Allow me to explain. These lines are based on values predicted by a formula developed by Dr. Lands that determines the proportion of omega-6 in tissue HUFA (highly unsaturated fatty acids; includes 20- to 22-carbon omega-6 and omega-3 fats), based on dietary intake of omega-6 and omega-3 fats. This formula seems to be quite accurate, and has been validated both in rodents and humans. As a tissue's arachidonic acid content increases, its EPA and DHA content decreases proportionally.On the Y-axis (vertical), we have the proportion of omega-6 HUFA in tissue. On the X-axis (horizontal), we have the proportion of omega-6 in the diet as a percentage of energy. Each line represents the relationship between dietary omega-6 and tissue HUFA at a given level of dietary omega-3.
Let's start at the top. The first line is the predicted proportion of omega-6 HUFA in the tissue of a person eating virtually no omega-3. You can see that it maxes out around 4% of calories from omega-6, but it can actually be fairly low if omega-6 is kept very low. The next line down is what happens when your omega-3 intake is 0.1% of calories. You can see that the proportion of omega-6 HUFA is lower than the curve above it at all omega-6 intakes, but it still maxes out around 4% omega-6. As omega-3 intake increases, the proportion of omega-6 HUFA decreases at all levels of dietary omega-6 because it has to compete with omega-3 HUFA for space in the membrane.
In the U.S., we get a small proportion of our calories from omega-3. The horizontal line marks our average tissue HUFA composition, which is about 75% omega-6. We get more than 7% of our calories from omega-6. This means our tissue contains nearly the maximum proportion of omega-6 HUFA, creating a potently inflammatory and thrombotic environment! This is a very significant fact, because it explains three major observations:
- The U.S has a very high rate of heart attack mortality.
- Recent diet trials in which saturated fat was replaced with omega-6-rich vegetable oils didn't cause an increase in mortality, although some of the very first trials in the 1960s did.
- Diet trials that increased omega-3 decreased mortality.
But the trend didn't continue into later trials. This makes perfect sense in light of the rising omega-6 intake over the course of the 20th century in the U.S. and other affluent nations. Once our omega-6 intake crossed the 4% threshold, more omega-6 had very little effect on the proportion of omega-6 HUFA in tissue. This may be why some of the very first PUFA diet trials caused increased mortality: there was a proportion of the population that was still getting less than 4% omega-6 in its regular diet at that time. By the 1980s, virtually everyone in the U.S. (and many other affluent nations) was eating more than 4% omega-6, and thus adding more did not significantly affect tissue HUFA or heart attack mortality.
If omega-3 intake is low, whether omega-6 intake is 5% or 10% doesn't matter much for heart disease. At that point, the only way to reduce tissue HUFA without cutting back on omega-6 consumption is to outcompete it with additional omega-3. That's what the Japanese do, and it's also what happened in several clinical trials including the DART trial.
This neatly explains why the French, Japanese and Kitavans have low rates of ischemic heart disease, despite the prevalence of smoking cigarettes in all three cultures. The French diet traditionally focuses on animal fats, eschews industrial vegetable oils, and includes seafood. They eat less omega-6 and more omega-3 than Americans. They have the lowest heart attack mortality rate of any affluent Western nation. The Japanese are known for their high intake of seafood. They also eat less omega-6 than Americans. They have the lowest heart attack death rate of any affluent nation. The traditional Kitavan diet contains very little omega-6 (probably less than 1% of calories), and a significant amount of omega-3 from seafood (about one teaspoon of fish fat per day). They have an undetectable incidence of heart attack and stroke.
In sum, this suggests that an effective way to avoid a heart attack is to reduce omega-6 consumption and ensure an adequate source of omega-3. The lower the omega-6, the less the omega-3 matters. This is a nice theory, but where's the direct evidence? In the next post, I'll discuss the controlled trial that proved this concept once and for all: the Lyon diet-heart trial.
52 comments:
Another excellent and clearly argued post.
We only need somewhere around 1/2% of calories as Omega 6 to be healthy which is about what the Kitavans get.
Deficiencies are difficult to generate but it is possible particularly in those with eating disorders.
Pregnant women will have higher needs.
Long term infection, increased cell renewal, septic events etc will increase usage.
It is important to consider the Omega 3 and 6 plant based fats separately to long chain fats as they have different roles.
