Tuesday, June 03, 2008

EFA deficiencies?

Arachidonic acid is essential. Apart from the fact that your brain is largely made out of it (I exaggerate here slightly) and it has a roll as a precursor to a myriad signaling molecules, there is a definite deficiency syndrome in the skin. The deficiency syndrome is a bit dubious in humans, especially adults, but pretty clear cut in lab animals, especially during growth. Chris Masterjohn covers this pretty thoroughly and it seems quite plausible.

In most adult humans there is enough linoleic acid stored in fatty tissue to act as a reservoir for the synthesis of arachidonic acid for a long time. Even after years on a PUFA free diet it is unlikely you could precipitate an arachidonic acid deficiency. Bear in mind that a completely PUFA free diet must be synthetic or largely so. No food, just a fat free protein source, sucrose, glucose and some multivits should cover it! Otherwise enough arachidonic acid would sneak in from meat and eggs to supply an adult's needs. Or maybe some linoleic acid from lettuce!

I suppose the flip side of this is that if you drop your PUFA intake deliberately it may well be quite a long time before you lower your blood linoleate levels. Obviously this depends on how much vegetable oil you've squirreled away in your fatty tissue, how much fat you (and your gut microbiota) actually own and if your hormone sensitive lipase ever actually gets working... And of course how low you think you need to get your linoleate level before a deficiency syndrome appears. No healthy adult has managed so far in the literature.

So arachidonic acid deficiency in an adult human seems to be very, very unlikely. Especially if they occasionally eat items of food.


What about DHA? Amongst the many things which control elongation and desaturation of fatty acids I posted about recently, the parent molecules, linoleic acid and alpha linolenic acids, are effective depressors of the system. That is, if you eat a diet absolutely loaded with linoleic acid there is a down regulation of its conversion to arachidonic acid. That's logical. No one would want an unlimited supply of arachidonic acid. It does a lot of things to you, all of which would want to be done under careful control. It doesn't seem to be possible to down regulate to the point of arachidonic acid deficiency though, some will get through even under very high linoleate intake. Not so DHA.

Exactly the same elongase desaturase system used to manufacture arachidonic acid converts alpha linolenic acid to EPA, heading for DHA. Down regulating the system with linoleic acid, as above, will down regulate DHA production too.


Anyone on a "healthy" oils diet may well need to be getting preformed DHA. As DHA is only available from animal (or algal) sources, the problem person here looks to be the high PUFA eating vegan. That's fair enough, that particular diet choice comes with its own special consequences!

The quote below, which comes from this paper, seems to sum up the current state of unknowledge as to whether this problem is real:

"individuals who adhere to vegetarian and vegan diets do synthesize small amounts of DHA, and evidence to indicate deficits in brain development among vegetarians has not been published"

Of course there is plenty of evidence that being on total intravenous nutrition (TPN), based on linoleic acid as your sole source of lipid, means that you will require more than an absolute minimum of alpha linolenic acid before you actually get any DHA produced at all.

Under these conditions there could easily be an absolute DHA deficiency. There often is.

I think a strong admonition to avoid abdominal gunshot wounds, or anything else requiring years on intravenous feeding, would (if heeded) improve your DHA status. If you must do the iv feeding thing, adding some ALA to the lipid emulsion might be a good idea. Getting pregnant under these conditions might not be the best idea either, even if you felt that way inclined and were adult...

If you are a pregnant mother who avoids fish because of the mercury concern, avoids liver due to the vitamin A concern, avoids animal fats due to the cholesterol concern then your child's eyes and brain might be marginal on the DHA front. Pregnancy and growth seems to be when the body needs bulk DHA. Again, working through this review will fill in the background. Being DHA deficient in utero and during early post natal development seems to be bad news, not fully correctable by later DHA supplementation.

Of course, once you have started eating food as opposed to junk, dumped your heart healthy oils and are eating a little liver occasionally, the chance of developing any sort of PUFA deficiency seems rather small. Occasional fish or a decent amount of ruminant meat would eliminate the risk.

The problem is, how many people eat food and how many live on junk? If everyone were to switch to eating food, would DHA supplements be needed? If the intake of linoleic acid is low enough no doubt even the alpha linolenic acid from green leaf vegetables might end up as DHA.

