109 replies to this topic

[Skötkonung]

I'd say probably ii, but, if 'm trying to keep PUFAs low, and that mean that I must skip on food regards as beneficials (nuts, oats) and need to use a supplement, such a vit E, which, using the precautionnary principle, are most of the time regards as bad, because not much supp. have huge amount of data backing them up as safe, i'm not sure this is a wise choice.

There is no need to supplement vitamin E. Do you think our ancestors relied solely on seasonal nuts and olive oil to get their vitamin E content? The solution is leafy greens and animal fats.

1/2 cup mushrooms has 9%
1 cup asparagus, raw, has 10% RDI
1 cup of mustard greens, raw, has 8% RDI.
4 tbsp of butter has 9% RDI.
1/2 salmon fillet has 7% RDI
1 cup parsnip has 13% RDI
5oz of spinach has 19% RDI
.25lb chicken liver has 6% RDI (organ meats are especially rich in this vitamin)

Etc, etc.

It is very easy to meet your RDI for vitamin E through diet. I'm usually within 90-100% of my RDI through diet and I rarely do nuts, grains, or legumes... just meat and vegetables.

 Picture_3.png   103.29KB   51 downloads

Edited by Skotkonung, 16 April 2010 - 08:12 PM.

[tunt01]

think skot is right on the evidence of nuts/n-6 pufa. it sucks. i love nuts. i love peanut, almond butter. this CR diet makes me crave pecan pie so badly. i have more energy and feel better, but it's like being a drug addict craving for a nut fix. it sucks haha.

[Skötkonung]

think skot is right on the evidence of nuts/n-6 pufa. it sucks. i love nuts. i love peanut, almond butter. this CR diet makes me crave pecan pie so badly. i have more energy and feel better, but it's like being a drug addict craving for a nut fix. it sucks haha.

Having high n-6 once in awhile can't be that bad I usually allow myself pie or a dessert item every few weeks.... and it is soo good. Not sure how dessert fits into CR?

Edited by Skotkonung, 16 April 2010 - 08:31 PM.

[oehaut]

I'd say probably ii, but, if 'm trying to keep PUFAs low, and that mean that I must skip on food regards as beneficials (nuts, oats) and need to use a supplement, such a vit E, which, using the precautionnary principle, are most of the time regards as bad, because not much supp. have huge amount of data backing them up as safe, i'm not sure this is a wise choice.

There is no need to supplement vitamin E. Do you think our ancestors relied solely on seasonal nuts and olive oil to get their vitamin E content? The solution is leafy greens and animal fats.

1/2 cup mushrooms has 9%
1 cup asparagus, raw, has 10% RDI
1 cup of mustard greens, raw, has 8% RDI.
4 tbsp of butter has 9% RDI.
1/2 salmon fillet has 7% RDI
1 cup parsnip has 13% RDI
5oz of spinach has 19% RDI
.25lb chicken liver has 6% RDI (organ meats are especially rich in this vitamin)

Etc, etc.

It is very easy to meet your RDI for vitamin E through diet. I'm usually within 90-100% of my RDI through diet and I rarely do nuts, grains, or legumes... just meat and vegetables.

 Picture_3.png   103.29KB   51 downloads

I've got to play more with my diet I guess. Thanks for the tips.

[Jay]

Vit E is necessary if you are consuming easily perishable fats stripped of their natural antioxidants. Fish come with CoQ10 or Astaxanthin, for example. Fish oil pills sometimes come with small amounts of vit E, but perhaps not enough to protect the fat once inthe body. Low doses of vit E (25-75 IU supplemental) are helpful in my opinion.

[oehaut]

think skot is right on the evidence of nuts/n-6 pufa. it sucks. i love nuts. i love peanut, almond butter. this CR diet makes me crave pecan pie so badly. i have more energy and feel better, but it's like being a drug addict craving for a nut fix. it sucks haha.

Still wondering.

Nuts have very good scientific data behind them as a food which affect positvely most biomarkers.

[Skötkonung]

think skot is right on the evidence of nuts/n-6 pufa. it sucks. i love nuts. i love peanut, almond butter. this CR diet makes me crave pecan pie so badly. i have more energy and feel better, but it's like being a drug addict craving for a nut fix. it sucks haha.

Still wondering.

Nuts have very good scientific data behind them as a food which affect positvely most biomarkers.

I think the evidence for nuts is skewed based on the composition of the control diets and organization of the studies:

Almonds decrease postprandial glycemia, insulinemia, and oxidative damage in healthy individuals.

Researchers fed 15 healthy subjects 5 meals providing a comparable amount of carbohydrate, fat and protein: 3 test meals (almonds and bread, parboiled rice, and instant mashed potatoes) and 2 bread control meals. Blood samples, taken before each meal and 4 hours afterward, showed levels of antioxidants increased after the almond meal, but decreased after the other meals. And not only did the almond meal increase antioxidant levels, but unlike the other foods, almonds also lowered the rise in blood sugar and insulin seen after eating.

Almonds and postprandial glycemia--a dose-response study.

In this study, after an overnight 10-12 hr fast, 9 healthy volunteers were randomly fed 3 test meals and 2 white bread (high glycemic) control meals on separate days. Each meal contained 50g of carbohydrate from white bread eaten either alone or in combination with 1, 2, or 3oz of almonds. To check subjects' rise in blood sugar, blood samples were taken for glucose analysis immediately after eating, and at 15, 30, 45, 60, 90 and 120 minutes. Eating almonds reduced the GI of the meal and subjects' rise in blood sugar in a dose-dependent manner - the more almonds consumed, the lower the meal's GI and the less the rise in subjects' blood sugar after eating.

Based on these types of studies, one could easily report that nuts reduce CVD. However, if you aren't consuming high GI foods, are the results relevant?

Edited by Skotkonung, 16 April 2010 - 08:48 PM.

[oehaut]

think skot is right on the evidence of nuts/n-6 pufa. it sucks. i love nuts. i love peanut, almond butter. this CR diet makes me crave pecan pie so badly. i have more energy and feel better, but it's like being a drug addict craving for a nut fix. it sucks haha.