Author Omega Six The Devils Fat
www.Omegasixthedevilsfat.com
Hi Stephan,
I am following your blog for a while, but because I am not a scientist I don't feel qualified to comment. I have lots of questions but while comments are accepted this doesn't seem to be like a forum so I don't want to intrude. However, related to the topic, can you comment on the Indian study Singh 2002 that is somewhat a continuation of the Lyon heart study? I did a search on Lyon heart study to find out more on it before your post and I got some excerpts from 'Coronary heart disease epidemiology' by Marmot and Elliot referring to this Indian study. It annoys me that 2/3 of the participants were vegetarians and they had about 60% from carbohydrate. (I am for Paleo/low carb) Anyway the point is the ALA consumption. We know that conversion to DHA is minimal. Is it enough to cut omega 6 by let's say not cooking anymore with sunflower oil but with olive oil and to add ALA in some form, nuts (very little in walnuts, bad ratio to LA) or flax to make a difference?
Sorry for the long post, my father is a vegetarian and at 72 he had a heart attack. The doctors are not giving him any recommendations regarding diet and he doesn't listen to me as I am not a doctor. I'm trying to find studies, to photocopy them and to take them to his doctors to make them change their attitude regarding omega 3 from fish oil supplements, CoQ10, avoiding omega 6, eating more eggs, supplementing B vitamins. Dr. Davis recommends eliminating wheat but he is not going to give it up.
Thank you.
Concerning Omega-6, is there any difference between natural sourced O-6 as found in nuts and seeds and industrial-sourced O-6 as found in vegetable oils? I seem to recall that natural sourced transfat is considered harmless/somewhat beneficial while man-made ones are really bad. Does the same logic apply to Omega-6?
Thank you for the great post.
I was reading on the Israeli 'paradox'. That's interesting. Low fat, high omega 6 to 3, similar incidence of cancers and CAD to US.
Another paradox that isn't a paradox.
small, dense LDL is a result of not enough SFA, and is concomitant with high triglycerides? (ref Krauss, Good Cal bad Cal)
it's the HUFA in small LDL that transforms it into ox-LDL at the drop of a dime?
are lesions in the arteries necessary for the atherosclerotic process to take place? (thinking glycation here, and gaps in glyccocalyx--the latter are very easy through high glucose)
high carbs ok as long as low fat (particularly HUFAs), but high carbs and high fats (HUFAs) is sure way to get CVD?
There are so many parts of this puzzle, but it feels like we're getting there....
hypothetical question.. what happens if we have large LDL from a high sat fat diet (which results in less LDL receptors), then we slip and eat highly unsaturated fats a few times--McDonalds fries, per say. Do the PUFAs get packaged in the large LDL that are to circulate longer than usual due to the lesser LDL receptors?
Sorry for the lack of references.
Alex
Makes you wonder if the apparent cases of success of Ornish type diet could be related to getting O-6's low enough that even with the carbs people can improve. I am strictly low carb because that works best for me but I suppose if your diet were <= 10% fat then limiting O-6's to <4% isn't so hard to do. Since reading this blog I have just decided to do both low carb and low O-6. I probably wasn't that high in O-6 before I just wasn't consciously trying to eliminate it.
To Darren,
Re:"I probably wasn't that high in O-6 before I just wasn't consciously trying to eliminate it"
I did an Atkins like diet for a long time. Atkins said the full-fat mayonnaise and salad dressings are OK because they're low carb. Actually preferred them to low fat versions, because the low fat versions had more sugar/carbs.
No mention that they are made with "soybean and/or cottonseed oil." While carb counting these are almost "free foods" so it's easy to consume quite a bit of them.
Also stuff like Wendy's chicken nuggets which are obviously fried in vegetable oil, and KFC fried chicken is relatively low in carbs and easy to manage in . Chicken fried steak, etc... by carb counting I could easily justify the relatively few amounts of carbs these foods had and finagle them into my Atkins-type diet.
When some of these fast food places went to "non-trans-fat" oils, while avoiding sat fats (or risk being sued by the lovely CSPI), the smoke-point dropped and some of these places became really smokey inside. This is scary because can u imagine the heat damage to the unsaturated fats one would consume?
The body appears to be well aware of the dangers of PUFAs. The digestive segregation of fats into the lymphatic system and carbs into the portal vein to the liver, is probably not mere coincidence.(1)
Probably no coincidence that saturated fat is packed into large LDL and ox-PUFA is "destroyed" in the liver via PERPP.(2) Because the body is NOT afraid of SFA as it knows it's not harmful. It's the very same type of fat that it makes in response to high carbohydrates.
I hypothesize that partially hydrogenated fats are as harmful as they are, because the body may confuse them for saturated fats, and thus pack them into large-LDL and with a lower LDL-receptor count and therefore uptake, these things would stay in the circulation longer than usual, wrecking potential havoc on the artery walls as they oxidize like common PUFAs. This is my own hypothesis and I have no references to back that up, just a guess of sorts.
