The most interesting finding is that the non-DHA effect is much stronger than the DHA effect. This doesn't align with the mechanistic explanation. Either this this is a novel and interesting result, or it's more evidence that we're just measuring wealth and health consciousness.
Observational studies like these are useful for guiding future research, but, on their own, they're essentially useless for informing lifestyle changes.
The non-DHA omega-3 EPA are good at preventing perivascular fibrosis and thus a better glymphatic system for the removal of beta-amyloid proteins. EPA also helps produce melatonin which kick off sleep and this whole process.
Natto-serrazime is probably an excellent complement as it is on the other side and is a dissolver. (Noteworthy: Pterostilbene + Glucosamine similar to EPA reduces fibrosis)
The interesting connection is how this is needed when we are older, but not younger. When younger ERa activates more which does this all on its own. This is the connection to why 2/3 of alzheimer's are post-menopausal women and why HRT is important.
The reduction in risk is 0.08 percentage points, not 0.08 percent. The "%" symbol always means "percent", not "percentage points". The 0.08 percentage point reduction is a 40% reduction.
Sure, because both are true (although that 0.08% is only over 8 years of known omega 3 consumption - as timescales increase the absolute risk moves towards the relative risk).
That 0.08% reduction would mean approximately 28,000 fewer EOD cases - not to be sniffed at!
The 40% (66%?) is the number that matters. Same way you wearing a helmet reduces your changes of brain damage in a motorcycle accident by 90%, yet you’re not on a motorcycle most of the time.
This is talking about early onset, which is a particularly terrifying outcome. And yes, 1 in 1000 for a horrible outcome sounds much better than 2 in 1000, doesn't it?
And to be clear, many things that people worry about is less likely than that. Homicides (over an 8 year period about about 0.04 per 1000 people), terrorism (vanishingly small), and on and on.
None of this means that people should stock up on omega-3s, and as likely the study is actually finding a correlation with something else (e.g. wealthier people enjoy more fish rich diets and are less exposed to toxins, or something else), but halving something terrifying that isn't that uncommon is legitimately newsworthy.
This could significantly underestimate the real impact. A single point measurement is perhaps a pretty noisy measure of long term average. If we had lifetime averages, the quintiles would be more purely differentiated by the variable of interest, and the risk would be as well.
from an actuarial perspective, these longitudinal studies on dementia are huge. early-onset is basically the hardest risk to price for long-term care because the tail of the claim is so long and expensive. finding a solid inverse correlation like this is the kind of thing that eventually shifts premium modeling for an entire generation.
It’s less about denying coverage and more about accurate risk pooling. If an insurer knows a specific marker leads to a 90% chance of a million-dollar claim, they have to price for that. If they don't, the 'healthy' people in the pool end up subsidizing the high-risk ones until the premium becomes too expensive for everyone and the pool collapses (adverse selection). The real challenge is that regulators often won't let insurers price high enough for those risks, which is why many companies just stop offering LTC (Long-Term Care) altogether.
that's the fundamental paradox of modern underwriting.
insurance relies on what philosophers call a veil of ignorance. it only works if we're spreading stochastic risk things that might happen to anyone.
once data gives us perfect foresight into a 90% chance of a million-dollar claim, it’s no longer insurance; it’s just a pre-funded bill. at that point, the pool isn't spreading risk, it's just facilitating a direct wealth transfer. the 'good' risks realize they're just subsidizing a known event for others and they flee the pool, which is exactly how the market for things like LTC collapses.
we're basically at a crossroads where better data is actually making 'insurance' as a concept mathematically impossible for certain risks.
YEsh, they'll both raise your rates for not submitting this data and raise your rates for being in the cohert that's susceptible; they'll also raise everyone elses rates for having to recalculate the tables!
Wow, that is a depressing point of view. Advancements in "not paying for things" accelerates while advancements in "preventing things" just inches forward.
yep. it's a total market failure. 20 years ago, carriers completely underestimated the tail of cognitive decline and priced it way too cheap. now the legacy claims are bleeding them dry, which is why new LTC policies are basically non-existent or priced for the moon. it's a tough lesson in what happens when the actuarial data lags reality by 20 years.
> Compared to participants at Q1 of DHA, those at Q5 of non-DHA showed a significant lower risk of EOD. A statistically significant lower risk was observed in Q3, Q4 and Q5 of non-DHA omega-3
If I'm reading this right, if you can't get many fish sources in your diet, it's better to increase the quantity of non-DHA sources (certain seeds, oils and vegetables). But my understanding is non-DHA is not helpful so I may not be understanding correctly
I think it's easy to take algal-based omega-3 supplements. They've gotten pretty good in the last couple years with gummies with a high dose and no algae test. And no fish killed!