Still wondering.

Nuts have very good scientific data behind them as a food which affect positvely most biomarkers.

I think the evidence for nuts is skewed based on the composition of the control diets and organization of the studies:

Almonds decrease postprandial glycemia, insulinemia, and oxidative damage in healthy individuals.

Researchers fed 15 healthy subjects 5 meals providing a comparable amount of carbohydrate, fat and protein: 3 test meals (almonds and bread, parboiled rice, and instant mashed potatoes) and 2 bread control meals. Blood samples, taken before each meal and 4 hours afterward, showed levels of antioxidants increased after the almond meal, but decreased after the other meals. And not only did the almond meal increase antioxidant levels, but unlike the other foods, almonds also lowered the rise in blood sugar and insulin seen after eating.

Almonds and postprandial glycemia--a dose-response study.

In this study, after an overnight 10-12 hr fast, 9 healthy volunteers were randomly fed 3 test meals and 2 white bread (high glycemic) control meals on separate days. Each meal contained 50g of carbohydrate from white bread eaten either alone or in combination with 1, 2, or 3oz of almonds. To check subjects' rise in blood sugar, blood samples were taken for glucose analysis immediately after eating, and at 15, 30, 45, 60, 90 and 120 minutes. Eating almonds reduced the GI of the meal and subjects' rise in blood sugar in a dose-dependent manner - the more almonds consumed, the lower the meal's GI and the less the rise in subjects' blood sugar after eating.

Based on these types of studies, one could easily report that nuts reduce CVD. However, if you aren't consuming high GI foods, are the results relevant?

Good point...

I should so much read full paper before commenting on anything

Obviously, anything is healthy compared to bread!

I'll have to look at the other studies I had and see compared to what they were ''healthy''

[tunt01]

I think the evidence for nuts is skewed based on the composition of the control diets and organization of the studies:

the evidence really seems to be coming out this way, at least as far as i can tell so far. it seems like an issue of trade-offs between "lesser evils" with minimal consumption being appropriate.

[Sillewater]

Some studies I found interesting:

Med Sci Sports Exerc. 2010 Feb 13. [Epub ahead of print]
Effect of n-3 Fatty Acids and Antioxidants on Oxidative Stress after Exercise.
McAnulty SR, Nieman DC, Fox-Rabinovich M, Duran V, McAnulty LS, Henson DA, Jin F, Landram MJ.

J Gerontol A Biol Sci Med Sci. 2009 Jun;64(6):646-52. Epub 2009 Apr 17.
Effect of dietary unsaturated fatty acids on senile amyloidosis in senescence-accelerated mice.
Umezawa M, Higuchi K, Mori M, Matushita T, Hosokawa M.

Neurochem Res. 2009 Jan;34(1):102-8. Epub 2008 Mar 29.
Reduced membrane lipids in the cortex of Alzheimer's disease transgenic mice.
Yao JK, Wengenack TM, Curran GL, Poduslo JF.

Curr Opin Clin Nutr Metab Care. 2010 Mar;13(2):123-4.
Dietary n-3 and n-6 fatty acids: are there 'bad' polyunsaturated fatty acids?
Deckelbaum RJ, Calder PC.

Br J Nutr. 2010 Feb;103(4):522-9. Epub 2009 Oct 13.
Membrane fatty acid composition of rat skeletal muscle is most responsive to the balance of dietary n-3 and n-6 PUFA.
Abbott SK, Else PL, Hulbert AJ.

J Nutr Health Aging. 2009 Jan;13(1):14-8.
Increased selenium intake in elderly high fish consumers may account for health benefits previously ascribed to omega-3 fatty acids.
Berr C, Akbaraly T, Arnaud J, Hininger I, Roussel AM, Barberger Gateau P.

Anal Biochem. 2010 Apr 1;399(1):30-8. Epub 2009 Dec 16.
Impact of phospholipid bilayer saturation on amyloid-beta protein aggregation intermediate growth: a quartz crystal microbalance analysis.

J Lipid Res. 2010 Mar 10. [Epub ahead of print]
Low dietary fish oil threshold for myocardial membrane n-3 PUFA enrichment independent of n-6 PUFA intake in rats.
Slee EL, McLennan PL, Owen AJ, Theiss ML.

Am J Clin Nutr. 2010 Jan;91(1):23-31. Epub 2009 Nov 18.
Linoleic acid is associated with lower long-chain n-6 and n-3 fatty acids in red blood cell lipids of Canadian pregnant women.
Friesen RW, Innis SM.

Prostaglandins Leukot Essent Fatty Acids. 2009 Apr;80(4):201-6. Epub 2009 Apr 8.
Dietary linoleic acid has no effect on arachidonic acid, but increases n-6 eicosadienoic acid, and lowers dihomo-gamma-linolenic and eicosapentaenoic acid in plasma of adult men.
Angela Liou Y, Innis SM.

Prostaglandins Leukot Essent Fatty Acids. 2010 Mar 3. [Epub ahead of print]
Polyunsaturated docosahexaenoic acid suppresses oxidative stress induced endothelial cell calcium influx by altering lipid composition in membrane caveolar rafts.
Ye S, Tan L, Ma J, Shi Q, Li J.

Good Review:
Metabolism and longevity: Is there a role for membrane fatty acids?
A. J. Hulbert1,*
* Metabolic Research Centre & School of Biological Sciences, University of Wollongong, Wollongong, NSW 2522, Australia
Kotarek JA, Moss MA.

I don't know what to make of all this, but my initial opinion is not that we should increase Vitamin E to satisfy our intake of PUFA's but to decrease our PUFA's to satisfy our requirements for RDAish Vitamin E intake.

Most of my reading on PUFA's are done on its relationship to AD and there's talks of rafts and Ca2+ channels and other mechanisms by which PUFA's possibly provide protection from AD but IMO its still quite speculative.

Also if you look at the third last paper I posted above it helps explain the relationship between LA intake and AA. Cron-O-Meter counts LA intake as O-6, while many studies look at long-chain (animal form) O-6 content in membranes. What is the relationship between LA and membrane O-6? Are nuts something we should be afraid of, or is the LA conversion just as bad as ALA.

