. In this post
Michael warns against Omega-3 higher than 3 g per day.

FDA concludes that the use of EPA and DHA omega-3 fatty acids as
dietary supplements is safe and lawful under 21 C.F.R. § 101.14,
provided that daily intakes of EPA and DHA omega-3 fatty acids do not
exceed 3 g/p/d from conventional food and dietary supplement sources.

> Are these warnings of hemorrhagic stroke
> overblown? Has anyone who's eating flaxseed or taking fish oil and
> getting much more than 3g experienced bleeding or bruising?

Real, provided that you're talking (as FDA evidently is) about
long-chain n3 (EPA & DHA): along with salt, it probably plays into the
high rates of haemorrhagic stroke in Japan. And see anecdotes from David
Dryden and others in the Archives on bruising, nosebleeds etc.

[Sillewater]

Did the olive oil have polyphenols?

Have you seen studies where they specify use of olive oil without polyphenols?

Nope, but just wondering. One problem with comparing dietary fats is that it is hard to compare just the effects of SAFA, MUFA, to PUFA, because with each fat source comes with not only a difference in the types of SAFA (this doesn't apply to MUFA because almost all of it is oleic), however oils do differ in PUFAs (which are very effective in lowering LDL). In the study above could be confounded by the polyphenols (it seems they controlled for the PUFA, but I'm wondering how).

Anyways, regarding the SAFA and lipid profile. There seems to be a really large variability in individuals reaction to SAFA. Some have better lipid profiles because SAFA doesn't affect them, but in others it seems to affect them a lot (as shown by a lot of paleo dieters increase in cholesterol, like mine). While Chris Masterjohn proposes that it is the increase in choline that contributes to this, I'm not so sure. In the various interventional studies where they just use butter to alter dietary fat ratios, a large increase in cholesterol in certain individuals are seen.

Anyways, I get most of this not from my own research but from a free ebook by Michael Gurr: http://www.pjbarnes....free/nutpdf.htm

It's a bit old (1999) but I find it is very accurate. Now all I have to do is review the more recent studies myself but have no time.

[sthira]

I realize I'm getting into very personalized nutrition questions with some of this stuff. But one reason I eat fruit is because I lead an active manual labor job often in a time crunch. I'm bouncing from video shoot to shoot with little down time. Fruit is great because it's easy, good for ya, clean, cheap, and not too alarming to spectators who already think you're an odd duck and you eat strangely.

So to tamp down BG readings, would it be better to A) not eat fruit, B) eat very little, C) combine it with some kind of fat like nuts?

[Mari]

Sthira, what about choline intake? The best sources are egg yolks and ruminant liver. Absence of choline seems to promote NAFLD and possibly weight gain (although not a problem for you). It also plays a role in brain functioning I believe.

You can get a bit from nuts or vegetables, but not as much as it seems is optimal. See here:
http://blog.choleste...ggs-organs.html

[sthira]

Hey Mari, thanks for that, I supplement choline. I tend to avoid turning my diet upside down in order to meet some one elusive food component or another. As time passes, the science progresses, I'm sure all of us will learn we're short and long on stuff. Big picture! I try to think big picture!

[Mari]

Ok. But what I'm confused about is why you're eating a diet that is producing nutrient deficiencies. I am quite hesitant to believe that that is optimal. Supplements are great, I use them myself, but I see them as additions to an already good diet rather than a necessary part that ensures I'm not short in something I could get from food. If you ate meat, even a little, this would provide taurine, carnosine, b12, choline, etc. If it was one nutrient I wouldn't change everything up either, but it just seems like maybe a some eggs or grassfed beef would be a good addition. Just something to think about.

[sthira]

The reason I'm a vegan is compassion for fellow critters. It's not because I believe this way is better for human health. While an intelligent vegan diet can be healthy for everyone, it also has drawbacks, flaws, weaknesses - some of which you're indicating clearly.

Edited by sthira, 22 March 2011 - 04:16 AM.

[Mari]

Ok, fair enough. I would also suggest eliminating the furniture polish. Uh, flaxseed oil. Too much omega 6 and ALA isn't converted well. There are omega 3 supplements from algae, as I'm sure you know.

[sthira]

I eat organic seaweed (nori, kombu) every now and then, does that count? It's insanely high in iodine, which may be a good thing given my pigginess for greens.

