Saturday, January 12, 2008

PUFA table

This post is for bruce. It's a copy paste of the table from:

Elgersma, A., S. Tamminga, and G. Ellen. 2003. Effect of grazing versus stall-feeding of cut grass on milk fatty acid composition of dairy cows. Proceedings of the Int. Occ. Symp. of the European Grassland Federation, Pleven, Bulgaria, May 2003. Grassland Science in Europe 8: 271-274.

I've no idea where I got the pdf from, it's just been lying around on my hard drive for ages. Not on pubmed.

The PUFA varied from 4.34 to 5.76, in the same 6 cows over a 5 month period. I don't really think of diet components in terms of accuracy to two decimal places. The figure of 5% is somewhere in the middle. My own PUFA intake estimate comes as total PUFA value from Fitday, so is USA based and probably bears little resemblance to values from parts of the world where cows are fed on grass! My estimate varies between 10 and 20g/d, depending on menu and how much I believe Fitday represents UK food. Even using http://www.nutritiondata.com/ the values in various types of cream and butter are wildly variable in their PUFA ratios. I just feel we can never really know exactly what is in a specific block of butter... Keeping it low is good, how low is low? I really dunno what I eat!

Sorry the table's a bit small, that's how it copy pasted

Peter

PS thanks for the reading pointers. Bear I've read, but not Peat.


16 comments:

g said...

What level of PUFA and omega-3's do you consume most days? I didn't realize that in France, there are recommendations for ALA 0.8/0.9% and DHA 0.05%/0.1?(young and aged populations)? See the end of the abstract. Europe is so progressive compared to the US!

J Nutr Health Aging. 2005 Jul-Aug;9(4):232-42.Links
Where to find omega-3 fatty acids and how feeding animals with diet enriched in omega-3 fatty acids to increase nutritional value of derived products for human: what is actually useful ?

Omega-3 polyunsaturated fatty acids have two major field of interest. The first lies in their quantitative abundance and their role in the development and maintenance of the brain. The second is their role in the prevention of different pathologies, mainly the cardiovascular diseases, and more lately some psychiatric disorders, from stress to depression and dementia. Thus, dietary omega-3 fatty acids are very important to ensure brain structure and function, more specifically during development and aging. However, concerning essential alpha-linolenic acid (ALA), most occidental diets contain about 50 % of the recommended dietary allowances. The problem is to know which foods are naturally rich in this fatty acid, and to determine the true impact of the formulations (enriched in omega-3 fatty acids, either ALA or EPA and DHA) in chows used on farms and breeding centres on the nutritional value of the products (meat, butter, milk and dairy products, cheese, and eggs, etc), and thus their effect on the health of consumers, especially to ensure adequate quantities in the diet of the aging people. The consequences (qualitative and quantitative) of modifications in the composition of animal foods on the value of derived products consumed by humans are more marked when single-stomach animals are concerned than multi-stomach animals. Because, for example, hydrogenating intestinal bacteria of the latter group transform a large proportion of polyunsaturated fatty acids in their food into saturated fatty acids, among others, thus depriving them of any biological interest. Under the best conditions, by feeding animals with extracts of linseed and rapeseed grains for example, the level of ALA acid is increased approximately two-fold in beef and six-fold in pork, ten-fold in chicken, and forty-fold in eggs. By feeding animals with fish extracts or algae (oils) the level of DHA is increased about 2-fold in beef, 7-fold in chicken, 6-fold in eggs, and 20-fold in fish (salmon). To obtain such results, it is sufficient to respect only the physiological needs of the animal, which was generally the case with traditional methods. It is important to stress the role of fish, whose nutritional value for humans in terms of lipids (determined by omega-3 fatty acid levels) can vary considerably according to the type of fats the animals have been fed. The aim of preventing some aspects of cardiovascular disease (and other pathologies) can be achieved, or on the contrary frustrated, depending on the nature of fatty acids present in fish flesh, the direct consequence of the nature of fats with which they have been fed. It is the same for eggs, "omega- 3 eggs" being in fact similar to natural eggs, were used in the formulation of certain formula milks for infants, whose composition was closest to that of breast milk. In fact, the additional cost on the price paid by the consumer is modest compared to the considerable gain in nutritional value in terms of omega-3 fatty acids content. Interestingly, in aged people, ALA recommendations in France are increased (0.8% daily energy intake in adult, 0.9 % in aged) and DHA is multiplied by 2 (0.05 % daily energy intake in adult, 0.1 % in aged; as well as in pregnant and lactating women).
PMID: 15980924 [PubMed - indexed for MEDLINE]