Since reading a bunch of studies, I've opted for a mix of ALA intake and fish oil intake (just to be on the safe side).

Reading all the posts here I tend to agree with most. PUFA should probably be kept low and the ratios kept below 4:1 ratio of O-6:O-3. I hope we can come to a pretty convincing consensus soon on this topic because its one of the things we can control pretty well.

[oehaut]

Some studies I found interesting:

Med Sci Sports Exerc. 2010 Feb 13. [Epub ahead of print]
Effect of n-3 Fatty Acids and Antioxidants on Oxidative Stress after Exercise.
McAnulty SR, Nieman DC, Fox-Rabinovich M, Duran V, McAnulty LS, Henson DA, Jin F, Landram MJ.

J Gerontol A Biol Sci Med Sci. 2009 Jun;64(6):646-52. Epub 2009 Apr 17.
Effect of dietary unsaturated fatty acids on senile amyloidosis in senescence-accelerated mice.
Umezawa M, Higuchi K, Mori M, Matushita T, Hosokawa M.

Neurochem Res. 2009 Jan;34(1):102-8. Epub 2008 Mar 29.
Reduced membrane lipids in the cortex of Alzheimer's disease transgenic mice.
Yao JK, Wengenack TM, Curran GL, Poduslo JF.

Curr Opin Clin Nutr Metab Care. 2010 Mar;13(2):123-4.
Dietary n-3 and n-6 fatty acids: are there 'bad' polyunsaturated fatty acids?
Deckelbaum RJ, Calder PC.

Br J Nutr. 2010 Feb;103(4):522-9. Epub 2009 Oct 13.
Membrane fatty acid composition of rat skeletal muscle is most responsive to the balance of dietary n-3 and n-6 PUFA.
Abbott SK, Else PL, Hulbert AJ.

J Nutr Health Aging. 2009 Jan;13(1):14-8.
Increased selenium intake in elderly high fish consumers may account for health benefits previously ascribed to omega-3 fatty acids.
Berr C, Akbaraly T, Arnaud J, Hininger I, Roussel AM, Barberger Gateau P.

Anal Biochem. 2010 Apr 1;399(1):30-8. Epub 2009 Dec 16.
Impact of phospholipid bilayer saturation on amyloid-beta protein aggregation intermediate growth: a quartz crystal microbalance analysis.

J Lipid Res. 2010 Mar 10. [Epub ahead of print]
Low dietary fish oil threshold for myocardial membrane n-3 PUFA enrichment independent of n-6 PUFA intake in rats.
Slee EL, McLennan PL, Owen AJ, Theiss ML.

Am J Clin Nutr. 2010 Jan;91(1):23-31. Epub 2009 Nov 18.
Linoleic acid is associated with lower long-chain n-6 and n-3 fatty acids in red blood cell lipids of Canadian pregnant women.
Friesen RW, Innis SM.

Prostaglandins Leukot Essent Fatty Acids. 2009 Apr;80(4):201-6. Epub 2009 Apr 8.
Dietary linoleic acid has no effect on arachidonic acid, but increases n-6 eicosadienoic acid, and lowers dihomo-gamma-linolenic and eicosapentaenoic acid in plasma of adult men.
Angela Liou Y, Innis SM.

Prostaglandins Leukot Essent Fatty Acids. 2010 Mar 3. [Epub ahead of print]
Polyunsaturated docosahexaenoic acid suppresses oxidative stress induced endothelial cell calcium influx by altering lipid composition in membrane caveolar rafts.
Ye S, Tan L, Ma J, Shi Q, Li J.

Good Review:
Metabolism and longevity: Is there a role for membrane fatty acids?
A. J. Hulbert1,*
* Metabolic Research Centre & School of Biological Sciences, University of Wollongong, Wollongong, NSW 2522, Australia
Kotarek JA, Moss MA.

I don't know what to make of all this, but my initial opinion is not that we should increase Vitamin E to satisfy our intake of PUFA's but to decrease our PUFA's to satisfy our requirements for RDAish Vitamin E intake.

Most of my reading on PUFA's are done on its relationship to AD and there's talks of rafts and Ca2+ channels and other mechanisms by which PUFA's possibly provide protection from AD but IMO its still quite speculative.

Also if you look at the third last paper I posted above it helps explain the relationship between LA intake and AA. Cron-O-Meter counts LA intake as O-6, while many studies look at long-chain (animal form) O-6 content in membranes. What is the relationship between LA and membrane O-6? Are nuts something we should be afraid of, or is the LA conversion just as bad as ALA.

Since reading a bunch of studies, I've opted for a mix of ALA intake and fish oil intake (just to be on the safe side).

Reading all the posts here I tend to agree with most. PUFA should probably be kept low and the ratios kept below 4:1 ratio of O-6:O-3. I hope we can come to a pretty convincing consensus soon on this topic because its one of the things we can control pretty well.

Thanks for all those posts, Sillewater.

This one,

Curr Opin Clin Nutr Metab Care. 2010 Mar;13(2):123-4.
Dietary n-3 and n-6 fatty acids: are there 'bad' polyunsaturated fatty acids?
Deckelbaum RJ, Calder PC.

Actually contradict your conclusion tho. It catches my eyes and was only 3 pages long so I read it and again, they say that PUFA-6 appears cardioprotective and that their consumption should be encourage... (based on an AHA review tho - which are know to produce low-quality evidence review)

That is the problem. The vast majority of the litterature point at them as being beneficial. All that we have here is speculation, while there are meta-analysis of prospective long-term cohort studies showing that they reduce CHD mortality & risk.

I'll try to read some of the other papers you posted.

I really wish too that this matter could come to an end. It's been debated forever.

EDIT: And just to make it clear, i'm simply playing the devil advocate here since I've always been of the opinion that PUFA-6 should me harmful myself hehe. Only, since I came here, I tend to be very skeptical of what I think.

Edited by oehaut, 16 April 2010 - 10:50 PM.

