1/ Have you seen the New Non-Nutritive sweeteners paper in Cell making the rounds!?! Fantastic!
Here's a video rundown:
And this thread contains a brief tweetorial...
2/ This study took 120 young health people who didn't consume non-nutritive sweeteners (NNS) and broke them into 6 groups, n = 20/group
👉 Control (no supplement)
👉 Glucose
👉 Sacchrin
👉 Sucralose
👉 Aspartame
👉 Stevia
7 day baseline, 14 day exposure, and 7 day follow-up
3/ There was a clear individualized response across NNS, with Sucralose and Saccharin having the largest impact on glucose tolerance on oral glucose tolerance test.
There were "responders" (who had worse glucose tolerance in response to NNS) and also non-responders.
4/ B = week 1, C = week 2, and D = follow-up (no sweetener)
Note how the pink and orange distributions get vertically squeezed in C compared to B. This appears to suggest that, overtime, non non-responders converted to responders
5/ Also, note in D (follow-up), that responders tended to revert to baseline, meaning the negative impact was reversible... PHEW!☺️
6/ The researchers were also able to show the effect was MEDIATED BY THE MICROBIOME
When then transferred fecal/microbiome transplants from participants to mice without microbiomes, the mice adopted the metabolic profiles of the responders/non-responders
7/ There were many brilliant nerdy nuggets throughout the paper. I'll highlight just one
When they look at profiles of responders vs non-responders for Sucralose, a major difference the popped out was baseline #ketone (BHB) levels
Look at top row...
8/ Responders (impaired glucose tolerance after Sucralose) had LOW ketone [dark blue]at baseline vs. non-responders had HIGH ketone [dark red] at baseline.
Then, levels went in opposite directions after exposure to Sucralose!
What gives?!
9/ While they data certainly do not confirm this, one might SPECULATE, that baseline metabolic state/dietary choice (re #ketogenic diet) could influence whether one is a responder/non-responder to Sucralose, which incidentally is the sweetener in @ketochow
10/ Speaking more broadly, I think it's possibly - if not likely - that dietary choice could influence how one responds to NNS
For example, it's previously been shown carbs + NNS might be worse than NNS alone
11/ Again, here's a link to a verbal video rundown. Certainly a stellar paper. The @Elinav_Lab group always produces incredible research! Very grateful for them!
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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.
Cholesterol Debates in the Era of Medical Mistrust
1/4) This graph shows the hazard ratio for coronary heart disease associated with insulin resistance score (LP-IR) versus LDL cholesterol.
It’s not even close. Insulin resistance dwarfs LDL—with a >14-fold difference in relative risk.
2/4) So why does LDL get all the attention?
Simple: It’s easy to manipulate—and highly profitable.
The statin industry alone generates over $20 billion annually. It would be naive to pretend financial interests don’t shape medical priorities.
That’s not a conspiracy theory. It’s acknowledgement of incentive structures that ultimately dictate the spotlight of research, guidelines and medicine.
3/4) And—despite better drugs and relentless focus on LDL as the biomarker cardiology loves to hate—CVD remains a top killer.
That shouldn't be acceptable. Big problems demand hard conversations—and honest autopsies on where we’ve gone wrong in medicine.
If we’re serious about orphaning cardiovascular disease, we must target the metabolic dysfunctions beneath the surface—the ones that often get overlooked and left in the shadows.