& of course, for those who have the time, I highly recommend reading the full paper, here: doi.org/10.1016/j.ajcn…
But for those who prefer video or TW thread... HERE WE GO...
3/18) What the researchers did in this paper is perform a secondary analysis of pre-existing data from a 12-month RCT: the DIETFITS trial in which 609 adults aged 18-50 without diabetes were randomized to either a 12 m Low-carb diet (LCD) or low-fa diet (LFD).
4/18) Initial data showed LCD led to more weight loss than LFD at 3 and 6 mo, but that the between group diff in weight loss lost significance at 12 months
This was taken to be evidence against the CIM. However, as this paper reveals, there is more nuance to the story...
5/18) One important ? is why significance was lost at 12mo?
2 reasons...
i) Participant dropout. Each group lost ~80 participants, diminishing statistic power
AND
ii) Diet convergence: ‘Carb creep’ in the LCD group (132g/d) + carb drop in the LFD group (213g/d)
6/18) Even setting aside the dietary convergence, when missing data was imputed, the LCD group did in fact lose more weight at 12 m than the LFD group at all time points.
7/18) Moving on, Fig 2 shows a model of predictors of weight loss ➡️ larger circumferences represent better predictors of weight loss
🍽️🍽️Total fat & Calories were poorer predictors of weight loss
🍩🥭Carbs & GI and sugar are the superior predictors
Consistent with the CIM
8/18) In Table are 2 models examining the mediators of weight loss
When you add in Glycemic Load (GL) is added to the model in model 2, GL is highly significant (p=5.7x10-5) and calories (p=0.80) LOSE significance!
Let’s expand on this point...
9/18) Many think that LCD works bc it just makes you eat fewer calories, but that it’s actually the drop in calorie intake that’s driving the weight loss. This certainly is a contributing factor but...
10/18) These results show that GL is better than caloric intake at predicting weight loss, which may appear counterintuitive BUT can be made intuitive if you think about the components of Energy balance: Calories in & Calories out...
11/18) The CICO model, when taken in CLINICAL practice, usually focuses on CI because accurately measuring CO accurately is next to impossible (think, NEAT, TEF, body temp, etc.)
12/18) By contrast, if GL influences the hormonal milieu of the body, it dictates NOT ONLY hunger and caloric intake (CI) but also homeostatic mechanisms to maintain energy equilibrium, or tip it one way or another, through CO: NEAT, body temp, etc.
13/18) Simply put, one could actually make the argument that the CIM is actually a superior real-life ‘CICO’ model than the standard cal counting CICO model itself!
LOL If that doesn’t make sense, read ^ again and watch video for completeness
14/18) Other cool data presented in this paper consistent with the results already shared is that, in fig 5, a biomarker of low-carb/GL (TG/HDL) was strongly associated with weight loss whereas a biomarker of fat reduction (LDL+HDL) was not.
15/18) Finally, and beautifully, the authors put a bold prediction of the CIM to the test which is that those with higher basal insulin secretion would benefit most for GL reduction. Again, this is b/c in the CIM GL influences insulin to cause fat storage.
16/18) So, if someone naturally is an insulin hyper-secreter, the effect of the model is simply going to be amplified. As a result, those who secrete a lot of insulin probably benefit the most from reducing GL. Is that the case? As it turns out yes!
17/18) Clearly see an interaction b/w GL reduction and basal insulin
As you can see in the back left row, these persons who reduced GL most and were the insulin hyper secreters, lost the most weight!
18/18) In summary, this paper provides powerful evidence for two prediction of the CIM: (1) GL > Calories as a predictor of weight loss and (2) insulin hyper secreters benefit most from carb reduction.
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.