Schizochytrium oil with DHA and EPA, which is sold as "algal" omega-3, for a lack of a correct word that could be understood by the general population (Schizochytrium is not an alga), is very good and no fish are killed for it.
Nevertheless, it remains at least 3 times more expensive than a fish oil, e.g. cod liver oil (I mean price per content of omega-3 fatty acids, not per volume; when not diluted to fool the customers, "algal" oil has a double concentration in comparison with fish oil, i.e. 5 mL of "algal" oil are equivalent with 10 mL of fish oil).
Taking daily a decent dose of "algal" oil can be more expensive than the daily protein intake required by a human, if that is taken from cheap sources (e.g. legumes and chicken meat). Allocating a major part of the budget for food to a supplement taken in minute quantities seems excessive.
I am not aware of any serious reason for the high cost of "algal" oil. A decade ago, it was much more expensive, e.g. 8 times or more in comparison with cod liver oil. Then the price has dropped to 3 times, and then it has diminished no more, remaining at 3 times for 5 years or more.
I believe that it should be possible to further reduce the cost of "algal" oil to make it an acceptable substitute for fish oil, but it seems that the producers are content with their niche market of rich vegans and they do not make any effort to reduce the cost in order to enlarge their market.
I have taken occasionally "algal" oil, to test it, but as long as it remains a luxury food I cannot use it to replace the cod liver oil that I am taking regularly, despite desiring to do so.
I think that it is a health tax, as many things are. For what it's worth, it costs me 50 cents a day. I'm not sure what semantics about it not being a "true" algae has to do with anything, though. If it's a protist or an algae, I'm not sure what that information does other than muddy the waters for people forming an opinion on non-animal based omegas.
If you consume "algal" oil of 50 cents per day, that must be some kind of capsule with a small amount of oil, e.g. a few hundred mg of DHA+EPA.
This is much better than nothing, but it is far from a daily intake comparable to that of the populations who live in places with access to cheap sea fish, where such fish are a significant fraction of their food (e.g. Japan).
If your target is to match the diet of such populations, that means e.g. 5 mL per day of non-diluted "algal" oil, i.e. a teaspoon of such oil (or 10 mL of fish oil), which contains around 2 grams of long-chain omega-3 fatty acids.
That would be much more expensive when using "algal" oil, at least judging after the prices seen e.g. on Amazon.
In order to not scare the customers, many sources of "algal" oil have a similar price with fish oil, but only because they contain much less omega-3 fatty acids per capsule. If you read the fine print, then you discover the true price ratio.
> They've gotten pretty good in the last couple years with gummies with a high dose and no algae test
Gummy supplements are questionable, especially for supplements that can have strong flavors and odors by themselves.
If you’re taking algal based gummies and thinking they taste good, they likely either have very little omega-3 or the ingredients have been so heavily processed that I’d start questioning if the omega-3 survived the processing
The "algal" omega-3 is not extracted from any algae, but it is extracted from certain cultivated strains of a fungus-like organism, Schizochytrium.
The cultivated strains have been selected and/or genetically engineered to have enhanced production of certain long-chain omega-3 fatty acids.
The composition of an "algal" oil ("algal" is the adjective derived from "alga", "algae" is the plural of "alga") depends on the particular strain that the vendor has used in production.
The first cultivated strains produced only DHA, but in recent years most vendors use strains that allow them to sell oil that has a mixture 2:1 of DHA and EPA, with minor quantities of other long-chain omega-3 fatty acids.
I do not think that growing is difficult, but extracting the oil from it in such a way that it will have a correct composition is likely to be impossible without complex chemical equipment.
For growing it would be difficult to obtain a good strain. The strains used by commercial producers were originally isolated from some mangrove forests or other such places on sea shores, but then they have passed through years of selection and/or gene manipulation. Even when a good strain would be available, a culture that is grown in less controlled conditions could be susceptible to being wiped out by a disease, I have no idea.
In any case, I think the difficulty is in the oil extraction, not in the culture. In industrial conditions the extraction could be made with supercritical carbon dioxide, for maximum cleanness of the extracted oil, but that would not be feasible at home. Using an organic solvent, like hexane, might be possible at home, but that would be dangerous and there is the risk of contamination of the edible oil with solvent residues.
