Healthy Fats Over 40: What Actually Works

Fat is not one category — it’s four different substances: saturated, monounsaturated, omega-6, and omega-3. Each behaves differently in the body. The real lever after 40 isn’t “eat less fat” — it’s shifting the balance between types.What ends up on my plate: olive oil as the foundation, fatty fish three or four times a week, nuts and avocado daily, saturated fat as an accent rather than the base. And the marker I track isn’t weight or total cholesterol — it’s ApoB, the count of atherogenic particles in the blood.

Fat Isn’t One Category — It’s Four

Until 45, I thought about fat the way most people who don’t dig into the topic do: fatty foods bad, “lite” foods good, avocado trendy, lard for retirees. That mental model held up for about twenty-five years. It explained things confidently — until I started actually looking at my bloodwork and stumbled onto ApoB, a marker most standard physicals don’t even mention. That’s when I realized my model worked roughly the way pre-Columbus maps worked: drawn from rumor.

Of all the dietary inputs that shape cardiovascular risk, the type of fat is one of the strongest — whatever the trending diet of the season says. Not calorie count. Not “how greasy” something looks. Type.

The single most useful exercise I did was stop talking about “fats” as one thing. It’s like talking about “carbs” as one thing without distinguishing broccoli from Coke. Technically yes, both are carbohydrates. But if you put them on the plate as equivalents, your metabolism is going to have a few questions.

When I broke it down, here’s what I got:

Saturated fats (SFA). Butter, coconut oil, lard, fatty meat, cheese. They raise “bad” cholesterol (LDL) and the count of atherogenic particles (ApoB) in most people — which is to say, they raise cardiovascular risk. Not poison — but a lever. Especially if you have heart disease in the family or your bloodwork is hinting that something’s off.

Monounsaturated fats (MUFA). Olive oil, avocado, almonds, hazelnuts. The mellow neighbor in the building. Almost always neutral or beneficial for the lipid profile. The one category where the scientific consensus hasn’t really moved in decades. If I could only pick one type of fat for the rest of my life, it’d be MUFA.

Polyunsaturated omega-6 (PUFA n-6). Sunflower oil, corn oil, soybean oil, nuts, seeds. The main character of the 2024–2025 nutrition culture war. Social media calls them “the poison killing us.” Recent meta-analyses say the opposite — they’re linked to fewer cardiac events, not more. Someone here is clearly wrong, and spoiler — it isn’t the scientists.

Polyunsaturated omega-3 (PUFA n-3). Fatty fish, flaxseed, walnuts, algae. Subdivided into EPA, DHA, and ALA — not one substance, which changes everything. Whole separate chapter coming, because the difference between “I bought an omega-3 capsule and handled it” versus “I bought an omega-3 capsule and think I handled it” is two different stories. They sound the same. They end differently.

Once I started thinking about these four categories separately, dietary advice stopped sounding contradictory. “Eat less fat” became “shift the balance between types” — a completely different task. The first one feels like punishment. The second one feels like tuning. I prefer tuning.

Omega-3 Over 40: What I Got After Sorting Out EPA From DHA

For a long time I didn’t take omega-3 as a supplement at all. The idea “I should drink fish oil” lived somewhere on the periphery, between “drink more water” and “find time to meditate.” Something I should do, but not today.

When I started digging seriously into my lipid profile and cardiovascular risk, it turned out omega-3 isn’t the vague “general wellness thing” I’d been quietly assuming. It’s a specific mechanism with specific effects. And there are details on the label that aren’t always obvious.

Omega-3 isn’t one substance. It’s three. ALA from plants (flax, chia, walnuts) converts to EPA and DHA in the body — but poorly, around 1–10% by various estimates. You can spoon down flaxseed and think you’ve covered your omega-3 quota. The biochemistry doesn’t share the enthusiasm.

EPA mostly drives the anti-inflammatory and cardiovascular effects. DHA is a structural component of brain and retinal membranes. These aren’t two flavors of the same thing — they’re two different jobs in the body. Buying “omega-3” as a single line item without checking the ratio inside means you’re skipping half the question.

Updated 2024–2025 meta-analyses rewrote part of my picture. The headline finding: across several large meta-analyses, EPA on its own outperforms the EPA+DHA combination for cardiovascular protection. So the move on the label is to stop looking at “total omega-3 mg” and start reading EPA and DHA separately. “1000 mg of omega-3” tells you nothing until you know how it splits between EPA, DHA, and whatever ALA was added for weight.