1.http://high-fat-nutrition.blogspot.com/search/label/AGE%20RAGE%20and%20ALE%20%284%29%3A%20segregation
2.http://high-fat-nutrition.blogspot.com/search/label/AGE%20RAGE%20and%20ALE%20%289%29%3A%20VLDL%20degradation%20and%20Fish%20Oil
mtflight: I agree that Atkins can certainly be done in a way that includes lots of O-6's but I wasn't really considering my diet Atkins and I have eaten little O-6's that I can think of for about the last year or so. My carb content is probably very Atkins-like but I really am not eating cheeses or bacon or even that much red meat.
I previously had some salad dressings which were more O-6's than what I am doing now for sure.
Chicken nuggets were never on the list anyway, chicken fried steak - don't think I've eaten that in 10 years...
Mtflight,
where did you get the idea that a high-sat-fat diet results in the downregulation of LDL-receptors?
Never heard that before.
Any info how grain finishing livestock affects the amount of omega-6 in the fat tissue? I often hear grass-fed beef as being higher in omega-3, is it also lower in omega-6? I would imagine that all the soy and corn being fed to cows would increase the omega-6 in their tissues, unless they have enzymes that can saturate the dietary fats. I ask this because grass-fed meat is more expensive, and from what I have tried I find that I prefer grain-fed as it is more tender and juicy.
paleord,
I have read somewhere that when the animal is grain fed, it converts alot of the grain into saturated fat and not omega 6. It also depends on the animals health. I don't think if your eating the muscle meats it makes that much of a difference if it is grain fed or grass fed....if your eating organs and glands, forsure get grass fed organic if you can.
I always choose grassfed if its available, but i will eat grain fed beef also.
troy
whoops...i think if you are eating the muscle meats it doesn't matter as much!
Braesikalla, quick Pubmed search came up with these, but I'm pretty sure I didn't just fabricate that.
"...long-chain saturated fatty acids further suppress hepatic LDLR activity, whereas several unsaturated fatty acids have the opposite effect."- Dietary Fatty Acids and the Regulation of Plasma Low Density Lipoprotein Cholesterol Concentrations. The Journal of Nutrition Vol. 128 No. 2 February 1998, pp. 444S-448S http://jn.nutrition.org/cgi/content/full/128/2/444S
I suspect this is due not by chance, but by the body's knowledge that PUFA-laden LDL should be cleared away as it is unstable (can become ox-LDL),while SFA-based LDL is more is more stable and there's no reason to be in a rush to clear it?
Saturated fatty acids and LDL receptor modulation in humans and monkeys. Prostaglandins Leukot Essent Fatty Acids. 1997 Oct;57(4-5):411-8.
http://www.ncbi.nlm.nih.gov/pubmed/9430388
LDL receptor activity is down-regulated similarly by a cholesterol-containing diet high in palmitic acid or high in lauric and myristic acids in cynomolgus monkeys. J Nutr. 1995 Aug;125(8):2055-63.
http://jn.nutrition.org/cgi/reprint/125/8/2055
Here I find Lauren Cordain, PhD says:
"As consumption of certain saturated fatty acids (12:0, 14:0, 16:0, but not 18:0) increases, the number of hepatic (liver) and peripheral low-density lipoprotein (LDL) receptors decreases which in turn causes serum concentrations of LDL cholesterol to rise (a process called down regulation). Down regulation occurs because internalization of 12:0, 14:0 and 16:0 within cells reduces the expression of genes which code for the LDL receptor protein. " no references to where he got it. http://www.ThePaleoDiet.com/faqs/#Fats
Unfortunately in the same page he falls back to the sat fat causes heart disease mumbo jumbo referencing everyone except Yerushalmy and Hilleboe.
I like Cordain, but he said something that upset me regarding the glycocalyx (the slimy layer outside the cell, in this case pertaining to the artery wall on the lumen side) ... he said "It is known that high-fat diets (which increase the rate of oxidized LDL formation) cause the glycocalyx size and mass to be reduced 18" citing http://ajpheart.physiology.org/cgi/content/full/290/2/H915
titled "Atherogenic region and diet diminish glycocalyx dimension and increase intima-to-media ratios at murine carotid artery bifurcation" which states the so-called high fat diet is "Diet-N; Hope Farms"
When you look up this diet, it is comprised of:
15% cacao butter,
0.5% cholate,
1% cholesterol,
40.5% sucrose,
10% corn starch,
1% corn oil, and
4.7% cellulose
(don't ask me where the remaining 27% is)--at 40% sucrose and overall 50% carbohydrate (excluding the cellulose as fiber), and only 16% fat.. I would hardly call it a "high fat diet" and blame "high fat" for damaging this impermeable barrier that protects the artery from blood-borne products like AGEs and glycated PUFAs. I'd blame sugar, which indeed is referenced in the same paper as high blood glucose destroying the glycocalyx in a matter of hours. SO take it with a grain of sand until I or someone else can find a better citation.