I like flaxseed oil, don't agree it tastes like furniture oil at all, and disagree that I'm consuming too much omega 6. Also, the jury's still out on "ALA isn't converted well."

Incidently, I just returned from the CRONA study in my role as a volunteer patient at UCSF. They disclosed some positive insights into my CR practice. For example, in the DEXA scan I learned my bone mass density is "in excellent shape" (nearly in the green zone) despite the fact that the DEXA also indicated that my body fat percentage is - in total - 4.4%. The scan operator's comment: "I wouldn't go much farther."

[Skötkonung]

Also, the jury's still out on "ALA isn't converted well."

Women's bodies are a little better at this conversion. Research has shown that young women convert 21% of ALA to EPA (compared to 8% in men) and 9% to DHA (compared to 0-4% in men). The difference, apparently, is linked to estrogen levels. So, unless you're a young woman, you probably aren't getting adequate conversion of long chain omega 3 fats. If you're a man, ALA might do more harm than good. Research has linked high ALA intake (from both flax oil and milled seed) with higher incidence of prostate cancer. ALA blood levels are higher in response to flax oil intake than they are with milled seed intake. Of coursefish intake (rich in both DHA and EPA) actually reduces the risk for prostate cancer. I guess all those "helpful" plant sterols aren't that helpful after all.

I think you're buying into a common misconception, especially amongst vegetarians and vegans, that our need for EPA and DHA can be met by consuming flax oil and other plant sources of ALA. But the conversion numbers above clearly indicate that this isn't the case.Studies have shown that ALA supplements (like flax oil) are unable to raise plasma DHA levels in vegans, despite low DHA levels at baseline.

Honestly, I don't see the controversy about whether the body needs long chain omega 3 fats (it does) and whether ALA is an appreciable source (it isn't). The controversy is around how much EPA and DHA one should take. The research indicates that once the RDA has been met, little further benefit can be derived from increased supplementation. Supplementing too much ALA, DHA, or EPA can actually be downright harmful.

I'll never understand the vegan mind.

Edited by Skötkonung, 23 March 2011 - 07:02 AM.

[sthira]

Thanks, Skot, I'm sorta relieved you don't understand my vegan mind despite what I keep writing about compassion for animals. I mean, who's reading? It would be creepy if anyone actually understood that revolutionary idea - perhaps even inhuman. Apes both wild and captive abuse the shit out of each other and anything else unfortunate enough to stand in the way - why should we be much different? The world is OURS, the Lord sayeth: use it up! Yet I'm positive we'll all eventually evolve despite participation in these many greedy-eyed side trips. Artificial meat = on the horizon.

Funny you should mention Lierre Keith's book, I've actually read it, it's poised on my shelf should we need to re-amp questions as to its intentions. Maybe we can discuss what a cretin I am for practicing a vegan diet in another thread and keep this one on CR?

Meanwhile on the ALA front, did you miss Rae's argument in the whirlwind of unread words above in this thread? Namely: "Also, the widespread notion, often repeated even in the scientific literature, that we need to get dietary EPA & DHA because ALA conversion rates are 'poor.'. This is a mechanistically-based, make-the-case petitio principii, which assumes that some higher rate is necessary, finds that it's lower, and gets worried, despite the overwhelming evidence that ALA conversion to EPA and DHA is adequate to ensure cardiovascular and other health outcomes. And, you (Sthira) are getting lots of ALA. As well, there's good reason to think that people on CR should minimize dietary EPA, DHA, & fish oil."

Edited by sthira, 23 March 2011 - 02:34 PM.

[Skötkonung]

Thanks, Skot, I'm sorta relieved you don't understand my vegan mind despite what I keep writing about compassion for animals. I mean, who's reading? It would be creepy if anyone actually understood that revolutionary idea - perhaps even inhuman. Apes both wild and captive abuse the shit out of each other and anything else unfortunate enough to stand in the way - why should we be much different? The world is OURS, the Lord sayeth: use it up! Yet I'm positive we'll all eventually evolve despite participation in these many greedy-eyed side trips. Artificial meat = on the horizon.

Funny you should mention Lierre Keith's book, I've actually read it, it's poised on my shelf should we need to re-amp questions as to its intentions. Maybe we can discuss what a cretin I am for practicing a vegan diet in another thread and keep this one on CR?