Accurate chemical analysis of the oil would be needed, to determine the fatty acid profile and validate the extraction method.
That's part of my question. ALA is supposed to not convert to DHA easily.
But these results seem to say at higher concentrations ALA lowers risk of EOD. Which tends to refute the belief that only DHA/EPA lower chronic inflammation or that EOD is not just a story about inflammation.
I cannot read the whole article, but the abstract says nothing about ALA.
The abstract only partitions the omega-3 acids in DHA and non-DHA.
While non-DHA includes ALA, without any concrete evidence that ALA has some direct role, it is more likely that the correlation seen with non-DHA refers not to ALA, but to the other long-chain omega-3 fatty acids besides DHA.
Humans can elongate ALA into useful long-chain acids, but the efficiency of this is typically lower in males than in females and lower in old people than in young people. Usually pregnant women have the best conversion efficiency.
Unless you monitor your blood composition, you cannot know if eating ALA (e.g. flax seeds or oil, or walnuts) can be sufficient for you. If you are an older male, it is very likely that eating ALA cannot be enough for avoiding deficiency.
I evolved to eat fish and meat killed. So did all other carnivores. I'm happy to continue eating and shitting and sleeping and having sex, I don't want supplements to replace food and AI to replace intellect and IVF to replace sex. I want to be alive.
Abstaining from killing animals is about the sober realization that we can have perfectly healthy and happy lives without killing animals, who have feelings and a sense of perspective and experience, just like us. Living with my values and actions as one give me a strong sense of life, and I love cooking every day. Plants taste great when cooked well!
> Abstaining from killing animals is about the sober realization that we can have perfectly healthy and happy lives without killing animals,
Maybe, maybe not. If one is lacking a hobby and happy to spend much time learning and obsessing and fiddling with what they eat, while accepting that they may be missing some vital things that we don't yet know about, then sure.
But I have enough hobbies and I don't want to risk missing some things we don't yet know about. I just eat what I evolved to eat.
Our species started out predominantly eating fruits, vegetables, nuts,.. As hunter gatherers, meat eating came later and initially was still not a dominant source of nutrition.
So yes, you eventually evolved for this, but it wasn’t the dominant food source for a loooooong time.
Homo sapiens? I don't think that's necessarily true. Older ancestors maybe. Home sapiens was probably mostly getting calories from fruit, tubers, and other animals, depending on season and what they could find.
Yes, but more likely insects as first small “animals”. Hunting animals takes more effort than eating fruits etc.
I know it’s all vague delineation of where our species really started, and at which point you would no longer consider it the homo line, but for a significant part of history we were a small predator that would eat whatever was _easily_ available. Hunting animals is not easy and it’s a risky endeavour.
I’m not saying meat wasn’t part of our diet obviously, but it logically wouldn’t have been as dominant a part of our diet as it is today.
The most likely hypothesis about how humans have become the most efficient hunters of the planet does not pass through catching insects and very small animals, but through eating the remains of the big prey killed by carnivores.
There are various bits of evidence for this, like the higher stomach acidity of humans, which resembles that of carrion eaters, like hyenas.
It is plausible that the ability to throw sticks and stones was used initially for scaring other predators and make them abandon their prey, and only later, after hundreds of thousands of years of evolution, it became accurate enough to be usable for hunting living animals.
The ability to use stones to break the bones and eat the parts inaccessible for the carnivores who had killed the prey, i.e. marrow and brain, which are rich in hard to get nutrients, e.g. omega-3 fatty acids, is also presumed to have played an important role in the development of a bigger and bigger brain.
It is likely that the gangs of humans acted in a very similar way with the packs of hyenas, which acquire much of their food by scaring away from their prey the other predators, e.g. cheetahs, wild dogs, leopards and even lions. Moreover, similarly to humans, the most important ability of hyenas is not speed, but endurance when pursuing a possible prey that is tired or weakened, e.g. by wounds. While hyenas rely on their big teeth to chase the other predators, humans have relied on their ability to throw things at a distance, for the same purpose. While humans are quite bad at running, jumping, climbing or swimming, in comparison with most mammals, their throwing ability is unmatched by any other animal.
And different populations evolutionarily "fine-tuned" in environments with different availabilities of various foodstuffs. While many dietary requirements are common to all humans (e.g. we lost the ability to synthesise vitamin C, making us all susceptible to scurvy), some are specific to individuals and (genetically-related) families.