Here's another "Among the saturated fatty acids (SFA), only lauric, myristic and palmitic acids (12:0, 14:0 and 16:0, respectively) reduce the level of hepatic LDLR activity"
Taurine Prevents Hypercholesterolemia in Ovariectomized Rats Fed Corn Oil but Not in Those Fed Coconut Oil. J. Nutr. 133:2616-2621, August 2003 but it is using the same reference as above:
Dietschy, J. M. (1998) Dietary fatty acids and the regulation of plasma low density lipoprotein cholesterol concentrations. J. Nutr. 128(suppl. 2):444S-448S
Glad I didn't just imagine this. whew.
mtflight
Thanks interesting posts.
Yes greater oxidation of frying fats is a concern.
Does this help?
http://www.jlr.org/cgi/content/abstract/38/3/459
Reducing saturated fat intake is associated with increased levels of LDL receptors on mononuclear cells in healthy men and women
VA Mustad, TD Etherton, AD Cooper, AM Mastro, TA Pearson, SS Jonnalagadda and PM Kris-Etherton
"Thus, an important mechanism by which reductions in dietary saturated fatty acids decrease LDL-cholesterol in humans is through an increase in LDL-receptor number. "
PaleoRD
Most of the trials I have read suggest that the Omega 6 in the grain in feed will increase the Omega 6 content in meat.
Robert Andrew Brown
Author Omega Six The Devils Fat
www.omegasixthedevilsfat.com
Another great post, can't wait for the ratio one. I used to do raw vegan and an interesting thing about that community is the typical pattern. People start out with lots of nuts and avocados, then feel crappy. Then they do a low-fat diet (ala Douglas Graham) of just fruits and greens and feel better and proclaim that fat is BAD. The Douglas Graham diet is pretty terrible in that long term adherents develop tooth decay among other signs of malnutrition and excess fructose, but it does tend to have a decent omega-3 to omega-6 ratio, which probably accounts for people initially feeling better.
That would lead me to the conclusion that the omega-6 in natural foods is not good, but there are so many coufounding factors. There are different types of omega-6 fats of course...and many nuts sold in stores are rancid.
The!kung do not seem to suffer from diseases of civilization, but their stable nut is high in n-6.
Thanks Robert, yup that helps. Off topic (well on topic since we're talking about eicosanoids and omegas) I just purchased your book yesterday. I'll get it in a few days and hopefully give it a read and add to my library.
Thanks,
Alex
With regard to ratios in grain fed vs. grass fed beef, the following information comes from Regina's Weight of the Evidence blog:
100 grams or about 3.5 oz
Beef, grass-fed
0.139g (n-6)
0.052g (n-3)
Beef, grain-fed, conventional
0.275g (n-6)
0.016g (n-3)
Beef, grass-fed
Ratio of Omega 6 to Omega 3
2.7 to 1
Beef, grain-fed, conventional
Ratio of Omega 6 to Omega 3
17.2 to 1
Melissa
"The!kung do not seem to suffer from diseases of civilization, but their stable nut is high in n-6."
Good find. I searched them on google - the San people of the Kalahari
Mongongo nuts 14% of calories 43% linoleic acid !! high in vitamin E and some minerals.
They spend 30 hours plus a week foraging.
They are thin !!!
Omega 6 only really starts to have a big negative effect once there are excess calories in the diet, logically the need for fuel must take precedence over other uses.
A trial on westerners suggest this may be the case.
mtflight
Very many thanks.
A new one is on the way which is a lot better I hope, and deal with the issues you have raised but I am sure you will find the current version thought provoking.
Author Omega Six The Devils Fat
www.Omegsixthedevilsfat.com
Revised version on the way that is hopefully a significant improvement.
Regarding grass-fed vs. grain-fed beef.
It is true that grassfeeding will increase the ratio of omega 3 to omega 6 but the overal proportion of PUFAs to other fats remains quite low anyway. Nick, those numbers are interesting because I have not seen such a dramatic difference in the study used by Sally Fallon. That's interesting. I would guess there may be some natural variation in these numbers.
However, I am not at all confident that grain-fed beef has more saturated fat. According to Sally Fallon (who cites a University of Nebraska study that I haven't actually gone to), all the increase in fat content in grainfed beef is monounsaturated. I believe this makes sense, since most of the fat gain when mammals gain weight is monounsaturated fat.
Another key difference in grassfed beef is the presence of conjugated linoleic acid, a natural trans fat alleged by some to have healthy properties. It gets eliminated in grainfed beef because the cows lose the gut microbes that make it from grass. I haven't looked at that research.
Lightcan
IF you have refs for the Indian trials that would be great. I have some but am always looking for more.
"Is it enough to cut omega 6 by let's say not cooking anymore with sunflower oil but with olive oil and to add ALA in some form, nuts (very little in walnuts, bad ratio to LA) or flax to make a difference?"