The 2024 caveat nobody mentions on biohacker Instagram. Across multiple meta-analyses, high doses of omega-3 — particularly EPA at pharmaceutical doses of 2–4 g per day and above — are linked to elevated risk of atrial fibrillation.

So the X enthusiast bragging about “6 grams of EPA daily because Attia said so” might post a follow-up thread next week titled “anyone else getting weird heart palpitations, asking for a friend.” This isn’t theoretical — it’s a pattern cardiologists have started seeing. I don’t go there. I built the system the other way around: most of my EPA and DHA comes from fish, the capsule covers the days fish doesn’t make it to the plate.

What I take now: two capsules a day, 300 mg total omega-3 each — adding up to 360 mg EPA and 240 mg DHA. Compared to the 4 g pharmaceutical dose in REDUCE-IT, this is modest. But if I’ve already had three or four servings of fatty fish this week, there’s no reason to chase a higher dose. The capsule isn’t therapeutic — it’s insurance.

A 1000 mg EPA capsule per day makes sense if you don’t eat fish at all. If you do — it’s just expensive piss.

What I’m planning to do:

• Test my omega-3 index — the percentage of EPA+DHA in red blood cell membranes. The commonly cited target is around 8%. Without that number, all the talk about “am I eating enough fish” is guessing.
• Switch to triglyceride-form capsules if the index says I need a higher dose. Triglyceride form absorbs better than ethyl ester (the cheapest version). Costs more, but if I’m spending the time on this, it might as well work.

Fatty Fish, Not Capsules: What’s In My Fridge

A capsule doesn’t replace fish. That’s the shortest version of what I learned digging into this. I could end the chapter here, but apparently people like the details.

When I look at the various sources of EPA and DHA, whole fish wins over capsules for reasons that don’t get discussed enough: it brings protein (~25 g per 100 g), vitamin D (especially salmon), and selenium as a cofactor. This is the food matrix effect — nutrients work better in combination than in isolation. Nature spent millions of years assembling fish — there was time to debug the recipe.

What’s usually in my fridge:

• Salmon — the most frequent guest. Sashimi, grilled, baked, in any form. About 2 g of omega-3 per 100 g. Forgiving in the kitchen — even if you overcook it, it’s still edible.
• Tuna — also regular, more often as sashimi. Important caveat about mercury: large species (bluefin, bigeye) accumulate it more. I keep it to a couple of times a week. Yellowfin runs lower. I’m not willing to skip tuna entirely just for mercury — it’s too good a package of taste, protein, and omega-3 to blacklist.

When I have the choice in restaurants, I almost always order black cod (sablefish). In my opinion, the most underrated fish on any decent seafood menu. Omega-3 close to salmon — about 1.5 g per 100 g — softer texture, milder taste, lower mercury. Japanese and Thai places often serve it as miso black cod, marinated in miso paste for a day and finished on the grill. It hits that rare combination of “tasty,” “good for you,” and “probably not overcooked.” Triple alignments are uncommon in restaurants.

What I don’t eat regularly, even though the EPA/DHA numbers are great: sardines, mackerel, herring. Just didn’t click. And that’s fine — fatty fish shouldn’t be a chore. If you’re forcing it, you’ll quit in two months. The “eat what you hate because it’s healthy” approach scales terribly across years. Better to get less omega-3 from fish you actually like, regularly, than a lot from fish you eat twice a year.In my system, fish sits at the intersection of protein and omega-3 — one product handling two jobs. More on the protein side: I wrote a separate piece on why men over 40 are chronically under-eating protein.

Extra Virgin Olive Oil — The One Fat I Almost Don’t Argue With

Of all the topics in this article, olive oil is the calmest. Scientists aren’t fighting, the industry isn’t lying, Instagram isn’t telling you to throw it out. If every food were this simple, nutrition would be a boring profession.

Recent 2024 meta-analyses are a rare moment of consensus in nutritional science. Researchers usually can’t agree on whether the sun rises in the east, but here two independent reviews land in roughly the same place: people who use olive oil regularly live noticeably longer — and more often, not from heart attacks.

The effect of olive oil isn’t only the monounsaturated fats. The real story in extra virgin is polyphenols — natural anti-inflammatory compounds. Their effect has been compared to low-dose ibuprofen, minus the stomach lining damage. A bottle of good EVOO is essentially a quiet pharmacy disguised as a grocery item.

