Anorexia is a devastating condition that increases risk of death >5X and is associated w/ high rates of relapse
There is desperate need for more effective treatment options
3/10) Common knowledge posits patients w/ anorexia should be discouraged from practicing food group restriction
But anorexia can be framed metabo-psychiatric condition that may benefit from treatment w/ metabolic health interventions w/ neuromodulatory properties, i.e. #ketodiet
4/10) In this case series, we report on 3 patients who -- after having little success with conventional approaches -- went into remission with an animal-based #ketogenic / #carnivore diet
5/10) Patient 1 (female):
👉BMI low 10.7 kg/m2
👉 complicated by starvation hepatitis, osteoporosis, anorexia-induced blindness, and cardiac arrest
👉 Quote: "My high-fat #carnivore diet saved me, and I feel I can now do anything. I'm never going back to the way I was"
6/10) Patient 2 (male):
👉BMI 13
👉 complicated by anxiety, low T, neuropathy, osteopenia
👉 Quote: "But when I started a carnivorous diet, my life changed! My anxiety diminished... I steadily gained weight... I'll never go back."
👉Total testosterone levels ⬆ 6X & free T ⬆ 10X
7/10) Patient 3 (female):
👉BMI low 11.8 kg/m2
👉 Complicated by OCD, depression, self-harm
👉 Quote: "I feel 100% in remission and confident it will stick.”
👉Suffered for 3 decades with treatment-resistant anorexia, before starting #ketogenicdiet; now in remission for > 5 years
8/10) This case series suggest #ketodiet may have clinical utility for some patients with treatment-resistant anorexia, consistent w/ the perspective of eating disorders as “metabo-psychiatric” conditions that can benefit from neuromodulatory interventions, including ketosis
9/10) We hope these cases inspire further research and attract funding for much-needed clinical trials for ketogenic diets for a variety of mental health conditions, including eating disorders.
10/10) YOU can help support this line of research by RETWEETING this thread and sharing the link to the paper on your social media share this thread LINK: insulinresistance.org/index.php/jir/…
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.