Meanwhile on the ALA front, did you miss Rae's argument in the whirlwind of unread words above in this thread? Namely: "Also, the widespread notion, often repeated even in the scientific literature, that we need to get dietary EPA & DHA because ALA conversion rates are 'poor.'. This is a mechanistically-based, make-the-case petitio principii, which assumes that some higher rate is necessary, finds that it's lower, and gets worried, despite the overwhelming evidence that ALA conversion to EPA and DHA is adequate to ensure cardiovascular and other health outcomes. And, you (Sthira) are getting lots of ALA. As well, there's good reason to think that people on CR should minimize dietary EPA, DHA, & fish oil."

It's not just mechanistic speculation. Did you miss this tidbit in my last post:
"Studies have shown that ALA supplements (like flax oil) are unable to raise plasma DHA levels in vegans, despite low DHA levels at baseline."

If ALA really provided adequate amounts of these essential fats, don't you think it would show more promise at raising plasma DHA levels? Hmmm...

Here's another study for you, and another.

I'll let the American Journal of Clinical Nutrition state my case for me:
"However, vegetarians and vegans have a relatively high intake of linoleic acid (18:2n–6; LA) (7, 8), which is largely derived from plant sources. EPA and DHA can also be synthesized in the body from α-linolenic acid (18:3n-3; ALA); however, this conversion is limited in humans (9), and possibly more in men than in women (10, 11). The conversion may be further suppressed by a high intake of LA, because the desaturation of ALA and LA involves the same rate-limiting Δ⁶ desaturase enzyme (12). Indeed, trials have shown that ALA supplementation increases plasma EPA and DPA but has little effect on DHA (13–15). As a result, vegetarians and vegans, who have a low dietary intake of DHA (and a correspondingly high intake of LA), have lower amounts of EPA and DHA in blood and adipose tissue than do omnivores (16–19).
...

In conclusion, in the present study of 659 British men, the proportions of plasma EPA and DHA were markedly lower in vegetarians and particularly in vegans than in meat-eaters. "

Would you really let your ideology get in the way of actually being healthy? Like the other poster said, I'd skip the "furniture polish" supplementation and eat real foods...

Thanks, Skot, I'm sorta relieved you don't understand my vegan mind despite what I keep writing about compassion for animals. I mean, who's reading? It would be creepy if anyone actually understood that revolutionary idea - perhaps even inhuman. Apes both wild and captive abuse the shit out of each other and anything else unfortunate enough to stand in the way - why should we be much different? The world is OURS, the Lord sayeth: use it up! Yet I'm positive we'll all eventually evolve despite participation in these many greedy-eyed side trips. Artificial meat = on the horizon.

I hope not. A world that's so crowded, polluted, and corrupt that we are all forced onto a artificial vegan diet is a dystopia if I've ever heard one.Thankfully it looks like people are coming to their senses..

Edited by Skötkonung, 23 March 2011 - 04:54 PM.

[ajnast4r]

I'll never understand the vegan mind.

this may help you better understand the vegan mind

It's not just mechanistic speculation. Did you miss this tidbit in my last post:
"Studies have shown that ALA supplements (like flax oil) are unable to raise plasma DHA levels in vegans, despite low DHA levels at baseline."

dont get me wrong... in my own experience, supplementing DHA provided benefits that ALA never did, but that study used only 2g ALA & did not go below a 6:1 n6:3 ratio. not exactly a crushing evidence.

Edited by ajnast4r, 23 March 2011 - 05:23 PM.

[Skötkonung]

I'll never understand the vegan mind.

this may help you better understand the vegan mind

Give me a break with that crap... Your sense of "compassion" tells us nothing about culture's impact on their land base. Your compassion is still part of the paradigm that's destroying the world.

By the way, the irony with your post is that the Dalai Lama is not vegetarian or vegan.
"In 1999, it was published that the Dalai Lama would only be vegetarian every other day and partakes of meat regularly."

Edited by Skötkonung, 23 March 2011 - 05:10 PM.

[Sillewater]

It's not just mechanistic speculation. Did you miss this tidbit in my last post:
"Studies have shown that ALA supplements (like flax oil) are unable to raise plasma DHA levels in vegans, despite low DHA levels at baseline."
If ALA really provided adequate amounts of these essential fats, don't you think it would show more promise at raising plasma DHA levels? Hmmm...

