Lipids & associated proteins have previously been identified as biomarkers of infection, including VLDL, HDL and various apolipoproteins, while both TAG and (serum) PUFA have been implicated as markers of severe disease outcomes
But what this paper adds
3/ Is an investigation (using mostly HEK293T-ACE2 and A549-ACE2 cells) of how the virus alters the lipidome and the importance of these changes in viral proliferation ... They found virus ⬆️TAGs, and PUFA chains were 2-8-fold more than saturated or monounsaturated species ...
4/ Several of the genes encoded by the virus - orf6, nsp1, nsp5, nsp13, nsp5, orf9b, orfc - appeared particularly important in the TAG-PUFA changes. And more interestingly...
5/ Drugs that alter fat metabolism, like an inhibitor of Fatty Acid Synthase (GSK2194069), strongly or completed blocked viral replication across viral strains.
6/ Those are the data. Now my questions
👉 Wondering whether intake of industrial oils could predispose to more severe infection?
👉 Could diets that alter fat metabolism, by doing so, lower infection risk/severity?
👉Are docs going to start prescribing Orlistat for COVID?
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Eating 1000 Sardines Gave Me THIS Superpower
(New 2026 Findings!)
1/8) I ran a self-experiment where I ate 1000 sardines in a month.
Sure, it made me stink—but it also gave me one epic superpower. Let me explain. 🧵 (link at the end)
We all know sardines make your breath stink and that they’re nutrient-dense.
That’s basic.
But eating that many sardines changed me. It gave me a “superpower” that had my inner Marvel nerd activated—and my scientist brain scrambling to explain it.
Eventually, I found those data.
2/8) It was new paper in a top journal turned confusion into clarity and left me in awe of how much we’re still uncovering about human physiology.
1/5) One meta-analysis of controlled human trials found that citrus bergamot extract lowers triglycerides, increases HDL, and lowers LDL — to a substantial degree.
But that’s not all... (link at the end)
2/5) More interestingly, one trial showed that while bergamot decreased small dense LDL, it increased‘large, fluffy’ LDL.
This shift towards a preponderance of large LDL vs small LDL is a metabolic fingerprint of improved metabolic health.
3/5) So how does citrus bergamot work?
Citrus bergamot isn’t a single nutrient — it’s a cocktail of polyphenolic compounds that influence multiple metabolic enzymes.
For example, the bergamot polyphenols inhibit the enzyme ACAT, contributing to downstream increase LDL receptor expression.
A strange new 2026 study suggests compounds in garlic might:
👉Extend lifespan (11.4% in animals)
👉 Improve insulin sensitivity (lower glucose and insulin levels)
👉Reduce fatty liver & reduce inflammation
Let’s break down this bizarre but compelling research.
2/7) Garlic is rich in diallyl sulfides (DAS) — sulfur compounds that increase hydrogen sulfide (H₂S) levels. H₂S acts like a hormone: it diffuses through membranes, triggering cellular pathways across the body.
Researchers fed mice a diet enriched with DAS, leading to an 11.4% increase in lifespan, more than double the effect of metformin.
3/7) Furthermore, on a glucose tolerance test, DAS-treated mice showed: Lower total glucose and much lower insulin levels
How Sleep Deprivation Causally Drives Atherosclerosis
1/5) It’s well established that poor sleep is associated with an increased risk of cardiovascular disease.
But the big question has always been: How… Exactly?
Impressive research published in Nature — one of the world’s top scientific journals — reveals a fascinating biological mechanism. (link at the end)
2/5) To test for a causal connection between sleep deprivation and atherosclerosis (the buildup of plaque in arteries), researchers sleep-deprived mice genetically predisposed to developing atherosclerosis.
Compared to well-rested healthy control mice, the sleep-deprived mice developed significantly more atherosclerotic plaque (quantified on the right).
But that’s not all…
3/5) The sleep-deprived animals also accumulated more inflammatory immune cells inside their arteries — the very cells that drive plaque formation and instability.
Below you can see a quantification of the immune cells (three types) in the arteries of sleep deprived animals (green) versus healthy controls.
As a Neuroscientist, this Graph changed how I think about Dementia Risk Factors
1/5) Microplastics are accumulating in the human brain at an alarming rate. Over the past ~8 years, brain microplastics have increased by ~50%.
But that’s not the worst part…
Consistently, microplastic levels in the brain are much higher in people with dementia (purple) than in those without dementia.
The association is so massive the graphs needs a Y-axis break!
2/5) The researchers behind this work hypothesize that the exponentially increasing concentrations of micro- and nanoplastics in the environment are driving a parallel increase in plastic accumulation in the human brain.
True—correlation ≠ causation. But you cannot do randomized controlled trials here. It’s neither ethical nor feasible.
And when an association is this large—and reverse causality is unlikely—it demands serious attention.
3/5) Mechanistically, this makes sense. Microplastics can drive oxidative stress, chronic neuroinflammation, and vascular injury—three core pillars underlying dementia.