Regular “pure olive oil” (refined) has almost no polyphenols. So EVOO isn’t just “olive oil” — it’s a different category. When you see a cheap bottle next to one three times the price, that’s not “premium versus generic.” Those are two different products, and what you’re paying for is polyphenols.

What I do:

• EVOO as the default — salads, dressings, finishing. 30–40 g per day. I pour generously, no rationing.
• Don’t fry on extra virgin — smoke point around 190°C, technically you can, but cooking oxidizes the polyphenols and they’re lost. No point paying premium for something that evaporates. Same logic as cooking down a good wine into mulled wine.
• For frying — regular olive oil. Smoke point around 240°C, fine for everyday cooking. Avocado works too if you need higher heat.

One quality signal I check: “harvest date” on the bottle, not “best before.” Good EVOO is worth buying within a year of pressing. By two years out, the polyphenols are mostly gone — at that point it’s just olive oil without its main feature. Which means a three-year-old bottle on sale isn’t a deal — it’s a demotion.

“Seed Oils Are Killing Us”: What 2024–2025 Science Actually Shows

This is the hottest zone in 2026. On social media, seed oils (sunflower, corn, soybean, canola, safflower) have been declared “the cause of all modern diseases” — from obesity and diabetes to bad Monday moods. The argument is standard: high linoleic acid → conversion to arachidonic acid → pro-inflammatory eicosanoids → chronic inflammation → end of civilization.

Sounds convincing. Especially when delivered by a fitness influencer with two million followers, an affiliate link to their supplement, and a caption reading “follow for more truth bombs.”

The problem is, 2024–2025 science says the opposite.

The most recent research measures linoleic acid directly in the blood — not via self-reported food diaries, which matters because people forget what they ate yesterday, never mind what oil was in someone else’s cooking. And the picture is consistent: the higher the linoleic acid level in plasma, the lower the inflammation markers (CRP, IL-6, and friends), and the better the metabolic health.

In other words, the exact opposite of what the TikTok theory predicts.

The most interesting part of the story is that the biochemistry doesn’t back the popular “ate sunflower oil → got inflamed” idea. The conversion of linoleic acid into pro-inflammatory metabolites in the human body works far worse than the textbook suggests. Recent research shows that increasing dietary LA does not raise arachidonic acid in plasma — meaning the chain everyone uses to argue against seed oils simply doesn’t fire in real bodies.

What I do with this:

• I don’t throw out my sunflower oil. I use it for neutral-flavor cooking when I don’t want the olive-oil note. Refined sunflower, used at home in normal amounts, is a normal product.
• I don’t buy ready-made food deep-fried in seed oils. Not because the oil itself is “toxic” — but because reused fryer oil + ultra-processed food is a different conversation. Oxidized lipids, refined carbs, salt, additives — that’s the cocktail, and the sunflower oil is the least of the offenders. If you’re worried about chips, worry about the chips part.
• Seeds and nuts in their original form — without hesitation. Walnuts, almonds, flax, chia. Came from nature, no bottle, no “cold-pressed” slogan needed.

The core mistake in the seed oils debate is conflating the substance with the products it shows up in. Linoleic acid by itself isn’t inflammatory. Potato chips fried in seven-times-reheated sunflower oil with salt and flavor enhancers — that’s a different dish, and yes, that one is bad for you. But not because of the sunflower oil. It’s because those are potato chips, somewhere near the top of the ingredient list of which a potato accidentally appeared.

Saturated Fat — The Most Confusing Story. What I Do With ApoB On Hand

If olive oil’s consensus is nearly settled, saturated fat is the opposite — a field where the science has been swinging back and forth for the past decade. First “dangerous for the heart,” then “rehabilitated,” then “no, actually still dangerous, but less so,” then “depends on what you replace it with.” At some point I stopped tracking each new turn — too much energy for one dietary variable.

The old model: saturated fat → LDL → atherosclerosis → heart attack. So: eat less.