Here's another study for you, and another.

I'll let the American Journal of Clinical Nutrition state my case for me:
"However, vegetarians and vegans have a relatively high intake of linoleic acid (18:2n–6; LA) (7, 8), which is largely derived from plant sources. EPA and DHA can also be synthesized in the body from α-linolenic acid (18:3n-3; ALA); however, this conversion is limited in humans (9), and possibly more in men than in women (10, 11). The conversion may be further suppressed by a high intake of LA, because the desaturation of ALA and LA involves the same rate-limiting Δ⁶ desaturase enzyme (12). Indeed, trials have shown that ALA supplementation increases plasma EPA and DPA but has little effect on DHA (13–15). As a result, vegetarians and vegans, who have a low dietary intake of DHA (and a correspondingly high intake of LA), have lower amounts of EPA and DHA in blood and adipose tissue than do omnivores (16–19).
...

In conclusion, in the present study of 659 British men, the proportions of plasma EPA and DHA were markedly lower in vegetarians and particularly in vegans than in meat-eaters. "

Would you really let your ideology get in the way of actually being healthy? Like the other poster said, I'd skip the "furniture polish" supplementation and eat real foods...

Well it still kinda is because you are saying that DHA in cells prevent cardiovascular disease.

MR (http://www.longecity...__1#entry423467) had a recent post here about ALA and prostate cancer referring to some recent meta-analyses showing "no convincing link".

[ajnast4r]

Give me a break with that crap... Your sense of "compassion" tells us nothing about culture's impact on their land base. Your compassion is still part of the paradigm that's destroying the world.

By the way, the irony with your post is that the Dalai Lama is not vegetarian or vegan.
"In 1999, it was published that the Dalai Lama would only be vegetarian every other day and partakes of meat regularly."

i knew someone would dig that up... the basic premise still stands... somehow i doubt that vegetarians are destroying the world

reading 'A. Perri's review on 'the vegetarian myth' is worthwhile...

The author cites 207 references in this book.
62 of those references are websites (~30%)
18 are newspapers and magazines (~7%)
32 are journals (~15%)
95 are other books (~46%)

First of all, think about that. 30% of the references in this book come from website information. Five of those 62 website references were Wikipedia. Wikipedia! One was Google Answers.

In reality less than 8% of the book is coming from peer-reviewed, fact-checked sources which can provide unbiased, neutral information.

Edited by ajnast4r, 23 March 2011 - 05:48 PM.

[Skötkonung]

Well it still kinda is because you are saying that DHA in cells prevent cardiovascular disease.

I believe adequate DHA consumption is necessary for optimal health and longevity. Not surprising given that it is an essential fatty acid. I don't think that DHA can be obtained in adequate amounts from a diet containing only ALA. If you have evidence showing DHA deficiency improves CVD risk, I'd like to see it.

Docosahexaenoic acid supplementation improves the moderately severe dementia from thrombotic cerebrovascular diseases

Is Docosahexaenoic Acid (DHA) Essential? Lessons from DHA Status Regulation, Our Ancient Diet, Epidemiology and Randomized Controlled Trials
"Human beings are poor DHA synthesizers, possibly because of their LC(n-3)P-abundant ancient diet. Dietary changes in the past century have lowered the (n-3) status to a current state of subclinical deficiency that is epidemiologically related to CVD, inflammatory disorders, mental and psychiatric diseases and suboptimal neurodevelopment. The strongest evidence comes from randomized controlled trials with LC(n-3)P, showing reduced mortality from CVD, improved neonatal neurodevelopment, and lower blood pressure in later life. With these studies as evidence, we conclude that DHA is likely to be essential."

