Why Omega 3 should be avoided and what to use/do instead

[Hans]

Since there are so many discussions and confusion on this forum around omega 3s, I thought I do a deep dive and write this article.
If there are so many studies showing that it's good and has so many benefits, how can it be bad?

Why Omega 3 should be avoided and what to use/do instead » MENELITE

Hopefully this article will ruffle some feathers…or scales… I’ll start with the core negative functions of omega 3 and then discuss some of its other “benefits” such as creating different prostaglandins, leukotrienes as well as a look into resolvins, etc. Basics on fats Saturated fat contains no...

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[Cloudhands]

Good in depth article. Appreciate your hard work hans ??

 

[Hans]

Good in depth article. Appreciate your hard work hans ??

Thanks man. And it's my pleasure!

 

[grithin]

Great article. It's good to see efforts to model how things work.

I expect most of the negatives relate not to natural intake of PUFA (via whole fish), but to fish oil in the form of supplements. The title, however, is probably usefully inflammatory. How much of the oil becomes oxidized from a fish oil capsule during digestion? How much of the concentrated burst of fish oil makes it past the liver and into the blood stream, b/c the liver can't burn it fast enough?

You have a quote

“A voluminous literature developed largely in Scandinavia prior to the time that EFA and tocopherol were discovered. Agduhr investigated the effects of cod liver oil upon several animal species and described abnormalities such as suppression of growth, leucopenia, haemorrhage of the myocardium, degeneration of the heart muscle, edema of the lungs, and necrosis of the liver. Slagsvold observed that cod liver oil poisoned cattle, with stiffness and muscle lesions as symptoms. In another study the toxicity of cod liver oil in calves was manifested as a severe muscular dystrophy…. The rats fed cod liver oil were sterile.” (R)

How did you go about extracting that? It is fully misleading. I'll explain:

1. the first part of the quote, ending with "necrosis of the liver", actually does not continue with Slagsvold. Instead, the context is:
"investigations of excessive doses of cod liver oil suggested it to be poisonous." [Your quote] "Normal doses for vitamin therapy did not produce these effects"

2. the second part, "Slagsvold observed..." is also in the context of excessive intake of cod liver oil

3. the third part, "rats fed cold liver were sterile" is more complicated. From the paper:

Burr and Burr reported in 1930 that reproduction is impaired by EFA deficiency 46 and that male rats become sterile and will not mate. ....
in his studies he developed severely deficient young rats by feeding the experimental diet to the mothers from the day of birth, and continuing the weanlings on the same diet which contained 10~o hydrogenated coconut fat and 0 or 1~ cholesterol.
....
The young rats developed characteristic symptoms of EFA deficiency, and 40 to 80 mg of cod liver oil given orally induced remarkable cures of skin lesions
....
Testes of male rats receiving 29/0 cod liver oil in the diet averaged 0.68~ of body weight compared with 0.98~ for rats fed soybean oil. The rats fed cod liver oil were sterile.

In other words, in rats with induced sterility by lack of polyunsaturated fats, with a diet including hydrogenated coconut oil, a 2% cod liver oil inclusion did not correct the sterility.

 

[Hans]

I expect most of the negatives relate not to natural intake of PUFA (via whole fish), but to fish oil in the form of supplements.

I'd say you can get away with consuming high omega 3 from seafood, but since it will still be incorporated into the cell membranes, it will still negatively affect cellular function. Plus, with all the stress, pollution and oxidative stress going on in modern society, those lipids will create a lot of lipid peroxides regardless if it's from fish or supplements.

How much of the oil becomes oxidized from a fish oil capsule during digestion?

Some supplements use krill, where the omega 3 is in phospholipids already, and it contains high anti-oxidant count, so you need a smaller dose and it's much less prone to oxidation. Same thing with the omega 3s from oysters. However, excess intake, if it's oxidized or not, will still be a problem. But why supplement if you can eat the food itself.

How much of the concentrated burst of fish oil makes it past the liver and into the blood stream, b/c the liver can't burn it fast enough?

These fats are found in tissue in a dose-dependent manner or at least depending on how abundant they are in the diet. I'm not sure how much of these fats the liver can take care of at once, but these highly unsaturated fat are oxidized (beta-oxidation) very rapidly, so that helps to prevent them from storing in the body. But still, they do accumulate, if it's from supplements or diet.