So it looks as if there are certain circumstances, especially with those junk food based vegetarian diets easily achieved today, when DHA may not be available to meet foetal and neonatal needs. Taking a little DHA supplement may well be needed at this time or, better still, eat some food. Food's a good idea.

That seems to sum up the risk of deficiency to me, as far as I can see. We need some EFAs, more during pregnancy and nursing. Arachidonic acid is not a problem, DHA looks to be the weakest link. TPN is bad news (in case you want more bad news than whatever the reason is for your being on intravenous feeding).

So should we all be taking fish oil supplements, all of the time? Do we need to do anything except to avoid frank DHA deficiency as a foetus or newborn baby?

Maybe, maybe not. That's another post.

Peter

30 comments:

donny said...

I seem to remember Dean Ornish saying something about it being very very easy to balance omega 3's and 6's, if you just avoid dietary fat like the plague. Just keeping Pufa's low sounds like a lot more fun.

Gyan said...

Vegetarian Hindus dont eat liver/fish/eggs but do consume a lot of ghee (say 2 spoons a day) and do not appear to have deficiencies in eyes.

So can I get all my DHA through ghee?

Peter said...

Gyan,

Probably so, the problem is that there is almost nothing about the DHA content of dairy on the net, which basically means that no one has looked. There certainly is a small amount of alpha linolenic acid in dairy fat, alongside a little linoleic. In a low PUFA situation the elongase/desaturase system will probably work well. The relatively high omega 6 in the rape seed oil won't help but will be offset by the omega 3s it supplies. If it's practical to avoid the rapeseed oil I'd agree with Bruce on this one. Problems are likely to be dose related and I don't see the need to exclude yourself from traditionally prepared meals at family gatherings, the way my wife and I need to for wheat products. No beef cooked in beer, that was a bad one we messed up on. Tasted great.

The other aspect of DHA is differentiating between specific neuro/opthalmic deficiency syndromes and using it as a pharmaceutical agent to manage problems generated by a high PUFA, high sugar diet. This is the thrust of modern research at the moment and is MUCH more contentious that I'd ever imagined.

I love ghee, just never get the time to make it nowadays.

Peter

Gyan said...

Nutrition Data site says one egg yolk has 600 mg of omega-6 (w6) and only 38 mg of w3.
So by eating six yolks per day, you are getting 3.6 g omega-6!
To balance, I suppose you would need at least 1.5 g omega-3.

Bruce K said...

"I seem to remember Dean Ornish saying something about it being very very easy to balance omega 3's and 6's, if you just avoid dietary fat like the plague. Just keeping Pufa's low sounds like a lot more fun."

A perfect statement of the flaws in Dean Ornish's theories. He does not isolate his variables. Maybe fat is bad, maybe PUFAs, maybe trans fatty acids, maybe MUFAs, maybe SFAs, and maybe w6/w3 ratios. We can sort all this out with a randomized, placebo controlled, double-blind study. But Dean doesn't even test one variable (fat) by itself. He throws in group therapy, meditation, exercise, stop smoking, etc. I will argue that you don't even have to worry about your w6/w3 ratios if you keep your PUFAs around 1-4% of calories.

Bruce K said...

"The deficiency syndrome is a bit dubious in humans, especially adults, but pretty clear cut in lab animals, especially during growth." (Peter)

The problem which Chris points out, is that lab animals are fed refined carbs, protein powders, and hi-PUFA oils, in short a totally artificial diet. The only way to cause EFAD in humans or animals seems to be using oils like safflower (255:1 n6/3 and 80% PUFAs), or totally hydrogenated coconut oil (100% saturated fat). I have yet to see a study that caused deficiency with normal coconut oil, beef fat, butter, macadamia oil, or other low-PUFA oils. The other food in the diet could also be depleting the body of various nutrients. EFAD has been cured with B-Vitamins, fat free liver extract, and minerals on a fat-free diet. Implying that they are not necessarily PUFA-deficient, but simply deficient in vitamins or minerals (due to processed chow).

http://raypeat.com/articles/nutrition/oils-in-context.shtml

Gyan said...

What of the studies that claim that DHA is essential for fetal eye and brain growth.
Or AA is large part of brain fats.
Are these studies misguided or confused?

Bruce K said...