[Jay]

Sillewater, those are interesting studies. I strongly suspect that over consumption linoleic acid (LA) causes disease, at least when combined with other ills in the western diet like sugar. That's based on the various findings I cited above (Lyon, Kitava, etc) and on the fact that so much more LA is consumed today on account of modern vegetable oils. However, one hypothesized mechanism for how LA causes disease has been losing support for a couple of years now. Specifically, many people have speculated that LA causes inflammation via its conversion to arachidonic acid (AA), which is a precursor for various "inflammatory" prostaglandins and leukotrienes. There have been some recent results (and you just posted one of them) that show that increased LA consumption does not lead to more AA. Moreover, AA is getting some good press of its own. For example, the expression of AA is important for mucosal GI defense. Too much LA does have consequences (less AA, EPA, and DHA) and that might be the problem...

Edited by Jay, 17 April 2010 - 02:45 AM.

[TheFountain]

Don't keep PUFAs low, keep 0-6 PUFAs low. Oatmeal is not high in 0-6 PUFAs. I am not sure where people get this idea from. My guess is that when 0-6 is consumed with 0-3 and MUFAs that the latter two clean up after the former, sort of. Of course eating too much 0-6 will result in linoleic overspill and we obviously do not want this as it might prevent the healthy fats from doing their thing.

[kismet]

Still wondering.

Nuts have very good scientific data behind them as a food which affect positvely most biomarkers. outcomes

Nuts are perhaps the single strongest nutritional influence on mortality and CVD that was ever studied in epidemiologic studies (and generally supported by said mechanistic studies). Nuts (or their equivalents) are not necessarily very high in PUFA. I wanted to mention that giving up nuts is a genuinely bad idea quite a while ago. Now it's done.

Edited by kismet, 17 April 2010 - 01:43 PM.

[Jay]

Still wondering.

Nuts have very good scientific data behind them as a food which affect positvely most biomarkers. outcomes

Nuts are perhaps the single strongest nutritional influence on mortality and CVD that was ever studied in epidemiologic studies (and generally supported by said mechanistic studies). Nuts (or their equivalents) are not necessarily very high in PUFA. I wanted to mention that giving up nuts is a genuinely bad idea quite a while ago. Now it's done.

How is that different than the data for vegetable oils? We know that PUFAs, like fructose, may be healthy for sick people, omega 3 deficient or diabetics as the case may be. Nut are sacks of linoleic acid, generally with antioxidants. They are also eaten by the more health seeking omega 3 deficient people. All in all it makes perfect sense that nuts have good data, given that soybean oil has good data! The debate is whether they promote optimal health among the non-omega 3 deficient.

[Jay]

A forth possibility (in addition to the (i), (ii), (iii)) I listed above, is that one should get a certain minimum amount (by weight, not percentage of energy) of long chain omega 3s and should make sure that other oils consumed are fresh and natural, with their innate antioxidants intake. This review seems to advocate for the minimum (by weight) long chain 3 approach. This may also explain the !Kung, who eat lots of mongogo nuts but still have little CVD. It might be as simple as getting 1 gram or less of long chain 3s and making sure to eat polyphenol rich oils like olive oil thereafter.

Edited by Jay, 17 April 2010 - 05:03 PM.

[kismet]

How is that different than the data for vegetable oils? It's considerably stronger and more consistent, coupled with much higher, both basic and "paleolithic", mechanistic plausibility.

We know that PUFAs, like fructose, may be healthy for sick people, omega 3 deficient or diabetics as the case may be. Yes, and lest we forgot, we know they may be beneficial for the healthy too. Or that they may be deadly weapons of mass destruction. That's why we use the word "may" to begin with.

Nut are sacks of linoleic acid, generally with antioxidants. Yes, and a few other substances you have forgotten like phytochemicals, phytosterols, fibre, micronutrients and phytic acid; which add to the mechanistic plausibility. And, no, they are not necessarily that high in PUFA and can be part of a low-moderate PUFA diet if you wish (hazelnut, macademia...)

They are also eaten by the more health seeking omega 3 deficient people. All in all it makes perfect sense that nuts have good data, given that soybean oil has good data! I don't think soy has that good data and PUFAs do have good epidemiology. The debate is whether they promote optimal health among the non-omega 3 deficient. Yes, and that's what the basic biology and epidemiology strongly implies (NB: epidemiology including data from seventh day adventists vegetarians, some of the strictest controlled and most powerful prospective cohorts on the planet and long follow-up which does address a few of your concerns)

But as always we can ignore stronger evidence and substitute it with weak speculation. Sometimes it's worth a bet, but the potential benefits of nuts are too large. I just can't bear that sort of dangerous advise. "Just cut out nuts". Yeah, that's nuts.   

Edited by kismet, 17 April 2010 - 05:48 PM.

[Jay]

One of the questions being debated on this forum, and elsewhere, is whether n-6 PUFA is unhealthy despite the epidemiological data that associates greater consumption of it with slightly better outcomes. It is important to remind people that PUFAs are backed by some good epidemiological results because some paleo people think demonizing PUFAs is a slam dunk. However, there is good reason to suspect that among omega 3 sufficient people, PUFAs may have the opposite effect and that the effect may be profound. It might be the difference between a 10% reduction in CVD and a 95% reduction. For me, that's the debate. Any additional evidence that n-6 PUFAs slightly promote health in severerly omega 3 deficient people doesn't add anything at this point.

I see 4 possibilities to explain the data.

1. Balanced 3/6;

2. Balanced and low 3/6;

3. Consumption of only fresh, natural sources of PUFA; and

4. Consumption of a certain minimum amount of LC n-3 PUFAs.

A few observations:

Using long chain n-3 rather than ALA seems to have the most support, except among MR.

Shooting for all four seems optimal to me given what I know. This has the advantage of being more immune to any change in our understanding.

You seem to think that one should shoot for just 3 and 4, right? You don't worry about excess LA consumption when the LA comes with good polyphenols/antioxidants (like nuts and olive oil), right? That could be sufficient to promote good health, but maybe not...