The new model is more nuanced:

1. Saturated fat does raise “bad” cholesterol (LDL) — but mostly through larger, fluffier particles that cling less to artery walls. Like the difference between a sedan and a freight truck: both are on the road, but they get stuck in traffic at different rates.
2. The smaller, denser LDL particles — the ones that actually do the damage — are driven more by refined carbs and insulin resistance than by a slice of butter. I covered this side of things in the post on carbs and energy after 40.
3. Replacing some saturated fat (butter, lard, fatty cheese) with unsaturated (olive oil, fish, nuts) cuts cardiovascular mortality by roughly 10–15%. Not magic, not “saved from a heart attack.” A two-percentage-point shift in your odds — but stack those small shifts across decades and they add up to a real difference. Health rarely moves in discrete leaps; it moves in percentages that eventually translate into years.
4. A 2025 meta-analysis (9 randomized trials, 13,532 participants) found no significant reduction in all-cause mortality, cardiovascular mortality, myocardial infarction, or major cardiovascular events from restricting saturated fat. That doesn’t mean saturated fat is harmless — but the blanket “everyone eat less saturated fat” rule isn’t as cleanly supported by hard mortality data as we used to think. The picture is messier than “eat less butter, live longer.”

What this means in practice:

I don’t treat saturated fat as poison — I just keep an eye on ApoB.

Here’s the part where most articles slide into a medical textbook. Let me try a different angle.

ApoB is a headcount of the cars that can clog your arteries. Every VLDL, IDL, LDL, and Lp(a) particle is one car. Each carries exactly one ApoB molecule. So if you measure ApoB, you know how many of those cars are driving through your arteries.

LDL cholesterol measures something different: how much cargo each car is carrying. Two different questions. You can have 10 cars with heavy cargo — that reads as “high LDL-C, normal ApoB.” Or 30 cars with light cargo — “normal LDL-C, high ApoB.” Atherosclerosis is caused by the traffic jam, not the weight of the freight. So counting cars matters more than weighing the cargo.

A 2025 review: in 9 out of 9 studies that compared ApoB with LDL cholesterol head-to-head, ApoB was the better predictor of heart attack risk. When the two markers disagree, ApoB is the one to trust. Which is why more and more clinical guidelines are shifting toward ApoB as the primary cardiovascular risk marker.

The logic for me looks like this: “eat less fatty stuff” is a useless advice that accounts for nothing. What’s needed is a systemic shift — less saturated, more mono- and polyunsaturated, plus tracking through bloodwork. Not “how I feel” and not “what I weigh” — a specific number in the blood. More on this logic in the pillar Risk Metrics: How To See Health Problems Before They Break Down.

Butter, lard, and fatty cheese are still on my plate — but as accents, not the foundation. Butter on toast once a week — yes. Butter at every meal, the way some carnivore influencers do it — no. They have their logic, I have mine; the difference is what’s in my head is meta-analysis data, not “Grandma lived to 95 on butter, so I will too.”

Fat And The Brain Over 40

The brain is roughly 60% fat by dry weight. Meaning when you “use your head,” you’re literally thinking with fat. Sounds undignified, but biologically that’s how it works — and DHA is one of the main structural fats in neuronal membranes.

The data that’s accumulated over the past few years all points the same direction: every additional 100 mg of DHA or EPA per day is associated with roughly an 8–10% lower risk of age-related cognitive decline. In people with genetic Alzheimer’s risk (APOE-4 carriers), omega-3 are particularly useful — they slow white matter atrophy on MRI. This doesn’t mean omega-3 protect against dementia. It means that, among dietary factors, this is one of the few where the brain data doesn’t contradict itself.

What I notice in myself:

Cognitive effects in N=1 are the least reliable thing in self-tracking. You drink coffee an hour later than usual and decide your brain is sharper because of omega-3. So I don’t make claims like “omega-3 made me smarter.” But WHOOP shows my HRV is steadily climbing — and I’m fairly sure the right fats play some role in that, alongside sleep, training, and the broader system.

One variable that shows up in HRV data just as consistently as fat intake is meal timing — specifically where the eating window sits relative to sleep. I looked at the 2025 cohort data on this separately: Meal Timing After 40: When the Eating Window Actually Works →

I don’t draw conclusions from this for anyone else. Just observing and noting it down.

Where To Find The Right Fats: Three Tables For Your Fridge

One of the more annoying things about this topic is that there’s no “healthy fats” aisle in the supermarket. They’re scattered across the whole store: fish in one corner, nuts in another, olive oil somewhere near the vinegar, avocado over with the produce. Apparently the supermarkets were designed by people reading a different article.

To avoid carrying that map in my head, I made three short lists by fat type — the ones my plate actually leans on. Not “everything about each type” — just what actually shows up in my fridge or on my plate.