That must help. Flax is good. The problem is there are many factors that block conversion to the longer fats including age and some medical conditions.
Men are often very bad at converting.
Alcohol depletes the body of Omega 3 DHA if it is not replaced.
So to be certain of getting a supply of long chain Omega 3 you need to eat it. Vegetarian supplements to exist.
I do not think that there is anything wrong with vegetarianism, the problem is that it is difficult to get the nutrients needed particularly once people start to move on to a refined diet, crops from depleted lands, refined oils, higher calorie intake etc.
I'm still a bit confused on whether "natural" sources of omega-6s should be eaten...such as nuts and seeds.
From what I can tell from these charts, you want to reduce your omega-6 as much as possible, meaning that nuts and seeds would not be a good idea.
What do you guys think? No nuts and seeds?
subscribing to follow-up comments
"flax is good"
but with n-3s being so delicate, unless it's been refrigerated and not exposed to oxygen, and not deodorized... and you have the ability to know when it's bad and avoid taking it.... it seems to be like a very sharp double-edged sword. All the peroxidation potential right there in a [hopefully] small bottle.
My guess would be to only recommend the sources of n-3 that are the most stable. As Stephan has suggested, possibly eating fish rather than taking fish oil.
If you consume lots of n-6 sure by all means try to raise n-3 intake to minimize the ratio a la Japan, but do so with caution. Better to just cut-out the n-6 and keep the omegas low by means of food choices.
I think the ratio of o-6/o-3 in beef depends greatly on the particular cut.
I've seen these often self-serving comparisons of grass- vs. grain-fed beef and finally went to the USDA Nutrient Database to find out.
100g of USDA Choice grade rib-eye (grain fed) has (.510+.020)/.24 = 2.2:1 ratio - not bad at all.
A New York Strip has a similar profile.
Ruminants - particularly cattle - don't react as poorly to a high grain diet as do pigs and chickens. I believe Peter at Hyperlipid discussed this awhile back.
BTW Stephan, this and the companion post are wonderful finds. Thanks for bringing them to light.
Since I carefully track my food intake with CRON-o-Meter (better than the online Fitday IMO) I was busily doing some calculations this morning... ;-)
Turns out I'm right on the 1% dietary o-3 curve at just under 40% o-6 HUFA. So I'm right between Japan and Greenland for CHD mortality by your first post. Good to know, but it's great to have some credible data to guide me in improvement.
Robert Anderw Brown
You said:
'Omega 6 only really starts to have a big negative effect once there are excess calories in the diet, logically the need for fuel must take precedence over other uses.'
Do you mean to imply that we don't need to worry a whole lot about our 6/3 ratio if we do not overeat and we are moderately active? Like Jesse, I wonder if foods like nuts should be eaten moderately due to Omega 6 content. Assuming most of us are no longer using any vegatable oils and supplementing with Omega 3 or eating fish a few days a week, how much math should we be doing?
Sam
Does Cron-o-Meter count Omega content?
Stephan
My question above in no way is meant to imply that your posts are not fascinating, important and essential work.
Having been raised on a farm, I don't know of any exclusively Grain fed or Grass fed cattle.
In the spring, summer and fall, the cattle grazed all day long in the pasture (cost..., Corn wasn't harvested till October). Then they wintered over using Alfalfa Hay and Corn. I have to believe that most dairy and beef sold in the late spring, summer and early fall is from predominately grass fed animals. I think the n6-n3 ratio must therefore have a seasonal variation.
I'd be keenly interested in the arachidonic acid content of animal fats, grass or grain fed. What mechanism is there to moderate inflammation from AA when dietary pre-formed AA is consumed?
Brian
Re: nuts and Omega 6
My strategy is to only eat raw Macadamia nuts, which have a fat content that is almost entirely monounsaturated.
Mtflight,
"I suspect this is due not by chance, but by the body's knowledge that PUFA-laden LDL should be cleared away as it is unstable (can become ox-LDL),while SFA-based LDL is more is more stable and there's no reason to be in a rush to clear it?"
That makes sense to me. Thanks for clarifying this.
what are the real sources of dietary omega6s?
we always talk about vegetable oils and french fries, industrial mayonaise, nuts, etc. I guess some people consume those a lot, but not all.
what about pork, chicken and eggs? the fat in these contains a relatively lot of omega6s (more than 10% of the fat?), especially when compared to beef, butter or milk products.
and if we try to minimize the intake of omega6s, it is easy to avoid vegetable oils and the products containing them. but it is very difficult to avoid eating pork/chicken/eggs. on a lowcarb diet one easily consumes them regularily. (can't afford to buy beef all the time, it is expensive in Europe).
how can you really avoid omega6s?
natural pork, chicken and eggs are not high in omega-6, look for the pastured ones (very hard to find though)
Nick
"Do you mean to imply that we don't need to worry a whole lot about our 6/3 ratio if we do not overeat and we are moderately active?"
