Post

@KenDBerryMD

@KenDBerryMD

More from @nicknorwitz

Nick Norwitz

@nicknorwitz

May 8

1/11) Since our KETO-CTA paper was published on April 7, 2025 there has been an undeniable and conspicuous spiral of events, leading to a strong diverse set of opinions on the data.

It’s also been noted that since around April 18th, my co-authors and I have been quiet regarding criticisms rendered. I’ll speak for myself when I say this wasn’t personal my preferred approach.

However, it was the strong preference of JACC Advances that we work through the preferred academic channels – namely, by responding to Letters to the Editors passed to us from the journal. Now that we’ve done so (links at the end), I’m pleased to break my silence and speak more freely.

2/11) First and foremost, I encourage everyone to listen to this recent hour-long conversation between Dave Feldman and Chris MacAskill about the controversy.

Truthfully, I think it was among the most honest, humble, and sincere conversations my ears have ever had the pleasure of capturing.

Please start there if you’ve been following the controversy and want a grounding perspective.
youtu.be/cM0KaSp5IIE?si…

3/11) The April 7th Paper was Fully Peer-Reviewed. But it Wasn’t Perfect

Now, here are some points I’d like to make to begin to reanimate productive discussion and resolve confusions.

First, let’s get this straight, the April 7th published paper was fully peer-reviewed and approved by all the authors. That’s not in question and was previously clarified in a joint statement.

Read 11 tweets

Nick Norwitz

@nicknorwitz

May 7

How to Start a Mediterranean Ketogenic Diet: A Step-by-Step Guide (Link to more🔗 in 5/5)

1/6) I started a ketogenic diet on June 1, 2019, and it saved me from debilitating inflammatory bowel disease.

But here’s a hard fact: despite its many benefits—including for obesity, diabetes, mental health, autoimmune and inflammatory conditions—ketogenic diets are still grossly misunderstood. Many people assume keto is all about bacon, butter, and steak, low in fiber, and at odds with what most have been taught, and internalized over their life courses, is “healthy.”

🚨That’s a huge misconception!🚨

Ketosis isn’t about specific foods—it’s about a metabolic state, where you’re producing ketone bodies. You can be keto while eating anything from a fully #vegan diet to a fully #carnivore one.

There is not one ketogenic diet. There are infinite.

And a Mediterranean ketogenic diet is an excellent entry point for many people because it balances the perceived health benefits of Mediterranean eating with the metabolic advantages of keto

Simply put, Medi-Keto is a low-friction dietary entry point to low-carb diets for many people.

Today’s Newsletter breaks down the how-to of Medi-Keto, including:

👉 4 ‘musts’ for preparing to start on your ketogenic lifestyle.
👉 My 9 favorite Medi-Keto foods and help flesh out your shopping list.
👉Common Q&A

In this thread, I’ll tease you with a few highlights…

2/6) Fatty Fish

Fatty Fish are a great source of protein, healthy fats, and micronutrients to support muscle growth, brain health, healthspan and even longevity.

Remember the acronym “SMASH” for Salmon, Mackerel, Anchovies, Sardines and Herring.

For salmon, I’d give Wild Alaskan Sockeye the edge of health and for Sardines, I suggest getting whole sardines (skin and bone) packed in BPA-free tins with water or brine, rather than with oil. (My personal go-to is Wild Planet)

3/6) Extra Virgin Olive Oil

If I were to do a video on all the health benefits of a good, true extra virgin olive oil it would be longer than the entire Lord of the Rings Saga (aside: Gollum was definitely oxidized).

But, practically speaking, what you need to know is how to pick a real extra virgin olive oil, as many bottles labeled “extra virgin” aren’t actually extra virgin and aren’t as healthy.

My top 3 tips for choosing a real extra virgin olive oil are:
(i) Dark glass or metal bottle, not plastic or clear
(ii) “Pressed” or “Harvest” date within the last 2 year
(iii) Look for a bottle that’s transparent about where the olives come from, ideally single source.

*What's the photo?

That's the TRPA1 receptor. The natural compound "oleocanthal" binds to this receptor in the back of the throat, and - if present in good amounts - should cause a burning sensation, and even make you cough. So, to really test for a good high polyphenol EVOO, take a shot and hope for a burning, stinging KICK in the back of your throat

Read 6 tweets

Nick Norwitz

@nicknorwitz

May 3

🚨How Chronic Stress Causes Depression🧠
(Link to Letter 🔗 at the end)

1/8) A new paper about the neuroscience of depression is the most fascinating mental health papers I’ve read in 2025!