On your other points, yes, those side effects are present with excess consumption, but smaller doses can also have a very mild effect in that direction. If it happens in a dose-dependent manner, what dose is considered safe? I'd say no dose of fish oil is safe, but only if you consume it from fresh food directly.

And lastly, in terms of sterility, many studies have shown that rats in an EFA deficient diet have double the testosterone levels than replete rats. PUFAs including omega 3 accumulate in the gonads and if they become oxidized there will cause testicular damage and dysfunction. Optimal testosterone production depends on high NAD levels and proper glucose oxidation, and excess omega 3 interfere with that process.

 

[grithin]

I'd say you can get away with consuming high omega 3 from seafood, but since it will still be incorporated into the cell membranes

I'll clarify what I was trying to push you towards.

When you eat salmon, the PUFA in salmon is stored in fat cells in lipid droplets (Lipid droplet - Wikipedia). If you've ever mixed bile and unsaturated fat, you'd notice they mix fairly easily. Omegas in lipid droplets in fat cells, even if the cells have been destructured by digestive enzymes, will not mix with bile as easily.
As such, the absorption of PUFA from fish, I would imagine, would be over a longer period of time and to a lesser extent when compared to a fish oil capsule.
You can then assess that the chylomicron composition resulting from fish oil consumption would be mostly PUFAs, in a sudden burst, whereas from fish consumption, the chylomicrons would have a broader range (b/c fish have more than just PUFA). I seem to recall that the composition of chylomicrons plays a factor in their oxidation and consequent deformity causing reduced uptake. Either way, this higher PUFA chylomicron, when absorbed by the liver, would result in higher PUFA vLDL, which does encounter issues with deformity.

The composition of tissues reflects lipid composition of diet, but not by much at all Fatty acid composition of membrane bilayers: Importance of diet polyunsaturated fat balance
This makes me curious as to why mitochondrial structures (PC, PE, CL) in Docosahexaenoic acid lowers cardiac mitochondrial enzyme activity by replacing linoleic acid in the phospholipidome were so drastically impacted by DHA. I suspect, however, that this was more a function of the absence of linoleic acid in the diet of the rats on WD + DHA, and DHA and its metabolites being use in place of the absent linoleic acid. This model is supported by the peanut oil study showing restoration of lipid composition (indicating there is no preference for DHA in composition).

Further, the presence of PUFA in diabetics, mentioned in that same study, is not necessarily indicative of consumption. Instead, a better model is there is something preventing the beta oxidation and clearance of PUFA that leads to it building up in diabetics. If you combine the two studies, you might realize that this is likely a result of deficient linoleic composition, that causes deficient IV activity, which holds up the chain, causing QH2 build up and ROS. High ROS would probably interfere with mitochondrial activity and might interrupt Enoyl CoA isomerase. The combination of ROS and ETC hold up would result in PUFA build up, which results in higher PUFA concentration in tissues (diabetics), and especially in mitochondria structures, where the PUFA is in queue to be beta oxidized.

And lastly, in terms of sterility, many studies have shown that rats in an EFA deficient diet have double the testosterone levels than replete rats

This wasn't something I was questioning. The matter was how did you come out with the poorly contexted quotes starting with "A voluminous literature developed"

Just to highlight a part of the poor context, your quote would lead people to think that consumption of cod liver oil leads to sterility when that is not at all what the quote meant in context.

excess omega 3 interfere with that process

The matter is what constitutes excess, and does the form matter. A factor as to what constitutes excess is how quickly cardiolipin composition, and other mito structures, change, and what determines their change (deficiencies, ratios, metabolism).

Again, I expect this is more an issue with fish oil rather than
- krill oil, taken in small amounts
- cod liver oil, taken for vitamin content
- whole fish

I find there is an optimal dose of DHA, and it is not 0, and not readily achievable without either brain or fish or krill.

 

[Hans]

I suspect, however, that this was more a function of the absence of linoleic acid in the diet of the rats on WD + DHA, and DHA and its metabolites being use in place of the absent linoleic acid. This model is supported by the peanut oil study showing restoration of lipid composition (indicating there is no preference for DHA in composition).