Monounsaturated fats (MUFA): the workhorse

The mellow type — almost always neutral or beneficial for the lipid profile. The base everything else builds on.

Product	Serving	MUFA inside	Note
Extra virgin olive oil	15 ml (1 tbsp)	~10 g	The main workhorse. On salads, drizzled over finished dishes.
Avocado	1/2 fruit (~100 g)	~10 g	Convenient breakfast block. Has to be ripe — underripe doesn't deliver half the benefits.
Almonds	30 g (handful)	~9 g	Default snack. Not salted, not roasted in oil.
Hazelnuts	30 g	~14 g	The most MUFA-dense nut. Pricier than almonds, but small portions don't break the bank.
Olives (pitted)	50 g	~5 g	For salad bowls. Green, in brine, no "improvements."

Omega-3 (PUFA n-3): the reason to keep fish in the fridge

The key rule — read EPA + DHA separately, not “total omega-3.” ALA from plants converts poorly.

Product	Serving	EPA + DHA	Note
Salmon	100 g	~2 g	Universal. Sashimi, grill, oven — works anywhere.
Mackerel	100 g	~2.5 g	One of the densest sources. If you don't like the taste — skip it, no torture.
Sardines (in own juice)	1 can (~100 g)	~1.5 g	Cheaper than salmon, almost no mercury. A good "rainy day" stockpile.
Black cod (sablefish)	100 g	~1.5 g	My favorite restaurant pick. Miso black cod is the best choice in Asian places.
Tuna (yellowfin)	100 g	~1 g	Better than bluefin on mercury. Still limit it — a couple of servings a week is plenty.
Walnuts	30 g	~2 g ALA	Plant omega-3, converts poorly. A complement, not a replacement for fish.
Chia / flax seeds	1 tbsp	~2 g ALA	Same story — support, not the foundation.

Omega-6 (PUFA n-6): the rehabilitated category

The same seed oils social media has labeled “poison.” Recent 2024–2025 science says the opposite — linoleic acid lowers inflammation and heart disease risk. Don’t throw your sunflower oil out.

Product	Serving	EPA + DHA	Note
Salmon	100 g	~2 g	Universal. Sashimi, grill, oven — works anywhere.
Mackerel	100 g	~2.5 g	One of the densest sources. If you don't like the taste — skip it, no torture.
Sardines (in own juice)	1 can (~100 g)	~1.5 g	Cheaper than salmon, almost no mercury. A good "rainy day" stockpile.
Black cod (sablefish)	100 g	~1.5 g	My favorite restaurant pick. Miso black cod is the best choice in Asian places.
Tuna (yellowfin)	100 g	~1 g	Better than bluefin on mercury. Still limit it — a couple of servings a week is plenty.
Walnuts	30 g	~2 g ALA	Plant omega-3, converts poorly. A complement, not a replacement for fish.
Chia / flax seeds	1 tbsp	~2 g ALA	Same story — support, not the foundation.

What I actually do. Olive oil, nuts, avocado every day, and fatty fish three to four times a week. Seeds and sunflower oil — without anxiety, in normal cooking amounts. No gram counting, no logging. Build the system once, then just steer.

Four Principles I Landed On

1. “Eat less fat” is outdated advice. The useful shift isn’t in volume — it’s in type. Less saturated, more monounsaturated and omega-3. Seeds and sunflower oil — fine. Coconut oil — no.

2. Buy the omega-3 capsule by label, not by brand. “Total omega-3 mg” is almost meaningless. What matters: how much EPA versus DHA, in what form (triglyceride beats ethyl ester), and what omega-3 index it actually produces in your blood.

3. Source beats dose. Fatty fish three times a week beats any capsule. Olives, avocado, and nuts beat seed oil that came pre-fried in a packaged meal. Not because supplements are useless, but because whole food works through several mechanisms at once.

4. If fat is affecting your risk, it shows up in bloodwork. Not on the scale. Not in how you feel. ApoB is the cleanest signal of whether the system is working or not.

I didn’t arrive at these all at once. The first couple of years I kept thinking of fat as one category and wondered why “healthy eating” wasn’t intuitively snapping into a clear picture. Once I sorted out the types and realized that the marker to track wasn’t total cholesterol but ApoB — the system clicked. Until then I’d been honestly working on a puzzle with half the pieces missing. And not realizing the other half was in the box.