Effects of Omega-3 Fatty Acids on Cardiovascular Disease
"Overall, consumption of omega-3 fatty acids from fish or from supplements of fish oil reduces all cause mortality and various CVD outcomes. The evidence for ALA supplements is sparse and inconclusive. "

Dietary reference intakes for DHA and EPA

Docosahexaenoic acid (DHA) and cardiovascular disease risk factors
"Numerous epidemiological and controlled interventional trials have supported the health benefits of long-chain omega-3 fatty acids in the form of docosahexaenoic acid (DHA, 22:6n-3) plus eicosapentaenoic acid (EPA, 20:5n-3) from fish and fish oils as well as from algal sources. The beneficial effects on cardiovascular disease and related mortality including various risk factors for cardiovascular disease (particularly lowering circulating triglyceride levels and the triglyceride:HDL-cholesterol ratio) have been observed in the absence of any concomitant blood cholesterol lowering. With appropriate dosages, consistent reductions in both fasting and postprandial triglyceride levels and moderate increases in fasting HDL-cholesterol levels have been observed with algal DHA in the majority of trials. These results are similar to findings for fish oils containing DHA and EPA. Related to greater fish intake, higher levels of DHA in circulating blood biomarkers (such as serum phospholipid) have been associated with reduced risks for the progression of coronary atherosclerosis and lowered risk from sudden cardiac death. Controlled clinical trials have also indicated the potential for algal DHA supplementation to have moderate beneficial effects on other cardiovascular disease risk factors including blood pressures and resting heart rates. Recommended intakes of DHA+EPA from numerous international groups for the prevention and management of cardiovascular disease have been forthcoming, although most have not offered specific recommendations for the optimal individual intake of DHA and EPA."

MR (http://www.longecity...__1#entry423467) had a recent post here about ALA and prostate cancer referring to some recent meta-analyses showing "no convincing link".

Is Rae guilty of confirmation bias? Hmm...

From one of the two studies mentioned in his post:
"High ALA intakes or high blood and adipose tissue concentrations of ALA may be associated with a small increased risk of prostate cancer."

Alpha-linolenic acid and risk of prostate cancer: a case-control study in Uruguay.
"In the time period of 1994-1998, a case-control study on diet and prostate cancer was carried out in Uruguay to examine the risk associated with fat intake. Two hundred and seventeen (217) incident cases afflicted with advanced prostate cancer were frequency-matched with 431 controls on age, residence, and urban/rural status. The analysis was carried out using unconditional multiple logistic regression. Alpha-linolenic acid was associated with a strong positive association (fourth quartile of intake odds ratio, 3.91; 95% confidence interval, 1.50-10.1) after controlling for total calorie intake and for the other types of fat. The effect was similar when alpha-linolenic acid was analyzed by its sources of origin (odds ratio for vegetable linolenic acid, 2.03; 95% confidence interval, 1.01-4.07). Including this report, five of six studies that have examined the relationship between alpha-linolenic acid and prostate cancer yielded a positive association, which was significant in four studies. Thus, there appears to be evidence of a role of alpha-linolenic acid in prostate carcinogenesis."

Dietary alpha-linolenic acid is associated with reduced risk of fatal coronary heart disease, but increased prostate cancer risk: a meta-analysis.
"The objective of this meta-analysis was to estimate quantitatively the associations between intake of alpha-linolenic acid [ALA, the (n-3) fatty acid in vegetable oils], mortality from heart disease, and the occurrence of prostate cancer in observational studies. We identified 5 prospective cohort studies that reported intake of ALA and mortality from heart disease. We also reviewed data from 3 clinical trials on ALA intake and heart disease. In addition, we identified 9 cohort and case-control studies that reported on the association between ALA intake or blood levels and incidence or prevalence of prostate cancer. We combined risk estimates across studies using a random-effects model. High ALA intake was associated with reduced risk of fatal heart disease in prospective cohort studies (combined relative risk 0.79, 95% CI 0.60-1.04). Three open-label trials also indicated that ALA may protect against heart disease. However, epidemiologic studies also showed an increased risk of prostate cancer in men with a high intake or blood level of ALA (combined relative risk 1.70; 95% CI 1.12-2.58). This meta-analysis shows that consumption of ALA might reduce heart disease mortality. However, the association between high intake of ALA and prostate cancer is of concern and warrants further study."