No.
My simplistic view is that in nature Omega six is scarce seasonal and we could never have achieved high levels of Omega six intake of the year round basis on a hunter gatherer diet.
Also the Omega three and six plant fats on a year-round basis would always have been more or less in balance.
On that basis alone it seems sensible to restrict the Omega six intake.
The Omega 3:6 balance impacts on body function in number of ways, and the eicosanoid pathway is just one.
If you are a San bushmen or an aborigine on a totally natural diet then the effects are likely to be lower than if your diet includes any Western refined foods.
What I am suggesting is that the negative effects of excess Omega six become turbo boosted with excess calories refined carbohydrates etc., and so we can see the effects in short-term trials.
The effects of a lifetime's excessive Omega six where our diets are in the sufficient calories bracket are going to be much more difficult to nail down.
If there are any San bushmen with undisturbed diets they would make a fascinating study on the long-term impact of Omega six on human cardiac health. They are very lean which suggests that a calorie intake is minimally sufficient. The body actively stores Omega six, and their lack of storage fat may reflect the wider metabolic fate of the Omega six they eat.
TTlaitin
"if we try to minimize the intake of omega6s, it is easy to avoid vegetable oils and the products containing them. but it is very difficult to avoid eating pork/chicken/eggs. on a lowcarb diet one easily consumes them regularily. (can't afford to buy beef all the time, it is expensive in Europe).
how can you really avoid omega6s?"
That is the dilemma. On a Western diet it is very hard to avoid Omega sixes. Vegetables fats are everywhere in processed foods. Grains are heavily used in the production of livestock.
This is why as well balancing the plant-based Omega threes and sixes, it is essential to get an adequate supply of long chain Omega threes.
As is illustrated by Stephan's post and the graphs you refer to Omega three intake will help mediate the effect of Omega sixes.
The problem is the supply sources of long chain Omega threes are limited. Marine fish and shellfish one of the best sources but we are depleting directions and polluting our estuaries and shorelines.
This is a helpful paper that illustrates how the need for long chain Omega threes change with increasing Omega six intake.
Healthy intakes of n–3 and n–6 fatty acids: estimations considering worldwide diversity – Joseph R Hibbeln, Levi RG Nieminen, Tanya L Blasbalg, Jessica A Riggs and William EM Lands
http://www.ajcn.org/cgi/reprint/83/6/S1483
For "directions" read "our oceans".
(I am using dictation software and missed the error) (-:
Wolong
"Concerning Omega-6, is there any difference between natural sourced O-6 as found in nuts and seeds and industrial-sourced O-6 as found in vegetable oils?"
There are huge differences.
Industrial processing leads to the creation of trans fats, and removes fat soluble vitamins and minerals.
The Omega three content is the most susceptible to structural alteration, and from what I've read most industrially processed oils contain some trans fats.
Processing also removes beneficial plants antioxidant compounds.
And as Stephan importantly identified production processes also damage vitamin K-1.
It may well be that the processing of these fats as other negative effects of which as yet we are unaware.
Author Omega Six The Devils Fat
www.Omegasixthedevilsfat.om
I just stumbled onto this link, which is a little dated, but apropos (warning: may raise blood pressure):
http://www.news-medical.net/news/2009/01/27/45299.aspx
Maybe someone here knows where this has already been discussed.
How is it that cardiologists are in charge of dispensing nutritional advice? Seems a bit odd to me...
Phil
Laughing once I realised what you meant.
Yes blood pressure must have gone up when I read that I was boiling.
Yes it has been discussed in previous posts.
Stephan had a few succinct words to say about it.
The arguments are very weak.
This is one of the comments which this excellent post of Stephan's refutes. The paper they cite to support this actually unsurprisingly goes against their argument.
"Eating less LA will not lower tissue levels of AA (the usual rationale for reducing LA intakes) because the body tightly regulates the synthesis of AA from LA."
And if you read the studies they cite there is no evidence I have seen that can justify this statement.
"Observational studies showed that people who ate the most omega-6 fatty acids usually had the least heart disease"
How do they sleep !!!
Melissa
I have spent much of the afternoon looking for data on the San. If you have any links that would be useful.
The only significant observation of diet was in a period of drought and the mongongo nuts were plentiful. There are suggestions that in the 1920 and 30s they were eating anything that moved, and were mal-nourished at certain times of the year. They were also reported as suffering from lung conditions and skin conditions in times of drought. There are a number of tribes involved and so things are far from clear. Another paper suggest that the nuts were not the most energy efficient food available to them so they would not have been a first choice. Clearly there are questions that it would be good to answer, including what their Omega 3 intake was like and where it came from.