Diet is one of the very few places where your genetic ancestry actually matters – although your gut microbiome, which evolves faster (https://doi.org/10.3389/fmicb.2014.00587), may not share quite the same ancestry as your human cell tissue.
There are many other intolerances, e.g. coeliac disease and the many different kinds of food allergies.
Besides these cases, which are obvious due to immediate harm, and which are the reason for laws about food labeling that mentions lactose, gluten and various allergens, there is a lot of variability between humans in the efficiency of digesting various foods and in the capacity of absorption for various nutrients.
Some people are able to eat pretty much anything, while others are aware that they do not feel well after eating certain things, so they avoid them.
They have found spears that are at least 400,000 years old, so we have hunted for food at least that long.
And if you look at our closest relatives chimpanzees, they also hunt without using tools. Humans and their ancestors probably ate whatever they had available, including meat.
“Evolution” is not a sound basis for most choices. We didn’t evolve to wear shoes, live in houses, to use powerful cleaning agents, indoor plumbing, decontaminated water, refrigeration, and pretty much all modern medicine, among about every other thing that is part of modern life.
This feels like a series of completely disconnected statements. The underlying theme seems to be that "living" is something that can only be realized by isolating behaviors to those that developed under specific niche conditions that applied pressure to our ancestors, and that this is good, and that deviating is bad. The word "living" and "alive" seems to be a proxy word for something like "happy" or "fulfilled"?
So many hoops to jump through to understand what the hell you're talking about, just to land on what could charitably be called the dumbest thing I'll read today if I'm lucky.
> But my understanding is non-DHA is not helpful so I may not be understanding correctly
Alpha-linolenic acid (ALA), the Omega-3 present in most plant sources, can get its chemical structure lenghtened to EPA and DHA in the organism. The problem appears to be, when people get older, the efficiency of this conversion takes a large hit.
It’s always a stretch too - takes something like 15x more ALA to convert to DHA when things are going well. Not nothing but if a substantial amount of DHA is protective, it’s hard to get there with only ALA.
> But my understanding is non-DHA is not helpful so I may not be understanding correctly
A lot of the common wisdoms about fish oil and omega-3 were based on early studies that had some too good to be true results. As studies were scaled up to more participants and more rigorous methods many of the amazing early results gave way to less impressive or even null results.
I think it’s a good idea to get a mix of omega-3s in your diet, but given everything I’ve seen I don’t think it’s all that important to start micro optimizing everything with isolated supplements. Consume a mixed variety of sources and try to get some fish in there every once while.
The importance of DHA specifically in this study is a good example of how individual studies don’t tell the whole story. This could be a spurious result that is correlated with something else that leads to elevated DHA in the blood (diet choices). Supplementing isolated DHA could miss whatever the real factor was.
The correlative effect is quite clear, i.e people who have high omega 3 levels (eat a lot of fish) have health benefits.
But in random controlled trials Omega 3 supplements have not had convincing effects.
It might be because the supplements aren't very good, or because there's actually something completely different going on, like fish displaces less healthy foods from the diet.
Fatty fish (salmon, mackerel, herring) has quite large amounts.
Some people aim for huge amounts of EPA/DHA but I don't think there's really much evidence that you need 3g/day or whatever the latest broscience is.
Mackerel is particularly high although it doesn't taste great to me compared to salmon, 100g of mackerel has ~4g of EPA/DHA so eating that a couple of times a week is probably more than enough.
Also there is some (although much less) in white fish, there can be significant amounts in shellfish, and tinned tuna has a surprisingly high amount. So all of that adds up if you eat those as well
Not sure what you can find in your country but we have tinned mackerel (with tomato typically) in Norway. I can highly recommend.
It's not thaaat fishy, I didn't grow up eating it. After having it a few times it really grew on me.
Super cheap and an easy way to get it into my diet. I have 2-3 tins per week. I eat it for breakfast mashed on bread (our bread is like a hard cracker), sometimes with a bit of mustard, or butter spread first.
Sardines, too, which are also fishier than salmon but tend not to be salted the way mackerel is.
Unless you’re also consuming all the oil from the can, prefer fish canned in water to canned in oil — because apparently the omega-3s can leach out into oil, but they’re not water-soluble.
Btw, trout is also up there (though not as high as salmon) and is a lovely mild-flavored fish.
What's also interesting that some recent studies show eating eggs every day actually is harmful, most likely due to the Omega3 to Omega6 ratio.
So here we go again. First it was cholesterol, which was then rebutted, so people (myself included) started eating eggs every day. And now this. You can't win!