Bruce said...

OK, they're including natural Trans Fat (like CLA and Vaccenic Acid) as PUFA. I would subtract those, since CLA is technically a MUFA. Just add the omega-3 and omega-6 and you get the key number. (NutritionData does not seem to include trans fat under the PUFA description.) Natural TFAs are not a problem, as they occur in small amounts in red meat and dairy products. PUFAs are best minimized, as I think we both agree. I have no problem with the CLA and VA in fats from ruminant animals.

Bruce said...

I checked the PUFA percentages for: half-and-half, heavy cream, coffee cream, light cream, and sour cream. They varied from about 2.8-3.7% of total fat on NutritionData. You are probably overestimating your total PUFA intake, but it's around 4% of calories, which is ideal IMO. I do not worry as much about the n-6/n-3 ratio. I notice the less n-6 I eat, the less I need n-3 to counter its toxic effects. Mead Acid will also compete with AA for eicosanoid and prostaglandin production. The more you get away from the typical high PUFA and high-carb junk food diet, the better off you will be.

Regarding g's comment, there are a lot of omega-3s in brain. It has a high ratio of n3 to n6, going from about 9:1 for pork brain, on up to 30:1 for beef brain. Loren Cordain and Anthony Colpo have both stated that primitives didn't eat fish or fowl regularly until 20-40 k years ago. They ate large ruminants, and got omega-3 from brains. But brain is not particularly high in PUFAs: (about 6-10% of calories). I don't agree with Cordain's views against saturated fat or that cave men ate high levels of PUFAs. I think that it is best to keep PUFAs low, with plenty of SFAs and MUFAs.

http://www.lowcarbmuscle.com/forums/showpost.php?p=924&postcount=24
http://www.thepaleodiet.com/articles/Final%20Fatty%20Acid%20PDF.pdf

Peter said...

My assumption re Cordain is that he's on a statin and it shows in his brain function. I remember following one his pro statin drivel papers through its refs. Initially it was self citation of another pro statin opinion paper. That self cited paper cited NCEP and a few junk science statin marketing studies. I have this vision of Cordain's hunter gatherer group bringing down a Mastodon in October in ice age northern Europe then carefully trimming all the fat off of their meat before eating it and discarding the abdominal tallow. Maybe greasing their boots with it. Meanwhile, just by looking at the home page of his website I can see that the women have gathered some black cherries, black grapes (big ones), a kiwi fruit, some commercial size strawberries and a seriously sweet looking orange. Gathering was good that day.

Peter

PS g, re PUFA, looks like not many! I still like to think I get a few grams of omega 3 a day. Not using the omega eggs etc though, cream and butter seem to do the job.

g said...

I'm trying to find long-term studies for 'high-dose' omega-3s -- the longest I think is 1yr. As you've written here there exist many culture how get in probably even more than 3-4 g DHA+EPA daily from diet sources (not high grade pharmaceutical pills).
Look, here are Americans who have brilliant thoughts like you...
I didn't know that cream had significant omega-3s! Would you say that even the non-grass fed cows produce sufficient quantities?

THANK YOU! g

http://nmsociety.org/index.php?option=com_content&task=category§ionid=4&id=14&Itemid=27
SEARCH FOR: Wat if Saturated Fat is Not the Problem?
b y Richard Feinman

Peter said...

