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/…
1/6) Maybe you've heard of the Wolverine Stack—a peptide combination of thymosin beta-4 (TB4) and BPC-157.
But I bet you haven't seen this… This is a mouse heart after a heart attack.
In the control group, the blue tissue is dead scar tissue. An entire section of the heart wall has died. Now look at what happens when the heart is treated one of the key components of the Wolverine Stack.
The red tissue is living heart muscle. As you can see, dramatically more of the heart survives.
In other words, this compound literally helped save heart tissue after a heart attack.
Sounds almost unbelievable. So, let's back up and look at the data.
2/6) Since I’ve covered BPC-157 at length before, let’s focus on TB4.
Is there evidence that it promotes tissue regeneration and healing?
Well… yes.
When I dug into the literature, I found Phase 3 double-blind, placebo-controlled human trials and papers published in journals like Nature. Not for every indication—and not for the combination itself—but there's far more science here than most people realize.
Now, let’s discuss some of the biology.
3/6) TB4 is a naturally occurring molecule found throughout the body. Its primary role is to act as a reservoir for actin, a critical structural protein involved in:
• Cell migration
• Tissue growth
• Wound repair
The theory is simple: more TB4 → more efficient repair.
How To Heal 20 Years of Gut Damage in 30 Days (link at the end)
1/7) When I was 21, I was diagnosed with severe inflammatory bowel disease that ruined my life. It took me years to claw my way back to health.
Now, after a PhD, an MD, and nearly a decade obsessively experimenting on my own body, I now have a set of tools I believe can help heal the gut quickly and aggressively.
In today’s deep dive, I walk through them. But let’s give you a taste, here and now.
2/7) Here’s a remarkable fact: You can feed your gut even when you’re not eating.
There are structures in your intestine called Brunner’s glands that secrete mucin to nourish gut bacteria.
And these glands are regulated by your vagus nerve… which is influenced by your mental state.
In other words: there is a direct brain-to-gut pathway through which your mental state can literally feed or starve your microbes.
And the consequences are profound.
3/7) Disrupt this brain-gut pathway or send too much of the “wrong” signal, like chronic stress, and you can trigger:
Should Everyone Be Taking GLP-1s? (link at the end)
1/7) Over the past few years, we’ve witnessed a massive societal shift in opinion on GLP-1s: from supreme skepticism to the provocative question: “Should almost everyone be taking a GLP-1?”
Honestly, my own perspective leapfrogged from: “These are overhyped” to “Maybe they’re not being hyped enough”
Or more precisely: The benefits people ARE hyping may only be the tip of the iceberg.
These aren’t just weight-loss drugs.
Today’s 6,000-word deep-dive (link at the end) is intended to be your one-stop shop for understanding GLP-1s.
So, let’s start with a few fascinating facts you may not have heard.
2/7) Starting with brain health. Higher GLP-1 signaling appears associated with less amyloid in the human brain.
Now of course, correlation ≠ causation.
But is there actually any mechanistic reason to think GLP-1s could protect against Alzheimer’s disease in a weight-independent manner?
Yes.
3/7) GLP-1 signaling appears to inhibit an enzyme called BACE, which helps generate neurotoxic amyloid oligomers from amyloid precursor protein.
At the same time, GLP-1 in the brain improves insulin sensitivity, which leads to the inhibition of GSK3-beta, decreasing formation of tau tangles.
In other words: GLP-1 receptor agonists may directly influence BOTH major pathological hallmarks of Alzheimer’s disease: Amyloid & Tau… and do so independent of weight loss.
1/7) This is, without a doubt, the craziest “diabetes drug” ever invented.
It’s completed Phase II human clinical trials showing efficacy for reducing blood sugar and improving blood pressure. But the promise may extend far beyond that. In preclinical trials, it:
• Reduces fatty liver
• Increases energy expenditure
• Improves exercise endurance
• Cuts fat without sacrificing muscle
It’s called ATX-304. But how does it work?
2/7) The mechanism centers on one of the body’s master metabolic regulators: AMPK.
AMPK functions as a kind of cellular fuel gauge. When it’s “on,” it shifts the body away from energy storage and toward energy production—pulling fat out of fat cells and sugar out of the bloodstream and directing them toward muscles and energy output.
For that reason, AMPK has long been considered a highly desirable metabolic target.
There have been challenges (discussed in the full letter), but the key point is this:
ATX-304 appears to be a powerful AMPK activator. Now let’s look at some data.
3/7) In this study, researchers gave animals a high-fat, high-sugar diet to induce obesity.
One group (black triangles) was started on ATX-304. As you can see, ATX-304 almost completely prevented weight gain.
Then the researchers “flip-flopped” the groups at day 15—and later again. As you can see, treatment with ATX-304 either prevented weight gain or actively caused weight loss.
1/5) Mitochondria are often called the “powerhouse of the cell,” as if they’re just little batteries.
But they’re so much more. They’re living, fluctuating, even dancing signaling networks that determine how your body generates energy — and even how you age.
For example, one striking feature of supercentenarians, including the woman who lived to 117, is remarkably robust and youthful mitochondria.
The amazing thing about mitochondria is that unlike a battery or car engine, they can recover, heal, and renew themselves.
And you can help them do this: through how you live, how you eat, how you sleep, and potentially through cutting-edge mitochondrial peptides.
In today’s deep dive (link at the end), we discuss: How to Reboot Your Mitochondria.
2/5) Let’s start with something free:
Morning sunlight. This isn’t influencer wellness woo-woo.
Morning light helps kick off your “mitochondrial dance.”
Mitochondria constantly undergo cycles of fusion & fission
• Fusion helps mitochondria become more efficient and powerful.
• Fission helps isolate damaged mitochondrial components so they can be recycled through a process called mitophagy.
And research suggests light helps orchestrate these cycles.
3/5) Now let’s get more cutting-edge. Take the peptide SS-31.
Inside mitochondria is a highly folded inner membrane where energy production occurs.
A molecule called cardiolipin helps stabilize this membrane and organize the energy-producing machinery.
SS-31 is a mitochondrial-targeting peptide that binds cardiolipin and helps stabilize mitochondrial structure and energy production.
Researchers are now exploring it in aging, metabolic disease, heart disease, and neurodegeneration.