The WD consisted of milk fat which does contain linoleic acid. Plus their fat intake was at 42%, which does give you a fair amount of linoleic acid.
The restoration of cardiolipin with peanut oil was because there wasn't any DHA (perhaps only trace amounts) in the diet so none could be incorporate. I've seen research showing that when the cardiolipin (containing linoleic acid) gets oxidized, it gets remodeled with AA and DHA upon availability. If ROS is low and mostly SFAs are available, such as with hydrogenated peanut oil or coconut oil, then the cardiolipin is able to remodel back to normal.

Instead, a better model is there is something preventing the beta oxidation and clearance of PUFA that leads to it building up in diabetics. If you combine the two studies, you might realize that this is likely a result of deficient linoleic composition, that causes deficient IV activity, which holds up the chain, causing QH2 build up and ROS. High ROS would probably interfere with mitochondrial activity and might interrupt Enoyl CoA isomerase. The combination of ROS and ETC hold up would result in PUFA build up, which results in higher PUFA concentration in tissues (diabetics), and especially in mitochondria structures, where the PUFA is in queue to be beta oxidized.

Yes, and what is preventing beta-oxidation? A dysfunctional mitochondria induced by PUFAs. On the contrary, excess linoleic acid will cause the same issues. Adding any vegetable or seed oil to increase linoleic acid levels will promote inflammation. The safest way to increase linoleic acid is by eating beef fat, dairy fat or some eggs. An EFA deficient diet doesn't cause the breakdown of cardiolipin and the mitochondria or reduce fat oxidation capacity. It actually improves mitochondrial function. Since PUFAs are more readily and quickly oxidized than SFAs, they will reduce the NAD faster, thus causing excess reduction and ROS. So PUFA buildup is caused by PUFA buildup. It all goes wrong with excess PUFA ingestion, which then leads to mitochondrial dysfunction and more PUFA buildup.

Just to highlight a part of the poor context, your quote would lead people to think that consumption of cod liver oil leads to sterility when that is not at all what the quote meant in context.

In small amounts cod liver oil will not be that harmful, but why use it for a little vitamin A and D, when you can get it in much higher amounts from much safer sources.

 

[grithin]

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[Hans]

This is 42% kcal of fat, of which 100% is milk fat. Milk fat is 4.5mg / g conjugated linoleic acid. IE, 0.45%. Presuming CLA and LA are indistinguishably interchangeable in composing mito structures, what makes you think a (42% * 0.45%) kcal CLA consumption is sufficient (https://www.intechopen.com/books/so...-acid-with-unique-health-benefit-properties)?

Why wouldn't it be sufficient?

Do you have the study reference for coconut oil? How would saturated fatty acids help remodel cardiolipin back to normal composition (normal composition being composed of linoleic acid)?

The hydrogenated peanut oil contained 0.27% linoleic acid, which is even less than milk fat. And they received only 0.5-0.7ml per day. Saturated fat food sources do contain small amounts of linoleic acid and possible by reducing oxidative stress, that small amount of linoleic acid are then successfully incorporated into cardiolipin without undergoing elongation and unsaturation to arachidonic acid for eicosanoid synthesis. They didn't check cardiolipin content, but they did check fatty acid composition of the muscle.

Again, this is a matter of concentration and amount. You can feed rats rancid highly concentrated linoleic acid and expect negative health outcomes. You can even feed rats non-oxidized, highly concentrated linoleic acid, past the rats ability to readily use (metabolize, incorporate), and expect to see negative health outcomes.

Where do you pull the line? Nut, seed and vegetable oils are best avoided, whereas smaller amounts from animal foods are much safer.

Who mentioned this that requires you to refute it?

Your speculation that low linoleic acid intake can lead to low cardiolipin function. Maybe I misinterpreted what you meant.

There is a reason this doesn't usually matter in the context of normal consumption of PUFA, but you still haven't answered my question about the out of context quotes I presented in my first post.

But what is normal consumption? Does the Inuit have normal consumption of fish oil?
As for out of context...I only quoted the article which did specify about excess.

Convenience. A bottle containing hundreds of little pills that can store in a refrigerator for a long time.

That's a poor reason IMO. Most people hate getting cod liver burps and as I mentioned, food (e.g. liver, milk, etc.) is much better and safer.

