Omega 3s and Omega 3/6 ratio questions


(Bob M) #1

Listened to this podcast with Nina Teicholz:

https://www.ihmc.us/stemtalk/episode-52/

At about 1 hour, 15 minutes, she discusses a chapter she left out of her book about Omega 3s. Basically, she says that there is no science to support that they are beneficial.

That seems reasonable to me, as I have seen large RCTs with excellent O3 supplements, with no benefits.

After this, they discuss the O3/O6 ratio. They state that the best way to make this better is to reduce your O6 content via eating fewer seed oils, for instance.

For this, I disagree. I have been avoiding seed oils for YEARS. If something has seed oils in it, I don’t eat it. I do, however, still eat some chicken and pork, and eat out at times. All of those have seed oils in them.

Here’s my ratio from 11/6/2020 (5.62):

Here’s my ratio from 8/20/22:

If the “desirable range” actually is desirable for us low carb folks (remember, all of these studies are on high carb folks), I’m nowhere near that, and I assiduously avoid PUFAs. On the other hand, I don’t eat much fish.

Your thoughts on this ratio? Is it actually better to have a higher ratio?

If so, for me, the only way I can do it is by eating more fish. I have seen people who eat nothing but grass-fed (only) beef, and they get good ratios, but I can’t afford that.

By the way, when I got the ratio in 2020, I had gained 20+ pounds trying the croissant diet and eating a ton of saturated fat; pants ballooned to 38 waist; for the one in 2022, I had lost all that and got back into all of my 34 pants. So, the ratio does not seem to matter at least from a weight loss/gain perspective.


(May the blessing of bacon be always with you) #2

How are you feeling? Are you well? Feeling healthy? If so, then I wouldn’t worry. I can’t believe that our bodies evolved to require a strict ratio between ω-3 and ω-6; surely our ancestors had no way to be so precise.

The main concern, as I understand it, is that the absorption of ω-3 and ω-6 is mediated by the same cell receptors, so that they compete to be absorbed. Therefore, we don’t want too much of one, because it might hamper us from absorbing enough of the other. On the standard American diet, the problem, as Dr. Phinney says, is not getting enough ω-6, it’s avoiding getting too much. I doubt there is much of an issue for someone eating a whole-foods ketogenic diet, especially if the meat is grass-fed (though apparently the profiles of grass-fed meats vary considerably, depending on the grazing practices of the farm).

We also know that even though ω-3 and ω-6 are essential to the diet, the absolute quantity needed is not much. My guess would be that, if you feel healthy, you are probably getting enough ω-3, regardless of what your ratio is. I’m pretty sure it’s also possible to get more ω-6 than one needs, but not enough to cause problems. Like you, I suspect that our picture of ω-3 and ω-6 and the ratio between them is biased because of the test population. And knowing how nutrition research works, I don’t feel I need to look at the studies to be pretty sure that the observed correlations are small and not all that clinically significant, regardless of their statistical significance.


#3

Hmm. Seems to be rather a lot of evidence to dispute that. A pub med search brings up scores of papers, particularly regarding Omega 3’s beneficial impact on inflamasomes.

Bikman is a fan as is Paul Mason I believe.

Also, plenty of papers on ratio e.g.


(May the blessing of bacon be always with you) #4

The alternative conclusion would be, not to increase ω-3, but rather to reduce ω-6. But we can’t seem to get our thinking around the idea that the industrial seed oils are far healthier for us than arterycloggingsaturatedfat.


#5

Well yes, eliminating seed oils and many processed foods will certainly make a big difference to the ratio.

But if you eat eggs, chicken, nuts, avocado but not much fish you’ll still be a long way from an “ideal” ratio. Does that matter? Each to their own I guess. Personally I try to eat oily fish at least twice or three times a week: tinned sardines (drained of brine or olive oil) are incredibly cheap and contain a lot of other micronutrients.


(May the blessing of bacon be always with you) #6

Do we really know? That’s the question, and given the poor quality of a lot of nutrition research, that’s an open question.