Excellent posts as usual, Stephan. Robert Andrew Brown is pursuing a thread on the San of the Kalahari that raises an intereting issue; calorie load and its impact on human health. If the diet is sufficient in micronutrients (at least minimally sufficient), then the first instinct of the body is to burn what comes in. This may save a lot of traditional cultures from somewhat out-of-balance macronutrient ratios.
It may only be necessary to concern ourselves with the issue of ratios as the calorie load increases.
Besides the CRON practitioners, I wonder what data may exist regarding the potential link between increasing over all calories and the various diseases of civilization? Of course, any links may be confounded by the macros consumed, so difficult to discern any patterns.
Just thinking aloud. I have been intermittent fasting off and on for a couple years and have slowly transitioned to eating just once a day. Eating real food, with a somewhat shrunken stomach, it is hard to eat too much at one meal so the calorie load decreases. It is amazing how the body can adapt to this though as I do fine with both hunger and activity level all day long. Makes me wonder what my body was doing with all the calories I used to eat.
Thanks for your efforts.
Scott W
So the way I see it, the human body is quite the Rube Goldberg contraption (obligatory fun link), with multiple inputs and outputs at every stage along the way.
Sounds like to have heart disease, you have a sequence of:
1) stress
2) signals
3) inflammation
4) damage
To combat heart disease, you can address it at any of the 4 levels.
1) Reduce stressors -- meditate, don't eat fructose or wheat, etc.
2) Reduce signalors (hey new word) -- reduce n-6, increase n-3 consumption
3) Reduce inflammation -- NSAIDs, probably other drugs
4) Reduce damage -- heart bypass surgery?
As Stephan pointed out in another comment, it's awful tough to wipe out step #1.
Reducing step #2 actually looks pretty easy....ish.... all of a sudden. No more corn oil, no problem! Just skip the entire salad dressing aisle at the grocery store.
Steps 3 and 4 have their own pluses and minuses of course.
Looking at it as a system, you can see why different interventions can have positive results even if they appear unrelated to each other, and why you can get conflicting results.
This was brought to my attention by Lani a stalwart on another board.
http://www.jbc.org/cgi/content/abstract/M109.004861
Effect of Dietary Fatty Acids on Inflammatory Gene Expression in Healthy Humans
"These data reveal that PUFA may exert their clinical effects via their capacity to regulate the expression of signal transduction genes and genes for proinflammatory cytokines."
Essentially Omega 3 reduces (and Omega 6 increases by implication) the expression of genes related to inflammation.
I have not seen the full paper as yet.
The genes obviously had not read the Medical News article posted by Phil and did not know they were not supposed to behave like this (-:
"Thus, it is incorrect to view the omega-6 fatty acids as 'pro-inflammatory,'" Harris explained.
http://www.news-medical.net/news/2009/01/27/45299.aspx
Author: Omega Six The Devils Fat
www.Omegasixthedevilsfat.com
Interesting new study: Omega Fatty Acid Balance Can Alter Immunity And Gene Expression
http://www.sciencedaily.com/releases/2009/05/090529183250.htm
"This study demonstrates, for the first time in humans, that large changes in gene expression are likely an important mechanism by which these omega fatty acids exert their potent clinical effects."
Robert,
Now that you point it out, I see I am late to the game. David spotted this six weeks ago, and Stephan had a few choice words.
It's interesting that the committee recommendation doesn't rest its case very strongly on the science they review, but rather on a survey of other authoritative bodies.
What fascinates me is that they're aware of the dangers. They point out we only need 0.5-2% omega-6 in our diet. They quote other authors who point out that no population has ever done what they recommend for a long period of time. And then... they go ahead and recommend the same old thing. It seems to me less like butt-covering and more like a habitual set.
Thanks Robert Andrew Brown,
This is the first link that I found and that you might be able to use as it refers to others.
http://eurheartj.oxfordjournals.org/cgi/content/full/27/13/1628
another one I found that I couldn't access
http://content.karger.com/ProdukteDB/produkte.asp?Aktion=showproducts&searchWhat=bookseries&ProduktNr=223966
Effects of an Indo-Mediterranean Diet on the Omega-6/Omega-3 Ratio in Patients at High Risk of Coronary Artery Disease: The Indian Paradox
Pella, D. ; Dubnov, G. ; Singh, R.B. ; Sharma, R. ; Berry, E.M. ; Manor, O.
Simopoulos AP, Cleland LG (eds): Omega-6/Omega-3 Essential Fatty Acid Ratio: The Scientific Evidence. World Rev Nutr Diet. Basel, Karger, 2003, vol 92, pp 74-80
it looks interesting. Here I found some free sample chapters
http://content.karger.com/ProdukteDB/produkte.asp?Aktion=showproducts&searchWhat=books&ProduktNr=232073
The Indian study related to a cardioprotective diet by Singh is controversial as the Lancet and the BMJ seemed to have 'concerns' about sloppy protocol, research and statistics.