It's really surprising how many people don't realise where omegas come from and just default to "more fish". Fish get omegas from alge. Simply skip the middle man and all the nasty side effects that has in the form of animal exploitation and harmful substances for humans they contain.
Cows eat grass for protein, we can't really skip the middle man and eat grass to get protein.
I don't know if it's true, but it wouldn't be unusual for there to be benefit from getting omega 3 from fish rather than algea because of something like this. AFAIK, we mostly only know about the benefits of eating fish.
It's seemingly dose dependent. Low omega 3 can seems to have the same mechanistic effect. As for what the dose should be? No clue, personally, and it depends on your heavily diet since even one fishy meal could provide as much as most supplements do. Personally, I don't eat much fish, so I'm comfortable with a supplement. If I ate even one piece of salmon in a day I'd skip the supplement that day.
If I had afib I'd talk to a doctor about it before taking it and probably would stay well under 1G on any day I don't eat fish and skip it entirely on a day that I do.
Not a dr, not a health professional, not anyone you should listen to perhaps at all, but this is my understanding.
The TL;DR (IIRC) is that we tend to only see this in trials where atrial fib is a tertiary endpoint so there’s not really compelling data to suggest AF is a risk.
But give it a listen and see what you think, it was a while ago I listened to it and I’m not qualified to give actual advice!
Omega-3 good, Omega-6 bad has been known for many years.
For example, Scott Alexander wrote in 2014 on his blog Slate Star Codex about how Omega-3 lowers crime rates and Omega-6 increases crime rates. And he links to some cool RCTs where you can check the methodology yourself.
Just get an omega 3 supplement that has a good amount of DHA and EPA. There’s not as much evidence to support it as there is to support eating fish, but that’s more due to a dearth of research on the subject than because the evidence suggests it has no effect.
Unfortunately it tends to be more expensive. I have recs if you’re in the UK but not much use otherwise!
I suspect the positive effects of consuming nutritious forms of fish-centric meals has as much to do with what you're _not_ eating in those meals as contents like omega-3s.
There's a bunch of less harmful stuff you can fill your diet with that just by virtue of displacing terrible things has positive effects.
Studies also show you do NOT need DHA and DHA can be detrimental, you want pure EPA or very high EPA to DHA ratio
if you want the purest Omega3 EPA without all the contaminants that are in OTC supplement nonsense (they are completely unregulated and untested by batch)
ask your doctor for a script of generic VASCEPA
CostPlusDrugs has the cheapest generic Vascepa that I've found
The dose is usually two pills a day but trust me on this, start with one for a long time, it takes your GI a long time to handle it without bathroom urgency
> "An X-ray diffraction study found that EPA and DHA exert different effects on the lipid bilayer of cell membranes. EPA readily incorporates into the cell membrane core and stabilizes it, whereas DHA does not"
> "Why does this matter? Cell membranes are essential for cellular function: not only do they provide structural support for cells, but they also facilitate cell-to-cell communication and nutrient/toxin transport. Different effects of EPA and DHA on membrane stability likely elicit different effects in cell signaling. A second study revealed that in addition to stabilizing cell membranes, EPA is also protective against harmful reactive oxygen species and lipid peroxidation"
basically EPA modulates the immune system, DHA does not
That's evidence of possible low-level protective mechanisms, but what really matters in the end is the effect on cognition, which in RCTs have favored DHA.
It's difficult if not impossible to increase your intake of omega-3 without increasing your intake of omega-6 even more. I am not sure that's worth it.
The O3:O6 ratio matters more. And with the right diet it's very easy to get tons of O3 with an excellent O6 ratio (1:4 vs. the 1:10+ of the standard western diet). Vegan with some seeds (hemp, flax, chia, etc.) and a fish oil or algal EPA/DHA supplement will do it quite easily. As long as you use olive/avocado oil over the O6-heavy cooking oils. Other diets are probably also capable of this.
I’m not aware of any compelling evidence that the n3:n6 ratio actually matters as long as you’re meeting the absolute required levels of each.
There was a big push for this hypothesis in the 2010s, but on closer inspection the only research that seemed to support it was where the “low n3:n6 ratio” cohort were there by virtue of low n3, not high n6.
Where studies compare groups of people where ratios were manipulated but both were at adequate levels, I don’t believe we see any evidence of a deleterious effect.
unfortunately the effectiveness from Omega 3 is from DHA and EPA but ALA (seed based omega 3) is minimal effective. Algae based omega 3 might be fine though