Hi g,

I think grain fed dairy is probably still adequate if your other sources of omega 6 are under control. My guess from carcass lipids would be there is 1 part omega 3 to 4 parts omega 6 in grain fed dairy. Acceptable. It does seem quite difficult to get hard data on these things. Long term omega 3 studies are not something I've ever chased really. It's unlikely that many would limit omega 6s, so it would be hard to pull meaningful information from them.

Don't forget mice contain nearly 50% calories from fat, unless they're starving!

Hee hee, joined nm society last week. Of course there are scientists in the USA, and it seems to me that the change in nutrition "research" from politics driven to science will have to come from the USA. Keys is dead. His legacy can't go on for ever. Even the USSR crumbled eventually!

Peter

Bruce said...

"My assumption re Cordain is that he's on a statin and it shows in his brain function."

I've never seen that theory before, but it would explain a lot of Loren Cordain's wacky ideas, like telling people to cook with canola oil, and add flaxseed oil to lean meat. He's convinced that primitives ate a lot of PUFAs, and very little saturated fat. Even if they did (which I very much doubt), I'd say that it's much healthier to minimize PUFAs and eat more SFAs and MUFAs. Mead Acid will substitute for omega-3, if we don't eat an excess of omega-6. It seems to me that excess omega-6 increases the need for omega-3. The studies I have checked talk about ratios, but they never try limiting the overall amount of PUFAs severely. They are ignoring a key variable, IMO.

HeartCipher said...

Hi Peter,

Found your blog as a result of your posting to Dr. Davis' blog... You may recall that I was amused in comments there by the irony of the fact that the ardent vegan, Dr. Fuhrman, has also written what Davis considers to be the best book on the health benefits of fasting...

I pulled out his book on fasting which I bought last month on the recommendation of Dr. Davis. In a section of his book on fasting, Fuhrman write a section call "The Biochemistry of Fasting". That section is summarized as follows:

"The unique nutritional adjustments that occur during a total fast, including the adaptation to ketone nutrition, apparently have long-term beneficial effects on brain function, improving psychological health as well as physical well-being. When EEG data and endocrine parameters are measured during and after fasting, it appears the homeostasis mechanism of the body significantly improves in the central nervous system." pp. 198-199

It sure looks to me like Dr. Fuhrman has the same basic understanding of fasting that you do... except...

He then proceeds to argue and write even more books on the benefit and even the necessity of a vegan lifestyle.

It would be interesting indeed to see a more blatant case of what Taubes has written about the fact that scientists do studies and then ignore the results of those studies.

Looking forward to reading more of your blog.

Just for fun, I spread your propoganda a bit at the ImmInst.org forum here:

www.imminst.org/forum/index.php?
showtopic=19699

Paste above two lines into a single link.

I'm going to post about you soon at my own blog Peter. You've got my head a spinnin'.

8-)

P.S. I see "g" is on the scene here too now. Wow! Hi g!

Peter said...

Hi heartcipher (wccaguy, yes?),

Nice to hear from you. I too really enjoy Dr Davis' blog. He has got to be absolutely the best source of personal accounts of the fallacy of the lipid hypothesis. You don't get those tales of people with "perfect lipids" producing explosive plaque growth anywhere else. I wonder what their post prandial insulin/glucose levels were???? I keep feeling there is hope for him nutritionally, but he can never quite make that break with vegetarianism and the lipid hypothesis. It's interesting to try and make him think beyond fasting and lettuce leaves. Hee hee.

Peter

g said...

I appreciate all your insights! The mice in our neighborhood looked even more chunky than most mice!! Probably 70% fat content! They were darn cute, except when their heads were half bitten off...

Does the UK have diet requirements for ALA and DHA?

That's hilarious!! -- I haven't had the time to go thru all the nm society stuff but they sure seem to have the correct thoughts, eh!

Hey ACipher -- funny seeing you here!