(Bob M) #7

@gaz3 I think the difference was that Nina was discussing RCTs, where they feed people O3s versus a comparison group, and then compare them.

That study you referenced appears to be based on epi data: in other words, people with certain O3/O6 ratios have good or bad effects. But that’s epi data, that’s not RCT data. For them to prove this, they would have to give them O3, raise their O3/O6 ratio, and have a proven benefit. And they didn’t do that.

Why is this important? It could be that people who have a higher O6 level do so because they eat worse. It might not be the O6 level at all, just the fact they eat crap. They could be poorer (can’t afford fish). They could drink more, smoke more, etc.

For instance, for the cancer implications, how do you know the people with higher O6 intakes eat more carbs, and the people with lower O6 intakes eat fewer carbs? You don’t. You’d need an RCT.

Unfortunately, that study is paywalled, so I can’t get to the meat of it.

I also realize what I show above is an “Omega 3 Index”, and not the ratio. Here’s the index, November 2020:

August 2022:

My O6/O3 ratio has gotten worse over time…interesting.

@PaulL That’s the problem. My O6/O3 ratio has gotten worse, while I’ve lost weight, feel better, have gotten much stronger, etc. As for “inflammation”, I don’t seem to have any or very low levels of it. I’ll have to get an HS-CRP done and maybe some others. It’s been a while since I’ve had those done.

So, it’s another area where I don’t know what the answer is.


#8

Yes, good point Bob. Epidemiological data isn’t the best but in the absence of RCTs, on balance I think it is worth paying attention to, as I can’t see any downside.


#9

This is the thing I just don’t care about as I could do whatever I want, my omega3/omega6 ratio always will be tiny. I live mostly on pork as it’s the healthiest and best woe I can do, we still spend most of our income on food. My genes are good, my body doesn’t complain so that’s it.
I don’t eat seed oils since ages but plants went, pork came and I eat better than ever now.

I don’t say I have ANY idea how important omega 3 and the ratio is, I just feel fine with what I have and I can’t change it anyway. So I don’t worry about it.


(May the blessing of bacon be always with you) #10

The downside of epidemiological associations is the risk of confounders. For example, shoe size correlates positively with reading comprehension. Will buying bigger shoes help us read better? Will learning to read better increase the size of our feet? Both ideas are ridiculous. The real association is with age and years of schooling, not with shoe size.

If you live in the state of Maine, there is a strong correlation between margarine consumption and the divorce rate. So does margarine cause divorce, or does divorce make people eat margarine? Or are the two completely unrelated?

So, when we observe a correlation, assuming it means that one thing causes another can be risky. Take the advice a few years back for women to supplement with hormones after menopause: when the randomised controlled trials were done, they showed that hormone therapy in many cases caused actual harm. So at best, an epidemiological study can suggest follow-up research, but it cannot safely assert causation.

The exception is data that meet Bradford-Hill’s criteria. One of them is that the observed correlation has to be at least 2.0 or greater, because anything less than that cannot be considered a signal, only noise. Another criterion has to do with how many people were studied; the more, the more reliable the data. Yet another is that there has to be a dose-response curve, so that more x strongly associates with more y and vice versa. Yet another criterion is that there has to be a plausible biological mechanism which can cause the harm or benefit we seem to be observing. And so forth.

By contrast, most epidemiological studies involve15 participants, with an observed correlation of 1.34 or so, and a p-value that is well above 0.001. Such a study is hardly worth getting out of bed for. And that’s leaving aside the clinical effect. Sure, taking a statin has been shown to prolong your life, but given the high incidence of side effects, is living for four or five extra days worth it?

These considerations represent quite a downside, to my way of thinking, which is why I’m no longer so ready to embrace each study as it comes out.


(B Creighton) #11

I’m not sure exactly what she said, but O3s are definitely beneficial. They are an essential fat. The brain is made up of large amounts of DHA. As for O3 supplements, they are often oxidized, and unusable by the body by the time people get them - esp fish oils. I use krill and calamari oil. They are generally less processed and have less mercury concerns. Also, natural krill oil has astaxanthin to protect DHA from oxidation. The other thing about them is free DHA is not readily transportable everywhere. It needs phosphatidylcholine to transport it into the brain for instance. That is readily available from lecithin.