Gyan, the body produces more DHA on low-PUFA than high-PUFA diet. It is almost impossible to deplete DHA in the body. The text Modern Nutrition in Health and Disease says it takes multi-generation studies to deplete animals of DHA. If they feed a high omega-6 diet with no omega-3, it is only reduced by 10-20% in the whole life-span. By avoiding of high-PUFA oils like soy, corn, safflower, and flax, we can get plenty of omega-3.

Peter said...

Gyan,

I don't see a conflict here. DHA and AA do appear to be essential for the functions you mention. How you set about getting a deficiency (it's very difficult) is what it boils down to.

Peter

Gyan said...

Here is Dr. Kendrick on the ad-hoc hypothesis:

But there is no evidence that any of these three factors [he’s just been talking about how people claim that garlic, red wine, and lightly cooked vegetables are protective against heart disease] are actually protective. NONE. By evidence, I mean a randomized, controlled clinical study. Not epidemiology, meta-analysis, discussions with French wine producers or green-leaf tea growers, or a trawl through the Fortean Times. In reality, the only reason that these three factors appeared was to protect the diet-heart hypothesis. They are what Karl Popper would call ‘ad-hoc hypotheses,’ which are devices that scientists use to explain away apparent contradictions to much-loved hypotheses.

Ad-hoc hypotheses work along the following lines. You find a population with a low-saturated-fat intake (and a few other classical risk factors for heart disease) – yet, annoyingly, they still have a very high rate of heart disease. One such population would be Emigrant Asian Indians in the UK. The ad-hoc hypothesis used to explain away their very high rate of heart disease is as follows. Emigrant Asian Indians are genetically predisposed to develop diabetes, which then leads to heart disease. Alakazoom! The paradox disappears.

On the other hand, if you find a population with a high-saturated-fat intake, and a low rate of heart disease, e.g. the Inuit, you can always find something they do that explains why they are protected. In their case it was the high consumption of Omega 3 fatty acids from fish. Yes, indeedy, this is where that particular substance first found fame, and hasn’t it done well since?

____________________________
So there is no need to take DHA while on low-PUFA high SFA diet (ghee, coconut, rapeseed)?

Gyan said...

I wonder how established w6/w3 imbalance hypothesis really is.
Does the mainstream likes it? If yes, then why does the mainstream speak out against excess consumption of vegetable oils?.
Or do their antipathy towards animal fats trumps w6/w3 concern?

Peter said...

Gyan,

Mainstream seems to say "try some fish oil, it might help your arthritis/alzheimers/heart disease etc etc etc", full stop.

Alties seem to go for 1:4 ish for maintenance and 1:1 therapeutic.

I would say I thought in altie terms but nowadays it's hard to see the logic.

Re the previous comment, just watch the omega 6s in rape seed oil

Peter

Bruce K said...

Gyan, rapeseed oil is high omega-6. I'd stick with butter/ghee, coconut oil, beef, lamb, duck, goose, lard, shellfish, and lean fish (like cod, pollock, whiting, tilapia, etc). If mercury is a concern, many fish are also high in that. I don't think we need supplements for DHA, but might benefit from a small amount of good cod liver oil for Vitamins A and D. I'd get the fermented cod liver oil like Blue Ice, if possible. There's no reason to supplement for omega-3 IMO, if you limit omega-6 and avoid most liquid vegetable oils. I'd use macadamia, olive, avocado, hazelnut oil in that order. Most liquid oils are best avoided, I think.

Gyan said...

If one has cancer (possibly because of w6/w3 imbalance)then should one supplement through DHA fish oil or cod liver oil?

Gyan said...

PS What exactly is fermented cod liver oil and why it should be preferred over non-fermented?

This is a question I have not found an answer to and would really appreciate it.

Peter said...

I read an account of traditional cod cod liver oil production. Throw half a tonne of raw cod's livers in to a large, non sterile, wooden barrel. Stand it in the Icelandic sun for 6m. Ladel the oil off of the gunge. Drink. "Ordinary" codliver oil seems to be a standard industrial process sterile food product. Plus all of the vitamins A and D are removed and replaced with RDA synthetic equivalents. UK CLO is not much like real CLO.