Fat is the fourth macronutrient in my system. They all work together on the same plate, alongside the rhythm — I’ve also written separately on fiber and breakfast for energy. The whole framework lives in the pillar — Fuel For Longevity: How I Think About Nutrition After 40.

FAQ

How much omega-3 per day is optimal for a man over 40?

Depends on whether you eat fish. If you eat fatty fish three or four times a week, the bulk of your EPA+DHA comes from food, and the capsule is just insurance — somewhere between 300–700 mg of total omega-3 per day covers the days fish doesn’t show up. If you don’t eat fish at all, aiming for 1000 mg of EPA+DHA per day from a supplement makes sense. Across multiple meta-analyses, pharmaceutical doses from 2 to 4 g and above are linked to elevated atrial fibrillation risk — I don’t go there without medical reason.

Krill oil, fish oil, algae oil — what to pick?

Algae oil is the only DHA source for vegans, with bioavailability comparable to fish oil. Krill has omega-3 in phospholipid form, which theoretically absorbs better — but it’s pricier, and the EPA+DHA dose per capsule is usually lower. Fish oil is the workable option for most people. Within fish oil, watch the form: triglyceride absorbs better than ethyl ester (the cheapest form), but costs more. If the label doesn’t specify the form — that’s a signal the brand is cutting corners on a key spec.

Can I get enough omega-3 from chia and flax?

Technically yes — if you eat a lot. Biologically, almost no. ALA converts to EPA at 5–10%, to DHA at 1–4%. Meaning 10 g of flaxseed (about 5 g of ALA) yields roughly 250 mg of EPA and 50 mg of DHA. To cover 2 g of EPA+DHA from flax alone, you’d need about 80 g of seeds per day. Not realistic, which is why for vegans the answer is algae oil — or a much more aggressive approach to fish alternatives.

Coconut oil — healthy fat or hype?

Hype. Coconut oil is butter dressed up in yoga-studio marketing. About 90% saturated fat, and it raises LDL cholesterol — and on average doesn’t look more cardio-protective than unsaturated plant oils. AHA published a Presidential Advisory back in 2017 with the explicit conclusion: there’s no scientific basis for calling coconut oil healthy. The data hasn’t shifted since. I don’t keep it at home — I have olive and avocado, and those photograph just as well on the Instagram shelf.

What oil should I cook on if I don’t want to dig into this?

At home I usually fry on regular olive oil — not extra virgin, just refined. Smoke point around 240°C, neutral flavor, the same MUFA-dominant profile as extra virgin but without paying premium for polyphenols (which oxidize during cooking anyway). Avocado oil works too, especially if you need higher heat. If you want one simple rule — regular olive oil handles 90% of everyday cooking.

What The Research Says

• Dinu et al., European Journal of Preventive Cardiology, 2024 — major meta-analysis on omega-3 and cardiovascular events. EPA on its own works noticeably stronger than the EPA+DHA combination.
• Mattumpuram et al., Clinical and Translational Discovery, November 2025 — updated meta-analysis across 42 studies. Confirms EPA monotherapy outperforms the combination.
• Yuan et al., Clinical Nutrition, March 2024 — 30 studies, 2.7 million people. Regular olive oil consumption is linked to noticeably lower cardiovascular and all-cause mortality.
• Maki et al., NUTRITION 2025 — circulating linoleic acid is associated with lower inflammation markers, not higher. A direct rebuttal to the “seed oils inflammation” narrative.
• Petersen et al., Nutrition Today, October 2024 — review explaining why the theoretical “LA → inflammation” chain doesn’t hold up in real human bodies.
• Yamada et al., JMA Journal, April 2025 — review on saturated fat restriction. The CVD effect is real, but not uniform across groups.
• Sniderman et al., Journal of Clinical Lipidology, June 2025 — ApoB outperformed LDL cholesterol as a heart attack risk predictor in all 9 studies analyzed.
• Wang & Liu, American Journal of Clinical Nutrition, 2023 — omega-3 and cognitive decline: more DHA, less risk of cognitive deterioration in middle and older age.

Disclaimer

I’m not a doctor, not a nutritionist, not a dietitian. The only blood panel I’m qualified to act on is my own. Everything above is the personal experience of someone who read more meta-analyses than he’d planned to in this lifetime and tried to assemble a working system out of it. Your genetics are different, your bloodwork is different, your plate is different — serious dietary changes are worth discussing not with a blog on the internet, but with a doctor who’s seen your actual data.

This article is for informational purposes only and is not medical advice.