It come down to what you fear more -- SFA or LA. I have almost no fear of SFA and am quite wary of excess LA.

Edited by Jay, 17 April 2010 - 06:02 PM.

[Skötkonung]

How is that different than the data for vegetable oils? It's considerably stronger and more consistent, coupled with much higher, both basic and "paleolithic", mechanistic plausibility.

We know that PUFAs, like fructose, may be healthy for sick people, omega 3 deficient or diabetics as the case may be. Yes, and lest we forgot, we know they may be beneficial for the healthy too. Or that they may be deadly weapons of mass destruction. That's why we use the word "may" to begin with.

Nut are sacks of linoleic acid, generally with antioxidants. Yes, and a few other substances you have forgotten like phytochemicals, phytosterols, fibre, micronutrients and phytic acid; which add to the mechanistic plausibility. And, no, they are not necessarily that high in PUFA and can be part of a low-moderate PUFA diet if you wish (hazelnut, macademia...)

They are also eaten by the more health seeking omega 3 deficient people. All in all it makes perfect sense that nuts have good data, given that soybean oil has good data! I don't think soy has that good data and PUFAs do have good epidemiology. The debate is whether they promote optimal health among the non-omega 3 deficient. Yes, and that's what the basic biology and epidemiology strongly implies (NB: epidemiology including data from seventh day adventists vegetarians, some of the strictest controlled and most powerful prospective cohorts on the planet and long follow-up which does address a few of your concerns)

But as always we can ignore stronger evidence and substitute it with weak speculation. Sometimes it's worth a bet, but the potential benefits of nuts are too large. I just can't bear that sort of dangerous advise. "Just cut out nuts". Yeah, that's nuts.

Let's see, Kismet's guide to optimal nutrition:

- Lots of nuts, roasted in vegetable oils of course as that is what is used in the studies. High in AGEs, salt, oxidized fats, etc.
- Industrially produced / refined vegetable oils.

These epidemiological studies you speak of aren't using organic, raw / sprouted nuts, they are being confounded by substitution. If you actually look at the food item as it is available to study participants and its constitute components, you will see that it is not nutritionally optimal.

As for PUFA, how do you reconcile this?
http://pmid.us/16620...976221 17702671
PUFAs are sensitive to oxidative damage and therefore species with long life spans tends to minimize their use.

[tunt01]

How is that different than the data for vegetable oils? It's considerably stronger and more consistent, coupled with much higher, both basic and "paleolithic", mechanistic plausibility.

We know that PUFAs, like fructose, may be healthy for sick people, omega 3 deficient or diabetics as the case may be. Yes, and lest we forgot, we know they may be beneficial for the healthy too. Or that they may be deadly weapons of mass destruction. That's why we use the word "may" to begin with.

Nut are sacks of linoleic acid, generally with antioxidants. Yes, and a few other substances you have forgotten like phytochemicals, phytosterols, fibre, micronutrients and phytic acid; which add to the mechanistic plausibility. And, no, they are not necessarily that high in PUFA and can be part of a low-moderate PUFA diet if you wish (hazelnut, macademia...)

They are also eaten by the more health seeking omega 3 deficient people. All in all it makes perfect sense that nuts have good data, given that soybean oil has good data! I don't think soy has that good data and PUFAs do have good epidemiology. The debate is whether they promote optimal health among the non-omega 3 deficient. Yes, and that's what the basic biology and epidemiology strongly implies (NB: epidemiology including data from seventh day adventists vegetarians, some of the strictest controlled and most powerful prospective cohorts on the planet and long follow-up which does address a few of your concerns)

But as always we can ignore stronger evidence and substitute it with weak speculation. Sometimes it's worth a bet, but the potential benefits of nuts are too large. I just can't bear that sort of dangerous advise. "Just cut out nuts". Yeah, that's nuts.   

same arrogant blathering nonsense we get from you in every other thread.

the seventh day adventist study does not address the issue in this thread. the issue is PUFAs and dietary intake. not nuts alone.

post studies, check your ego at the door, or F*** off already.

[oehaut]

the issue is PUFAs and dietary intake. not nuts alone.

Well, we have gotten to a point in this thread that because of their PUFAs content, we are saying to avoid nuts. I think he was only saying this might not be a wise idea, because nuts have indeed a lot of other interesting nutritional components.

Nuts and health outcomes: new epidemiologic evidence.

This article reviews recent epidemiologic evidence on nut intake and health outcomes. It focuses on studies in which nut consumption is directly assessed or when nuts are included in a dietary score or pattern. Epidemiologic studies have been remarkably consistent in showing an association between nut consumption and a reduced risk of coronary heart disease (CHD). Some evidence has emerged recently to suggest health-protective benefits of nuts other than CHD. Frequent nut intake probably reduces risk of diabetes mellitus among women, but its effects on men are unknown. Evidence on the anticarcinogenic effects of nuts is somewhat limited because studies in the past 2 decades have examined only 3 tumor sites, and the benefits appear to be manifested only in women. However, the protective benefits of frequent nut consumption on gallstone diseases are observed in both sexes. Long-term nut consumption is linked with lower body weight and lower risk of obesity and weight gain. A dietary pattern or score that includes nuts is consistently related with beneficial health outcomes, and this provides an indirect evidence of the salutary benefits of nut consumption. More longitudinal studies are needed to clarify the possible effects of nuts on diseases other than CHD.

Regular consumption of nuts is associated with a lower risk of cardiovascular disease in women with type 2 diabetes.