Re omega 3 vs 6 for cancer therapy, these are questions I've never addressed. If omega 3 supplementation works for breast cancer it will undoubtedly be a form of chemotherapy. This falls in to the big controversy I'm wading through re potential uses for omega 3s as opposed to that of avoiding DHA deficiency.

Peter

Bruce K said...

Like Peter said, Gyan, I think that fermentation is the traditional way to make cod liver oil. Nowadays, it is common for oils to be exposed to extreme heat, solvents, and various toxic chemicals during preparation. I'd stick with the traditional ways until a better method is developed. For example, I use coconut oil that is centrifugally purified, but it's made without any heat or chemicals.

Re: cancer. It seems clear that an excess of PUFAs (of any kind) will cause cancer. Gary Taubes pointed this out in his book, how studies blaming cancer on fat all used the high-PUFA oils. Saturated fats did not cause cancer, unless you added PUFAs to them. Taubes also pointed out that a high-calorie intake may be involved. Limiting both omega-6 and omega-3 to <10% calories seems like a good idea. <4% even better.

More research is needed, concerning whether a diet high in calories and fat, but low in PUFAs, will promote cancer. Ray Peat believes PUFAs are "essential" to cancer and other bad diseases, but not "essential" for a human to eat in large amounts. He's in line with Chris Masterjohn's new PUFA Report, saying that 0.5% PUFAs or less is adequate even for growth and development. But many financial interests have led people to eat 20 times that level of PUFAs.

http://raypeat.com/articles/articles/fats-degeneration.shtml
http://raypeat.com/articles/nutrition/oils-in-context.shtml

Bruce K said...

Peter: "I read an account of traditional cod cod liver oil production. Throw half a tonne of raw cod's livers in to a large, non sterile, wooden barrel. Stand it in the Icelandic sun for 6m. Ladel the oil off of the gunge. Drink."

I assume 6m stands for 6 months? Is that right? Wow! There are still a few companies using the traditional fermentation process. It's costly, but the dose you need is very small (like 1-2.5 g/ml a day). It's also supposed to be easier to digest, as fermentation breaks it down.

Peter said...

The link is here, it was of course a Weston A Price Foundation page. Half way down, January to June I think...

Peter

Gyan said...

Ray Peat?.
Are his views on CO2 therapy likely?. That it is possible to avoid/cure major illnesses just by taking in more CO2.

Although I should tell you that here it is quite popular esp among women to take fizzy drinks
when troubled gastrically.

Peter said...

Hi Gyan,

I have attempted Ray Peat on a number of occasions at Bruce's prompting. I find him particularly difficult as I frequently disagree on the interpretation of PUFA studies he cites. You also get a very one sided view. Omega 3 fatty acids encourage metastasis in certain rat models of cancer. You can find this out from RP. But you have to go to the study authors to find that the same model developes less cancers in the first place on the same omega 3 based semi synthetic diet... Chris Masterjohn gives a far more balanced view, even citing lack of MDA production with cod liver oil (if it's the real vitamin A rich stuff).

Having struggled to accept that RP may well be correct on PUFA despite disagreeing on references, I still find it hard to accept his other ideas.

Peter

Bruce K said...

"I have attempted Ray Peat on a number of occasions at Bruce's prompting. I find him particularly difficult as I frequently disagree on the interpretation of PUFA studies he cites." (Peter)

What's the alternate interpretation that you think is correct? You have never clarified this, AFAIK. I feel he's only wrong in some of his more extreme views, like saying lard is similar to corn and soybean oil if the pigs eat corn and soyeans. That is clearly false, because lard has 12% PUFAs, but corn and soybean oil have 60% PUFAs. I think he's right that lard is worse than coconut or butter/ghee or beef fat, but he is wrong in comparing lard with those oils. Even the worst lard would be several times better than corn and soybean oil.

"Chris Masterjohn gives a far more balanced view, even citing lack of MDA production with cod liver oil (if it's the real vitamin A rich stuff)."

That doesn't prove anything, since MDA's only a marker, not an actual measure of lipid peroxidation. The long-term mortality and morbidity might show something else entirely. I think animals will die faster on a high fish oil diet (or fish eggs) than a beef suet, coconut oil, and ghee diet. What about you?

"Having struggled to accept that RP may well be correct on PUFA despite disagreeing on references, I still find it hard to accept his other ideas."

