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/…
1/10) No word yet from 'Dr' Johnson. So, I've decided to use this as a springboard to deeper learning.
Quick review: in a recent Twitter exchange between @chamath and @bryan_johnson, Bryan proclaimed: “Definitely do not stop statins.”
Today, we deconstruct common logical missteps that could lead to this misguided medical mandate.
A 🔗 to the full letter is at the end.
This won't be shallow reaction content, but an opportunity to dive deep...
2/10) Main Point #1: Causality is Overrated
Just because a molecule or biomarker plays a causal role in a disease process does not mean it is sufficient to cause disease.
More importantly, it does not mean intervention is the prudent path.
The presence of a “causal” variable does not ensure disease nor is the treatment benign.
3/10) Let me emphasize the point with an intentionally absurd analogy.
A penis is part of the causal pathway by which a biological male contracts a sexually transmitted disease. Amputation of the causal variable will reduce STD risk.
But in this case, as with the case of LDL cholesterol, presence of the causal variable does not ensure disease nor is the treatment benign.
1/6) The bile acid and supplement, TUDCA, has the potential to reduce atherosclerosis.
And it appears to do so not by lowering cholesterol, but by reducing inflammation inside arteries. (Red = fatty deposits in arteries)...🔗 in 6/6
2/6) In atherosclerosis, macrophages in the artery wall take up too much oxidized LDL.
This can trigger *ER stress* and activate inflammation, pushing the macrophages into *foam cells* that are a cause and hallmark of atherosclerosis.
3/6) In TUDCA supplementation experiments, TUDCA did not alter total cholesterol or LDL cholesterol levels but led to a significant reduction in arterial fatty deposits in arteries (red staining).
5 Things to Know About Cholesterol-Lowering Drugs 🧵
1/6) Statins are the go-to prescription — but with baggage.
They can:
👉Deplete GLP-1
👉Cause insulin resistance
👉Trigger muscle pain/damage and potentially muscle loss
These risks aren’t often mentioned, but they should be part of a real cost-benefit analysis.
🔗 to the letter at the end, including all hyperlinked references
2/6) Lp(a) and Drug Effects
👉PCSK9 inhibitors = tend to lower Lp(a)
👉Statins = tend to raise Lp(a)
This often-overlooked detail could matter a lot depending on your individual risk profile.
3/6) Ezetimibe blocks cholesterol absorption in the gut — both dietary and recirculated. Liver compensates by increasing LDL receptors.
Its effects are usually modest compared to statins and PCSK9 inhibitors, but if you're low-carb/high-fat you’re naturally recirculating more cholesterol + bile.
Thus, if you’re low-carb, ezetimibe becomes a much more powerful tool for ApoB and LDL lowering.
Creatine Explained: How One Molecule Boosts Muscle and Brain Health 💪🧠🧵
1/11) Creatine is one of the most extensively studied performance-enhancing supplements in the world of exercise science and nutrition.
And yet, despite its popularity, few people truly understand how it works or what its full range of effects might be.
So, let’s break down what you need to know about creatine.
💪Muscle Hypertrophy Mechanisms
💪Brain Health
💪Protocols
2/11) There are several mechanisms through which it can support muscle growth (a.k.a. hypertrophy):
First, Satellite Cell Activation
When muscle fibers grow, they require additional nuclei to manage the increased protein production.
Unlike most cells, which contain only one nucleus, muscle cells are multinucleated. These extra nuclei come from satellite cells—a type of muscle stem cell.
Combined with resistance training, creatine stimulates satellite cell activity, which helps supply growing muscle fibers with the extra nuclei they need to expand.
In simpler terms: creatine makes it easier for your muscles to grow by helping recruit and integrate new cellular “command centers” (nuclei) into the muscle fibers.
3/11) ii. Cell Volumization: Creatine draws water into muscle cells, increasing intracellular hydration.
This “cell swelling” is more than just cosmetic—it acts as a signal that stimulates protein synthesis.
Over time, this contributes to an increase in muscle mass.
Never get Alzheimer’s Disease: The NAD+ Breakthrough
1/9) This graph hints at a potential breakthrough in Alzheimer’s disease.
It shows that NAD+, a key energy carrier in the brain, is depleted in Alzheimer’s—but preserved in cognitively healthy brains.
Restoring it may not just protect memory—it might reverse dementia.
2/9) What is NAD+? NAD+ is an essential energy carrying molecule in the brain.
Most major energy metabolism pathways (carb burning via glycolysis, fat burning via beta oxidation, TCA/Kreb cycle, mitochondrial metabolism) rely on NAD.
When NAD drops, the brain fails.
3/9) In Alzheimer’s, NAD+ levels don’t just drop—they correlate with a core Alzheimer’s biomarker: phospho-tau.
Even more intriguing: some people have Alzheimer’s pathology (amyloid)… but if their NAD+ is high, they don’t tend to develop dementia.
This suggest NAD+ could be a resilience factor in the aging brain… So… what happens if you restore NAD+?