Higher nut consumption has been associated with lower risk of coronary heart disease (CHD) events in several epidemiologic studies. The study examined the association between intake of nuts and incident cardiovascular disease (CVD) in a cohort of women with type 2 diabetes. For the primary analysis, there were 6309 women with type 2 diabetes who completed a validated FFQ every 2-4 y between 1980 and 2002 and were without CVD or cancer at study entry. Major CVD events included incident myocardial infarction (MI), revascularization, and stroke. During 54,656 person-years of follow-up, there were 452 CHD events (including MI and revascularization) and 182 incident stroke cases. Frequent nut and peanut butter consumption was inversely associated with total CVD risk in age-adjusted analyses. After adjustment for conventional CVD risk factors, consumption of at least 5 servings/wk of nuts or peanut butter [serving size, 28 g (1 ounce) for nuts and 16 g (1 tablespoon) for peanut butter] was significantly associated with a lower risk of CVD (relative risk = 0.56; 95% CI: 0.36-0.89). Furthermore, when we evaluated plasma lipid and inflammatory biomarkers, we observed that increasing nut consumption was significantly associated with a more favorable plasma lipid profile, including lower LDL cholesterol, non-HDL cholesterol, total cholesterol, and apolipoprotein-B-100 concentrations. However, we did not observe significant associations for HDL cholesterol or inflammatory markers. These data suggest that frequent nut and peanut butter consumption is associated with a significantly lower CVD risk in women with type 2 diabetes.

Nuts, inflammation and insulin resistance.

The beneficial effects of nut consumption on cardiovascular disease (CVD) have been widely documented. These protective effects are mainly attributed to the role of nuts in the metabolism of lipids and lipoproteins. As chronic inflammation is a key early stage in the atherosclerotic process that predicts future CVD events and is closely related to the pathogenesis of insulin resistance, many recent studies have focused on the potential effect of nut consumption on inflammation and insulin resistance. Through different mechanisms, some components of nuts such as magnesium, fiber, alpha-linolenic acid, L-arginine, antioxidants and MUFA may protect against inflammation and insulin resistance. This review evaluates the epidemiologic and experimental evidence in humans demonstrating an association between nut consumption and these two emergent cardio-protective mechanisms.

etc, etc.

It was pointed out, and it's a very valid point, that nuts in the SAD diet can indeed be an healthy food, compared to the crappy food most SADers eat, but for us, with a very good diet already and looking for optimal nutrition, they might not be a good choice because of the PUFAs.

But let's not forget that they are a good source of phytochemicals, antioxydants nutrients, minerals and fiber. Is the risk/benefits worth it? Don't know.

I think 2 brazil nuts are enough to get my selenium for the day. So maybe there no need to exclude them, but not over do it, as with many other things.

[oehaut]

Just sharing other papers i've found while downloading the one proposed here, for whoever interested


Mitochondrial membrane peroxidizability index is inversely related to maximum life span in mammals.

The oxidative stress theory of aging predicts a low degree of fatty acid unsaturation in tissues of longevous animals, because membrane lipids increase their sensitivity to oxidative damage as a function of their unsaturation. Accordingly, the fatty acids analyses of liver mitochondria from eight mammals, ranging in maximum life span from 3.5 to 46 years, show that the total number of double bonds and the peroxidizability index are negatively correlated with maximum life span (r = -0. 88, P < 0.003; r = -0.87, P < 0.004, respectively). This is not due to a low content of unsaturated fatty acids in longevous animals, but mainly to a redistribution between kinds of the polyunsaturated n-3 fatty acids series, shifting from the highly unsaturated docosahexaenoic acid (r = -0.89, P < 0.003) to the less unsaturated linolenic acid (r = 0.97, P < 0.0001). This redistribution pattern strongly suggests the presence of a constitutively low delta6-desaturase activity in longevous animals (r = -0.96, P < 0.0001). Thus, it may be proposed that, during evolution, a low degree of fatty acid unsaturation in liver mitochondria may have been selected in longevous mammals in order to protect the tissues against oxidative damage, while maintaining an appropriate environment for membrane function.

N-3 polyunsaturated fatty acids impair lifespan but have no role for metabolism

Although generally considered as beneficial components of dietary fats, polyunsaturated fatty acids (PUFA) have been suspected to compromise maximum lifespan (MLSP) in mammals. Specifically, high amounts of phospholipid PUFAs are thought to impair lifespan due to an increase in the susceptibility of membranes to lipid peroxidation and its damaging effect on cellular molecules. Also, there is evidence from in vitro studies suggesting that highly unsaturated PUFAs elevate basal metabolic rate (BMR). Previous comparative studies in this context were based on small sample sizes, however, and, except for one study, failed to address possible confounding influences of body weight and taxonomic relations between species. Therefore, we determined phospholipid membrane composition in skeletal muscle from 42 mammalian species to test for a relation with published data on MLSP, and with literature data on BMR (30 species). Using statistical models that adjust for the effects of body weight and phylogeny, we found that among mammals, MLSP indeed decreases as the ratio of n-3 to n-6 PUFAs increases. In contrast to previous studies, we found, however, no relation between MLSP and either membrane unsaturation (i.e. PUFA content or number of double bonds) or to the very long-chain, highly unsaturated docosahexaenoic acid (DHA). Similarly, our data set gave no evidence for any notable relation between muscle phospholipid fatty acid composition and BMR, or MLSP and BMR in mammals. These results contradict the 'membrane pacemaker theory of aging', that is, the concept of a direct link between high amounts of membrane PUFAs, elevated BMR, and thus, impaired longevity.

Well, it's very possible that both PUFA-3 & -6 should be kept low and probably balance.

So maybe they are cardioprotective, but impair lifespan?

If that's the case, since most of us here, unless some genetic disorder that we don't know, are not at high risk of suffering from lifestyle-induced CHD, it probably would be wise to keep them low.

Edited by oehaut, 17 April 2010 - 10:14 PM.

[Sillewater]

Yea oehaut, I agree with that.

Here is some more studies to add to the analysis:

Lipids. 2010 Jan;45(1):1-10. Epub 2009 Nov 5.
Early and sustained enrichment of serum n-3 long chain polyunsaturated fatty acids in dogs fed a flaxseed supplemented diet.
Dunbar BL, Bigley KE, Bauer JE.

Could someone explain what this is saying? (Warning for this one I just read the abstract) It seems to be saying that ALA consumption helps save DHA for the brain. Would this be good for longevity? Keeping it out of the peripherals?