Chris Masterjohn has said the same thing that Ray Peat has said, that the need for PUFAs is 0.5% or less if other factors are optimized. He used to say the opposite. The only problem I have with Ray Peat is in some of his conclusions about food, not the idea that less PUFAs would be better than more PUFAs.

If you look at studies that purport a benefit from omega-3, you see the same problem. They fail to test the other sides of the issue: limiting omega-6, limiting total PUFAs, and limiting carbs (esp refined sugars and flours). Testing MDA levels on cod liver oil doesn't prove that a reduction in lipid peroxidation is occurring. You have to control for the anti-oxidant enzymes, like SOD, peroxidase, catalase, etc. I don't pay much attention to studies that fail to produce death or morbidity or both. Why? Because those are the only meaningful results, not saying one animal had less MDA or a lower cholesterol or a higher blood sugar or anything like that.

Gyan said...

Re: the w6/w3 balance hypothesis, are all w3 fats the same?>
Is taking 5 g w3 in form of ALA same as taking 5 g DHA?
I should suppose not- as it is claimed that human body manufactures DHA out of ALA with 1% or so efficiency and if 5 g of ALA is plenty then surely taking 5 g of fish oil is extreme and could over-balance one's w6/w3 balance.
Is it line of argument OK or am I missing something

Peter said...

It looks like fish oil at 5g/d may be far more than is necessary in a patient who is not overloaded with omega 6 fatty acids. If you are overloaded with omega 6 fatty acids, then you can probably take as much ALA as you like and little will get elongated/desaturated to DHA. Under these circumstances fish oil might be of benefit as it has the DHA ready formed.

This still leaves you with how much DHA is really needed per day outside of pregnancy and early growth to weaning. That I don't know, but the amount seems to be low.

The other aspect is whether there is a toxicity problem from the ALA/LA which accompanies the DHA in fish oil. This is the largest unknown to me. Is the benefit of correcting a DHA deficit which may or may not exist worth having compared with the toxicity form increased PUFA intake, which also may or may not exist at 5g/day fish oil?

Answers on a post card to.....

Peter

Gyan said...

Pace Masterjohn, on a 2000 cal diet with 0.5% PUFA--- that is just 1 g PUFA.
Is it 1 g AA+DHA or LA +ALA?
I suppose it is AA+DHA since minimal PUFA diet would avoid LA/ALA.
With 1.5:1 ratio, it gives 400 mg DHA.

Peter said...

Hi Gyan,

Not too sure it matters because with this low an intake of PUFA the desat/elong system would be working very efficiently and whatever DHA or AA was needed could be synthesised form ALA or LA, whether these came from green leaf vegetables or the fat of a ruminant....

Peter

Aravind said...

Hello Peter,

I know this is a really old post. I'm trying to clarify my understanding regarding EFAs.

I have this recollection that you have written extra O-3 may not be healthy on a high carb diet, but perhaps good on LC/HF diet. However I cannot find where you wrote that or if I am misremembering.

Chris Masterjohn has recently suggested that for adults (excluding pregnant women) that 1% PUFA intake might be adequate and I am questioning if O-3 supplementation is necessary even as a vegetarian if you have killed the vegetable oils in the diet and are eating dairy and eggs.

Your thoughts?

Warm regards,
Aravind

Peter said...

Hi Aravind,

I stopped omega 3 supplementing about 3 or 4 years ago, mostly influenced by Chris Masterjohn. I think the dairy and eggs probably provide quite adequate amounts of DHA provided the dairy is in part grass fed. We do eat fish fairly regularly, say once a fortnight. The situation may not be so straightforward in places like the USA where dairy production appears to be designed to eliminate the omega 3 content.

I think there is no doubt at all that bulk calories from any PUFA are probably the main driver of cirrhosis, but that's not saying that 1-5g/d of fish oil will do this...

All the best

Peter

Aravind said...

Thanks for the response Peter!

So regarding the relative goodness or badness of O-3 based on % of carbs vs fats in ones diet, did you ever write anything about that or am I misremembering?

Peter said...

No sure, but I would suspect that the correcting a gross omega 3 deficiency might be worth doing and beyond that limiting omega 6 would be the important goal. You still have to think about how relevant conditions like fatty liver are if you are on a low carbohydrate diet and your liver is running on fat all the time anyway...