I have had very interesting observations with THyroid replacement and Vitamin D replacement. Have you noticed any changes in your animals? What I've seen is individuals (humans) require less LT4 levothroid once they are vitamin D replete. does that make sense? similar phenomenon occurs with hormone replacement in post-menopausal women. FASCINATING!

Thank you! g

g said...

I assume your lipoproteins are spectacular and phenomenol... as well as insulin levels... btw, have you ever had an EBT/CT scan? In your experience, is the high fat nutrition effective at preventing all human plaque development and growth? THanks, g

Peter said...

Hi g,

Lipids and plaque are two very complex subjects. I really must get a post together on this some time. It's clear from George Mann's work with the Maasai that they do not develop IHD but DO develop extensive arteriosclerosis. Unfortunately the full texts are not easily available but I guess Gary Taubes went to the originals when he cited them. The Maasai have lipids even a modern cardiologist would be happy with, lots of plaque and no IHD. Kitavans have appalling lipids, low HDL, high trigs, high LDL. Lindeberg was not set up to look for plaque in Kitava, so all we have here is the near total absence of overt IHD and angina throughout the population. Whether they resemble the Maasai in that they have plaque, we don't know. Their lipids are as bad as people in Sweden. So where does that leave the lipid hypothesis?

My own lipids are HDL around 60, trigs around 80 and TC 335 (I just checked my lab report, I remembered it as higher than this but no, 8.6mmol/l it is). You can imagine what my LDL calculates out at, but NMR for lipids is not available in the UK (as far as I know). EBCT is around $1000 a shot in the UK so I'm saving. My insulin was half the bottom of the lab reference range 2 years ago, can't remember the units. HbA1c is currently 4.4%.

My feeling is that low HDL, high trigs and small dense LDL simply reflect hyperinsulinaemia. Hyperinsulinaemia drives the arterial proliferation which is the normal repair process (gone wild) for glucose induced arterial damage. Or any other damage for that matter, such as homocysteine or even mechanical stress.

The Kitavans appear to maintain insulin sensitivity despite a diet of yam and sweet potato. That's their "trick" in avoiding cardiac disease, as far as I can see...

Obviously a EBCT score of zero is very nice. An explosive rise would be frightening. Between is interesting, but on the SAD and no sunbathing any plaque score is probably rising. I can certainly see why Dr D aims for reversal. This is his tool and he has a way to monitor it which works. His lipid manipulations are all fine and good, especially if they happen to involve dropping insulin and glucose levels. I'd even accept the antithrombotic effects of statins if they didn't drop cholesterol levels.

Peter

PS re thyroid. I believe most thyroid deficiency is auto immune in origin and certainly vitamin D might affect the underlying process. I rarely have the option to measure vitamin D in my patients as it is very expensive and there is no veterinary clinical precedent for using D to manipulate the immune system. As I'm nowadays a part-timer my veterinary work is very much more mainstream than is good for my patients. I'll even only explain rawfeeding when clients ask me point blank what I feed my own cats.

HeartCipher said...

We need to get you an NMR test and a CAC scan Peter.

I've got a friend in the UK who is going to be asking his doctor about lipoprotein subfraction testing in the near future. If he comes up with anything, I'll let you know.

aka wccaguy

g said...

Right, without a CAC score/EBT you don't really know the actual health of the endothelium (hopefully 'gone MILD' not wild *ha ha*)... You may be like the Vytorin sub-pop that's been getting all the media -- the high LDL is clearly not atherogeneic as pre-diabetic/T2DM LDLs.