 

[grithin]

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[Cheese liver]

Taking into account all the factors, are PUFAS in any amount bad or when taken in excess they can promote degeneration and damage ? Do small amount of PUFAS help in any way ? On a further note I have heard that vitamin-E protects the PUFAS from oxidization . So can supplemental vit-E negate the negative effects that are coupled consuming high PUFA foods ?
Can anyone also explain what is the furan that also prevents oxidative damage from PUFA ?

 

[Hans]

Taking into account all the factors, are PUFAS in any amount bad or when taken in excess they can promote degeneration and damage ?

In smaller amounts, they are definitely less harmful, since your body will be better able to deal with them. If you eat lots of eggs and oysters and consume like 10g PUFAs per day, you should still be fine since these foods contain compounds that prevent the oxidation of PUFAs. However, with accumulative intake, they do still accumulate and can cause harm. So I try to limit my intake to 4-5g daily.
In someone that is already full of inflammation, then limiting PUFAs as much as possible is probably best.

Do small amount of PUFAS help in any way ?

Not really no. But even if we as humans had zero requirements for PUFAs, it's impossible to avoid it completely and to eat in a sane way, you'll be consuming PUFAs if you want to or not.

On a further note I have heard that vitamin-E protects the PUFAS from oxidization . So can supplemental vit-E negate the negative effects that are coupled consuming high PUFA foods ?

It can only partially protect. But as I mentioned, foods like oysters contain their own anti-oxidants that make these lipids more stable.

Can anyone also explain what is the furan that also prevents oxidative damage from PUFA ?

It's furan fatty acids. "Furan fatty acids are very effectively acting as radical scavengers. In this process dioxoenoic fatty acids are formed, which are by themselves very unstable and form thioethers with thiols such as cysteine or glutathione.[17] As potent antioxidants, they specifically trap hydroxyl radicals.[18]"

 

[FitnessMike]

Very interesting, thanks.

 

[Cheese liver]

Thank you @Hans

 

[Cloudhands]

@Hans Have you any idea about the relationship between pufa and sunburn? Ive heard people say that once youre completely pufa depleted you wont sunburn, but i have trouble believing such a heavy statement.

 

[Hans]

@Hans Have you any idea about the relationship between pufa and sunburn? Ive heard people say that once youre completely pufa depleted you wont sunburn, but i have trouble believing such a heavy statement.

You can still sunburn, but the inflammation will be much less and will resolve much faster. Plus, you're much less likely to get sunspots if you're PUFA depleted.

 

[Cloudhands]

You can still sunburn, but the inflammation will be much less and will resolve much faster. Plus, you're much less likely to get sunspots if you're PUFA depleted.

Do you have any recommendations for preventing sunburn? Looking for something besides the obvious sunscreen and shade, thanks for answering my questions btw man

 

[Hans]

Do you have any recommendations for preventing sunburn? Looking for something besides the obvious sunscreen and shade, thanks for answering my questions btw man

Np man.
Building up slowly is probably the best way. Virgin coconut oil is good, but it's not very practical to be oily all the time. There are natural sunscreens with zinc oxide without other harmful ingredients that can also work.

 

[hclh]

I think the big question is the relationship between cardiolipin and omega-6.
And the question is why cardiolipin in general has a bigger proportion of omega 6 than other parts of th cell?
Why is prefered by the metabolism to use omega 6 rather than saturated fats? Even animals fed with mostly saturated fat, their cardiolipin is mostly unsaturated.
I think that is proved in the cientific literature and however that probably leads to mitochondrial membrane unstability.
Why?
I really do not know

 

[Hans]

I think the big question is the relationship between cardiolipin and omega-6.
And the question is why cardiolipin in general has a bigger proportion of omega 6 than other parts of th cell?
Why is prefered by the metabolism to use omega 6 rather than saturated fats? Even animals fed with mostly saturated fat, their cardiolipin is mostly unsaturated.
I think that is proved in the cientific literature and however that probably leads to mitochondrial membrane unstability.
Why?
I really do not know

It still depends on how much PUFA you have in your diet, but yes, linoleic acid seems to be the preferred fat for cardiolipin. Some studies show that linoleic acid consists of between 60-80% of all the fatty acids in the cardiolipin, so if you reduce PUFA intake, that number will be closer to 60% and perhaps even lower. MUFAs and Mead acid can also be incorporated if extra flexibility is required.