Prediagnostic level of fatty acids in serum phospholipids: omega-3 and omega-6 fatty acids and the risk of prostate cancer.
"Ecological and case-control studies have demonstrated a positive correlation between consumption of fat and the risk of prostate cancer. Two recent human studies have focused on alpha-linolenic acid as a risk factor for prostate cancer. Animal experiments have shown that dietary omega-6 polyunsaturated fatty acids have generally stimulated tumour development, whereas omega-3 polyunsaturated fatty acids have diminished it. The aim of our study was to investigate the association between these fatty acids and the subsequent risk of prostate cancer. Blood donors to the Janus serum data bank in Norway, who later developed prostate cancer, were matched to blood donors without prostate cancer (141 matched sets); the proportional level of fatty acids measured before diagnosis in the donors' serum was examined. The risk of later prostate cancer was analysed by conditional logistic regression. Increasing risk for prostate cancer was found with increasing quartiles of palmitoleic, palmitic and alpha-linolenic acid. An inverse risk association was found with increasing levels of tetracosanoic acid, for the ratios of linoleic to alpha-linolenic acid and arachidonic to eicosapentaenoic acid. There was no clear association between the risk effect of total omega-3 and total omega-6 fatty acids. There were no indications of a relationship between fatty acids and more aggressive cancers. Our results verify recent findings of a positive association between alpha-linolenic acid and a negative association between the ratio of linoleic to alpha-linolenic acid and the risk of prostate cancer."

That's enough to make me think twice about supplementing ALA in any purified form. Here is an interesting news article on the possible mechanism:

"At first we thought that ALA was associated with a higher risk of prostate cancer because men who consumed more ALA also consumed more meat," says Walter Willett, who chairs the nutrition department at the Harvard School of Public Health in Boston. "But now it looks like the ALA in oils like soy and canola are also linked to prostate cancer."
So it seems surprising that flaxseed, one of the richest sources of alphalinolenic acid, lowered PSA levels (from 8.5 to 5.7, on average) in a pilot study of 15 men who were scheduled to have a repeat biopsy. (2) (The men added an ounce a day of ground flaxseed to a lower-fat diet for six months.)

"The findings are conflicting, but people don't eat isolated nutrients--they eat foods," says researcher Wendy Demark-Wahnefried of Duke University in Durham, North Carolina. "We tested the whole flaxseed, which has a host of nutrients--not just ALA, but lignans, which are fiber-rich plant estrogens."

A recent study at the University of Michigan found that ALA promoted prostate cell growth, she notes. "But that was a study done in cell lines, not in people or even animals. And they used purified ALA, which is devoid of antioxidants and is kept at high temperatures, not ALA as it is found in the body."

Demark-Wahnefried's studies have found that flaxseed slows the growth of prostate tumors in mice. (3) "Those results, plus the slower cancer growth and the drop in PSA we found in men who are flaxseed during the month before surgery, are compelling," she says. "But I wouldn't stand on a soapbox and tell men to eat flaxseed. We first need well-controlled trials to find out if it can help."

She has now started a clinical trial that will give a low-fat diet supplemented with flaxseed to cancer patients who are scheduled to have their prostate glands removed. (Most weeks before the surgery can be performed.)

"Then when the prostate comes out, we can measure the cell proliferation rate," she says. "That's more reliable than measuring PSA."

Demark-Wahnefried suggests several mechanisms to explain why flaxseed might work. "The lignans could be acting like estrogen," which slows prostate cell growth. "Or they could bind to testosterone in the GI tract, just as the beta-glucan fiber in oat bran binds to cholesterol. That would enhance testosterone excretion."

But until more research results are in, it makes sense to avoid too much ALA, especially from concentrated sources like flaxseed oil supplements.

"We found an increased risk of prostate cancer in men who consumed 1.5 grams of ALA a day compared to those who got 0.7 grams," says Ed Giovannucci of the Harvard School of Public Health. Every 1,000 mg of flaxseed in a typical supplement contains roughly 500 mg (0.5 grams) of alpha-linolenic acid.

Increased risk at 1.5g... I wonder what 9g would do?

reading 'A. Perri's review on 'the vegetarian myth' is worthwhile...

Interesting, but that analysis is somewhat pointless: 1.) the book is partially an editorial if anything and 2.) the review assigns no hierarchy to the importance of the sources and their relevance to the author's supposition. For instance, the core premise of Lierre's book could be based on those 8% of peer reviewed sources or the book references could be written by experts in their field.

... somehow i doubt that vegetarians are destroying the world

Its probably better than the standard American diet... but not by much. I wouldn't say it deserves a "compassionate for the planet" label, either.

Edited by Skötkonung, 23 March 2011 - 06:57 PM.