I disagree too. The best way to get a good ratio is to eat only natural fats. That involves avoiding omega 6 rich seed oils, but also increasing Omega 3s.

The ideal ratio is probably somewhere close to 1:1. Most researchers seem to suggest something equal to or less than omega 6 7:1 omega 3

Grass fed beef has about a 1.5:1 ratio. If you eat it, you inherit that natural ratio. The grain finished beef has more like a 7:1 ratio which is still better than the average American. Just a few months back Sam’s Club had organic grass fed ground beef for $5/lb. Surely, you can afford that. Some of the smaller Kroger affiliated stores seem to clearance it when it gets close to the sell by date.I also eat fresh/frozen Pacific Salmon, and canned salmon, tuna and sardines. However, the chemicals used for the can lining may be lipophilic, like BPA was, so don’t scrape the sides out.

Also Flax and chia are high in the omega 3 ALA. The body can convert about 10% of ALA into DHA and about 20% into EPA - but probably only does it when it deems it needs it. So, this would be a source for vegans. Making flax seed wraps is an option for keto. I soak chia seeds and add them to a fat bomb I make. I will also add chia seeds to soups.


(May the blessing of bacon be always with you) #12

BJ’s also has grass-fed beef at a reasonable price.


#13

It all depends on your level of inflammation and if your particular type of inflammation is exacerbated by a high omega6:3 ratio.

My type of inflammation requires a strict 1:1 ratio. I am pain free as a result.

So chicken is out & pork once in a while. I don’t eat much omega 6 foods & I eat plenty of fatty fish for Omega 3. I would say I eat fish two out of four weeks of the month). If I get that ratio up even slightly in favour of omega 6, pain comes back immediately (although still not as bad as when I was on the standard high omega 6 diet).

So…it depends. There are other good side effects I have noticed from high omega 3 intake but the key one for me is inflammation.


(May the blessing of bacon be always with you) #14

I think you meant a high ω-6 to ω-3 ratio, am I correct?


#15

Correct! High 6:3 = bad.


(Michael) #16

I balance my intake. I get a ratio of no more than 2:1, and normally 1:1. I eat salmon daily for this and vitamin D. Not sure how much it matters, but I feel good so I will keep it up.


(Ohio ) #17

It’s largely thought that humans weren’t consuming omega 3 throughout evolution until the stone ages. Then, all the sudden, we started catching fish. This is why our brains, doubled in size, in short period of time.


(May the blessing of bacon be always with you) #18

I’d have to say that either there were enough ω-3 fatty acids in what our ancestors were eating before, or else there was a sudden mutation that prevented us from making our own, that spread rapidly and made dietary ω-3 essential for everyone.

Also, skeletal remains show that our ancestors’ brains began to grow even before they made it to the shore, and were able to obtain fish, so the other hypothesis is that it was the eating of meat, first from scavanged carcases and later from animals we hunted ourselves, that caused the brain growth.

There is a strong impulse to deny that our ancestors could possibly have thrived on mostly meat, despite the evidence of a number of tribal peoples whose traditional diets excluded plant foods (studies comparing Maasai who remained on their traditional diet with their relatives who moved to the cites and adopted the standard Western diet are quite illuminating). This is probably partly leftover thinking from early Seventh-Day Adventist writings, since their prophetess, Ellen G. White, believed that eating meat stimulates lust. (Her writings are the origin of vegetarianism and veganism.)


(Ohio ) #19

There’s a snippet in “The Salt Fix” that goes over it. On an evolutionary scale our craniums doubled in size due to o3 dominating our diet. Someone is borrowing my copy but I’ll photograph it and post it.

I’ve washed my hands of any doubt this wasn’t the case. Kill or be killed is the backbone of evolution. But there’s also a strong impulse to deny that ancestors carnivores diets weren’t tethered to lengthy fasting durations.


(May the blessing of bacon be always with you) #20

I don’t understand that one, either. Clearly we evolved to fast, as well as to feast.