Dietary n-3 LCPUFA from fish oil but not -linolenic acid-derived LCPUFA confers atheroprotection in mice
Chiara Degirolamo, Kathryn L. Kelley, Martha D. Wilson and Lawrence L. Rudel*
Wake Forest University School of Medicine, United States

But ALA might not protect against heart disease? (Be aware these are not in humans)

Saturated fat doesn't look to good in this one, but we can't get all our fat calories from O-3.
Prostaglandins Leukot Essent Fatty Acids. 2010 Mar 4. [Epub ahead of print]
N-3 vs. saturated fatty acids: Effects on the arterial wall.
Sudheendran S, Chang CC, Deckelbaum RJ.

Found this one quite interesting but don't know the implications:
Biochem Biophys Res Commun. 2010 Feb 5;392(2):135-9. Epub 2010 Jan 7.
n-3, but not n-6 lipid particle uptake requires cell surface anchoring.
Murray-Taylor FM, Ho YY, Densupsoontorn N, Chang CL, Deckelbaum RJ, Seo T.
(What is Lactoferrin's effect on ApoE genotypes?)


Some more reading on Lipid Rafts if your interested:
Curr Opin Clin Nutr Metab Care. 2010 Mar;13(2):156-66.
The nutritional and clinical significance of lipid rafts.
Yaqoob P, Shaikh SR.

And many of the studies posted on nuts still seem to suggest that nuts are good:
Clin Nutr. 2010 Jan 9. [Epub ahead of print]
Effect of nut consumption on oxidative stress and the endothelial function in metabolic syndrome.
López-Uriarte P, Nogués R, Saez G, Bulló M, Romeu M, Masana L, Tormos C, Casas-Agustench P, Salas-Salvadó J.

A Roundtable Discussion
Discussion on dietary fat

When I came upon this study, it reminded me of a post by Peter at Hyperlipid. I can't find it right now but he was talking about how DHA was protected because it was unstable.
Prostaglandins Leukot Essent Fatty Acids. 2009 Feb-Mar;80(2-3):157-63. Epub 2009 Feb 23.
Rapid beta-oxidation of eicosapentaenoic acid in mouse brain: an in situ study.
Chen CT, Liu Z, Ouellet M, Calon F, Bazinet RP.

This was a very interesting review:
Curr Treat Options Cardiovasc Med. 2009 Aug;11(4):289-301.
Dietary fat quality and coronary heart disease prevention: a unified theory based on evolutionary, historical, global, and modern perspectives.
Ramsden CE, Faurot KR, Carrera-Bastos P, Cordain L, De Lorgeril M, Sperling LS.

[tunt01]

Dietary n-3 LCPUFA from fish oil but not -linolenic acid-derived LCPUFA confers atheroprotection in mice
Chiara Degirolamo, Kathryn L. Kelley, Martha D. Wilson and Lawrence L. Rudel*
Wake Forest University School of Medicine, United States

lot of Lawrence Rudel's work is interesting. i read this one earlier today and basically have been going through all his studies. he did the provocative work on monounsaturated fats being atherogenic.

it's difficult to find very clean data on the issue, on an isolated basis. a lot of the studies are colored by using hyperlipidemic patients or non-human subjects, etc.

[Sillewater]

lot of Lawrence Rudel's work is interesting. i read this one earlier today and basically have been going through all his studies. he did the provocative work on monounsaturated fats being atherogenic.

it's difficult to find very clean data on the issue, on an isolated basis. a lot of the studies are colored by using hyperlipidemic patients or non-human subjects, etc.

O yea, that's what I forgot to mention. The whole thing about oleates being atherogenic. There's some studies from the 1950's (or so) showing this fact and monounsaturated fats increase the production in the liver.

[tunt01]

O yea, that's what I forgot to mention. The whole thing about oleates being atherogenic. There's some studies from the 1950's (or so) showing this fact and monounsaturated fats increase the production in the liver.

It also contributes to the problem of all these studies being "incomplete". There are plenty of studies which show SFA vs. PUFA vs. MUFA. They show the LDL, HDL, Total Cholesterol. But they don't dig into the details, they don't show the oleate issue.

I may just email Rudel and ask him what he thinks. Maybe it's so recent a development, that the detail we aspire to see doesn't exist.

btw oehaut- thx for posting this http://www.ncbi.nlm....pubmed/17156083, that is a very interesting datapoint.


If you just sit down and do the math on how much omega-3 you can get in a day from a little bit of fish (against the RDI of protein for an adult, etc.), the other datapoints we have on omega-3 intake (Bill Lands's model, etc.) and posit that against a balanced 1:1 n-3/6 intake, then it's really hard to get any kind of substantial nut intake. Just something very modest and small. I tend to agree w/ oeahut/others that PUFA should be kept low + balanced.

I think a lot of the beneficial effect of walnuts is coming from sources like ellagic acid, which can be readily obtained from pomegranate juice or raspberries/strawberries anyway.

Edited by prophets, 18 April 2010 - 02:28 AM.

[TheFountain]

Oh the limitations of language.

Once again we have a black and white argument escalating into stupidity.

AVOID PUFAs or suffer!

We have seen this approach before with many things on this forum.

There is just too much evidence, epidemiological and otherwise, that 0-3 consumption lowers inflammation and CVD risk. Not to mention the suggestive evidence of its potential role in alzheimers. A quick look at PUBMEDs database simply typing in 'omega 3' in the search box indicates that this debate is silly and that people who are saying 'PUFA is bad' are performing a disservice to us. Use the correct language! 0-3 PUFA, good. 0-6 PUFA, not so good. okay?