Nick,
Thank you very much.
The first link to the letter contains some interesting material, and it fits very well with what I am working on in terms of the impact of excess calories.
The second goes to Simopolous's books which I have not read as they are expensive !!, but Simopoulos has some great papers and a big reputation.
The third to Okuyama is useful. He is very perceptive and brings together powerful material I keep finding free chapters to this book and it is excellent. I have seen 1 but not the other two. I know Stephan has seen the whole book.
Phil
I agree with you. One has to wonder how they came to the conclusion that they did. I wonder how much heated discussion there was in coming to an agreement as to the content of the paper. A lot is suspect. (-:
Many thanks
My salad dressing: Carlson's Norweigan Lemon Flavored Fish Oil (800 EPA,500 DHA per teaspoon), balsamic vinegar, Pensky's spices kept in refrig. I also steam asparagus then add a little Carlsons. Easier than popping alot of fish oil gelcaps.
Is life worth living with fish oil as your salad oil?
---- I'm kinda making a joke here.
Lightcan,
Everyone is qualified to comment on this blog! I'm not familiar with that study. I do think it's ideal to include some animal omega-3 for the DHA. But that can also be found in pastured eggs (or "omega-3 eggs" in the grocery store) and pastured dairy. I think flax isn't ideal but it's better than nothing.
WoLong,
That question has not been answered fully to my knowledge, but my opinion is that omega-6 from nuts is probably healthier than omega-6 from vegetable oils. But I still believe that excess omega-6 from any source is likely to be a problem.
Alex,
I think you raise some interesting questions. I can't answer them at this point. I like your theory on trans fats being treated as saturated fats in lipoprotein particles.
Darren,
Maybe. Here's the thing though. I don't believe his diet/lifestyle actually works, because it hasn't demonstrated any survival advantage in controlled trials. He likes to cite a very small study he did showing that his diet/lifestyle increased the diameter of a few peoples' coronary arteries, which is well and good until you have a heart attack anyway. But there may be some individual successes due to reducing omega-6.
PaleoRD,
Cows hydrogenate unsaturated fats in their digestive tract, rendering them saturated. So beef always has a low proportion of PUFA regardless of diet. The ratio will change based on diet, but it's easy to balance the small amount of extra omega-6 with a little bit of seafood or fish oil. In my opinion, there are many reasons to eat pastured beef besides the fatty acid balance.
Melissa and Robert Brown,
The !Kung do get a large proportion of their calories from linoleic acid. However, from what I understand, mongongo nuts are eaten seasonally. During the mongongo season, they eat very little carbohydrate as well. I'd be interested to know what their average yearly intake of omega-6 is. But anyway, I acknowledge that there are other factors involved.
Jesse,
My opinion is that high-omega-6 nuts are best eaten in moderation. Nuts lower in omega-6 include macadamias, hazelnuts and cashews.
Carl,
Typically, modern grocery store beef is raised first on pasture with some grain supplement to the diet, plus hormones, then it's taken to a feedlot to fatten for the last 6 months or so of its life, where it eats a largely grain-based diet. Tissue omega-3 content plummets during a cow's time in the feedlot.
Brian,
The mechanism is competition from omega-3s. Pastured meats will contain omega-3 HUFA as well as omega-6 HUFA.
Scott W,
I suspect that our increased caloric intake in the US is more a consequence of our health problems than a cause. We're metabolically deranged and our appetite control systems are damaged. When you feed rats junk food, they eat more calories too. But that doesn't rule out other possibilities such as cultural factors.
Ed,
That's consistent with my current thinking.
Robert B,
Great study, I'm going to have to check out the full text.
Carl, there is no such thing as grain-fed cattle in New Zealand. :) I spent months on a ranch down there and I never saw any cows or sheep eating any other grains than the few seeds that might have occurred naturally in the fields.
You make a good point that there's always been a history of grain feeding in this country, though. This really took off in the late 1800s when industrialists figured out how to feed cattle industrial waste products of germ and bran (from making white flour) instead of washing it down the Mississippi. (They later marketed bran and germ as a health food to humans.)
Still, the way cattle are raised has changed pretty dramatically in the past 50-60 years. They used to graze on much more diverse pasture (including oats) over a longer period of time. Only about 1/4 of the total cattle are on a feedlot 100% of the time at any given time in the year.
Many people who raise their own cattle just slaughter baby beef. To my tastes, it's much better than feedlot beef and they are raised almost entirely on mother's milk and grass and the calf gets fat pretty quickly.
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