You're so funny with the latest post! You are sounding a bit like a big rant like DR. D! Thank you for all your insights in illuminating the biochem and health horrors of wheat... You and Dr. D have a lot in common (biochem wise) than you could ever know. I have some more questions for you :)
I have a BSc in Nutri Sci and Food Science... however a lot has advanced since then. I've learned a lot from your posts and links!! It's neat that you were/are an athlete too. I started jogging half-marathons recently and discovered how we can train and be more efficient metabolically. Didn't know that KBs were so involved. what i've read is about fatty acids in skeletal muscles and the 'remodeling' and increased mitochondria that occur with endurance and exercise training. Any thoughts? Does the body prefer fatty acids linked to albumin, KBs, or TG-rich lipoproteins during physical exertion? For me, I actually run better RIGHT after a small meal (like cheese, peanut butter and 2 bites Ezekiel toast -- yeah sounds gross but tastes really good -- trust me *ha*). obviously I'm not training well lately w/the cold b/c I 'bonked' the other day on a little hill when I skipped breakfast AND lunch -- forgot what that felt like.

It's been so neat to find you -- i'm so glad that you started on the heartscanblog (with your anti-veggie/SFA rhetoric no less!) somewhere in the middle I'm sure the truth will lie. My wise friend Tina always says -- we should eat what our 'ancestors ate'. so perhaps you are the progeny of strong Siberian or Russian stock obtaining Vit C and folate sustenance only from carnivorous sources! I think us Asians are genetically accustomed to a little more green sources? dunno...

Peter said...

Hi wccaguy,

It's something I'm quite interested in getting done, the EBCT rather more than lipid particle sizes. In exactly the same way as I monitor my glucose system I'm interested in my cardiovascular system too, though you have to realise that a cholesterol skeptc is unconcerned by a TC of 8.6mmol/l. My interest is to find out whether what I' doing is effective as a whole, never mind the LDL level. As we know, EBCT seems to be the best way to get marks out of 10 CV system-wise....

There is a system for assessing aortic stiffness based on the time between the systolic peak of the blood pressure in your finger to the secondary peak which occurs during the fall down to diastolic. For years I'd noted this secondary peak on arterial pressure traces, you can even see it on the plethysmograph trace of a good quality pulse oximeter. I'd never really thought about what caused it. It's the pressure wave being reflected from you lower limbs back up your aorta and down to your finger/radial artery/wherever. As such, the time interval between the two peaks gives information about transit time of the secondary pulse wave. The stiffer your aorta, the faster the wave travels and the shorter the time interval. Factor in height to account for the distance travelled and you have an index for aortic stiffness, or how "old" your aorta is. Mostly looking for central vascular disease, people argue about how indicative this sort of information is re coronary arteriosclerosis. I got chance to play with a machine. My aorta is 32 years old, I'm 51. So far so good, and a very cheap measurement (it was free).

Needless to say I was a little stressed on the day of the aortic pulse wave analysis, my first ever marks out of 10 for several years LC high fat eating. Turned out to be cool.

The machine's owner is younger than me and had an aortic age >70. I gave her Life Without Bread. She's down to chronological age and dropping. I think that was over about 6 months.

Anyway, that's still a very indirect look at CV function!

EBCT is where it's at....

Peter

Peter said...

ah, g,

Ancestors! I'm a mix from the Western Ukraine and the Glasgow east end! Breadbasket of Russia and Celt... Probably either leaves me with lots of options or none!

Not sure about the Asians and greens link, the rice and metabolic syndrome seems quite nicely linked though, even without lectins.

I see you forget to eat occasionally, it's so easily done! My exercise is a bit limited too at the moment and I've never really looked at FFA vs chylomicrons vs ketones as fuel personally. It's probably way too early to go find subtleties in the literature yet. I would comment that I routinely go in to ketosis post prandially and I suspect either my vascular lipoprotein lipase spills FFAs directly in to my bloodstream or my liver picks up chylomicrons and churns out ketones.... Perhaps this is what best fuels your running?

From general reading on ketones they appear to be able to generate more ATP per unit oxygen than FFAs. Presumably this has to be paid back somewhere? Maybe in the liver, but not acutely in the muscles, so perhaps there is a serious roll for ketosis in hard endurance work...

BTW if I ever get tested for heterozygous FH and come back negative I will be very disappointed! I did once get a TC below 7.0mmol/l but that was probably a lab error!

Peter