BACKGROUND: The benefit of n-3 polyunsaturated fatty acids (PUFA) supplementation for mortality and cardiovascular events after myocardial infarction is well documented, but the effect of n-3 PUFA in Caucasians without established cardiovascular disease is not known. Our aim was to examine the influence of supplementation with eicosapentaenoic acid and docosahexaenoic acid on all-cause mortality and cardiovascular events in elderly men at high-risk of cardiovascular disease. DESIGN: In the Diet and Omega-3 Intervention Trial, 563 Norwegian men, 64-76-year old and 72% without overt cardiovascular disease, were randomized to a 3-year 2x2 factorial designed clinical trial of diet counseling and/or 2.4 g n-3 PUFA supplementation. The n-3 PUFA arm was placebo-controlled (corn oil). METHODS: Demographic parameters and classical risk factors were obtained at baseline. Deaths and cardiovascular events were recorded through 3 years, and the effects of n-3 PUFA-intervention on these outcomes were evaluated in pooled groups of the n-3 PUFA-arm. RESULTS: There were 38 deaths and 68 cardiovascular events. The unadjusted hazard ratios of all-cause mortality and cardiovascular events were 0.57 (95% confidence interval: 0.29-1.10) and 0.86 (0.57-1.38), respectively. Adjusted for baseline age, current smoking, hypertension, body mass index and serum glucose, hazard ratios were 0.53 (0.27-1.04, P=0.063) and 0.89 (0.55-1.45, P=0.641), respectively. CONCLUSION: We observed a tendency toward reduction in all-cause mortality in the n-3 PUFA groups that, despite a low number of participants, reached borderline statistical significance. The magnitude of risk-reduction suggests that a larger trial should be considered in similar populations.

[oehaut]

Oh the limitations of language.

Once again we have a black and white argument escalating into stupidity.

AVOID PUFAs or suffer!

We have seen this approach before with many things on this forum.

There is just too much evidence, epidemiological and otherwise, that 0-3 consumption lowers inflammation and CVD risk. Not to mention the suggestive evidence of its potential role in alzheimers. A quick look at PUBMEDs database simply typing in 'omega 3' in the search box indicates that this debate is silly and that people who are saying 'PUFA is bad' are performing a disservice to us. Use the correct language! 0-3 PUFA, good. 0-6 PUFA, not so good. okay?

We're saying to keep them low and not overdo it. Not to avoid them entirely. Even PUFA-6 are good, in the good amount and in the good ratio. Even PUFA-3 can be bad, if overdosing it and screwing the ratio.

But I do think that it does not justifiate yet, based on these evidence, to avoid minimal consumption of nuts such as walnuts or macadia nuts.

[Skötkonung]

Oh the limitations of language.

Once again we have a black and white argument escalating into stupidity.

AVOID PUFAs or suffer!

We have seen this approach before with many things on this forum.

There is just too much evidence, epidemiological and otherwise, that 0-3 consumption lowers inflammation and CVD risk. Not to mention the suggestive evidence of its potential role in alzheimers. A quick look at PUBMEDs database simply typing in 'omega 3' in the search box indicates that this debate is silly and that people who are saying 'PUFA is bad' are performing a disservice to us. Use the correct language! 0-3 PUFA, good. 0-6 PUFA, not so good. okay?

Of the limitations of your brain. Don't you feel embarrassed writing such crap without even bothering to review the discussion in the thread? By the way, you can't even spell "O-3 / O-6" correctly. The "O" stands for Omega. There isn't a zero in the name. LOL! Anyways, it is primarily called n-3 / n-6 in the literature, which refers to the position of the carbon–carbon double bond shared by all PUFA.

But I digress, no one here is saying n-3 is bad, it is an essential fat. So is n-6. Without either, you cannot survive. However, the arguement is in what quantity and what ratio.

We know that too much n-3 can cause problems with prolonged bleed times (induced hemophilia). It thins the blood excessively. Too much n-6 raises inflammation and is thought to contribute to CVD. Too much n-3 / n-6 de-saturates cellular membranes and makes them more prone to oxidative damage. PUFA also contributes to aging via ALEs. N-3 and n-6 work synergistically, even in a situation where one is consuming extremely high levels of n-3 in relation to n-6, it doesn't provide any more reduction in systemic inflammation. In fact, the best combination seems to be balanced levels.

[TheFountain]

Oh the limitations of language.

Once again we have a black and white argument escalating into stupidity.

AVOID PUFAs or suffer!

We have seen this approach before with many things on this forum.

There is just too much evidence, epidemiological and otherwise, that 0-3 consumption lowers inflammation and CVD risk. Not to mention the suggestive evidence of its potential role in alzheimers. A quick look at PUBMEDs database simply typing in 'omega 3' in the search box indicates that this debate is silly and that people who are saying 'PUFA is bad' are performing a disservice to us. Use the correct language! 0-3 PUFA, good. 0-6 PUFA, not so good. okay?

Of the limitations of your brain. Don't you feel embarrassed writing such crap without even bothering to review the discussion in the thread? By the way, you can't even spell "O-3 / O-6" correctly. The "O" stands for Omega. There isn't a zero in the name. LOL! Anyways, it is primarily called n-3 / n-6 in the literature, which refers to the position of the carbon–carbon double bond shared by all PUFA.

But I digress, no one here is saying n-3 is bad, it is an essential fat. So is n-6. Without either, you cannot survive. However, the arguement is in what quantity and what ratio.

We know that too much n-3 can cause problems with prolonged bleed times (induced hemophilia). It thins the blood excessively. Too much n-6 raises inflammation and is thought to contribute to CVD. Too much n-3 / n-6 de-saturates cellular membranes and makes them more prone to oxidative damage. PUFA also contributes to aging via ALEs. N-3 and n-6 work synergistically, even in a situation where one is consuming extremely high levels of n-3 in relation to n-6, it doesn't provide any more reduction in systemic inflammation. In fact, the best combination seems to be balanced levels.

I'm using the 0 so I don't have to capitalize the o fool! You're talking about a fucking fatty acid with ALOT more evidence behind its positive effect against CVD and inflammation than the one you taut on this forum non-stop. I.E saturated fat! And you're talking about the limitations of my brain? Bottom line is I am not saying to O.D on 0-3 I am talking about balance using the correct language, unlike you and most other people here. PUFAs are not bad. Just too much 0-6 PUFA is. I know you're not saying 0-3 is bad but use the correct language so lay people who visit this site are not confused to fucking oblivion! And it is likely that ALL lipids contribute to aging, not just those found in PUFAs!

Edited by TheFountain, 18 April 2010 - 09:15 PM.