It reveals a possible central biological mechanism by which chronic stress can contribute to depression and opens doors to innovative solutions for improving mental health. (link at the end)

Let’s get into it…
#depression #mentalhealthmatters #autophagy
cc/of interest @janellison @ChrisPalmerMD @NTFabiano @KetoCounselor @TuitNutrition @hubermanlab @AllyTransforms @bschermd @Metabolic_Mind

2/8) Background to Know: Lateral Habenula 🌶️ & Autophagy♻️

The habenula is a region in the middle of the brain important in processing
aversive and unpleasant stimuli and in the stress response.

🌶️Because I love memory tricks, the way I remember this is: habenula sounds like habanero, the spicy pepper that can be 100x hotter than a jalapeño — and is therefore an aversive and unpleasant stimulus for most people. So now you won’t forget it! Specifically, the lateral habenula is important in processing responses to unpleasant stimuli and stress.

♻️Think of autophagy as your brain’s janitor crew. It’s a built-in cleanup and recycling system within cells. When proteins get old or broken, a membrane wraps around them like a trash bag, isolating the waste from the rest of the cell. That bag — called an autophagosome — then fuses with the cell’s digestive center and breaks the waste down into reusable parts.

But here’s the catch: under chronic stress, it’s like the janitors go on strike. The trash piles up, the system clogs, and neurons start to malfunction. That’s where things start to go wrong — and potentially spiral toward depression.

And that’s what they show in this paper — at a high level — autophagy within the lateral habenula is impaired, contributing to depression.

3/8) Chronic Stress Inhibits Autophagy in the Lateral Habenula

First, it’s important to note that there are already data suggesting autophagy markers are impaired in people with mental health disorders, including depression.

To demonstrate a causal relationship, the researchers subjected mice to various chronic stress protocols designed to model depression. This decreased autophagy, specifically in the lateral habenula.

You can see that here (Figure 1G): the result of an experiment where they exposed mice to acute or chronic stress and measured levels of a protein called p62, which is normally broken down by autophagy.

👉Taller bars = less autophagy👈

And you can see taller bars in the chronic stress condition — meaning autophagy is inhibited by chronic stress.

Read 8 tweets

Nick Norwitz

@nicknorwitz

Apr 20

🚨 New Genetic Discovery: Why Some People Naturally Eat Less Sugar & Stay Lean 🍫➡️🚫 (link at the end)

Scientists may have just uncovered a hidden biological quirk that makes some people naturally eat less sugar, crave less sugar, and stay lean.

1/5) A paper just published in Gastroenterology found that people with mutations in a gene coding for a carbohydrate-digesting protein called “sucrase-isomaltase” had:
✅Lower intake of added sugar
✅Lower BMI
✅Improved metabolic health

But here’s the kicker: there may be a way to hack this system, even if you weren’t born with these lucky genetics 👀…

#SugarCravings #Metabolism #NutritionScience #GLP1 #FunctionalFood #Genetics #HealthHack

2/5) Researchers found that people with a Sucrase-isomaltase mutation that reduces this protein’s function not only consumed less sugar but also experienced better metabolic health overall.

🍭 Voluntarily ate less sugar
🥤 Drank less sugary fluids
🔁 AND released more GLP-1 in response to sugar

3/5) The whole metabolic cascade isn’t fully understood yet, but another key player might be acetate, a molecule that increased in both the mice and humans with this mutation.

Researchers suspect this acetate signals the brain and nervous system to boost GLP-1 levels and curb sugar cravings.

And here’s something else really fascinating part: the more sugar a food contained, the less people with this mutation liked it—compared to those without it!

Read 5 tweets

Nick Norwitz

@nicknorwitz

Apr 19

'Lettuce' Be Honest: Fiber Isn’t Always the Answer🥬🤥(Refs linked in letter at the end) 🧵

1/6) We’ve been told for years that fiber is a must-have for gut health—that without it, your microbiome will crumble faster than a stale bran muffin.

But what if I told you… you don’t actually "need" fiber?

But before you throw your kale smoothie at the screen, let’s break down the science—because the truth about fiber is way more complex than a simple 'good' or 'bad.'

#fiber #microbiome #guthealth #educational #SCFA #ketodiet #carnivore #plantbased #metabolism #metabolichealth

2/6) Fiber & Inflammation🔥🥬

Some people argue that fiber-rich foods are anti-inflammatory. But that’s not entirely true.

For example, a landmark randomized controlled trial published in Cell found that some people were inflammatory responders to dietary fiber. Reading from the paper, “Taken together, these data suggest divergent immune system responses to the high-fiber intervention, with high-inflammation participants exhibiting broad increases in steady-state immune activation.”

To be clear, this was NOT the majority of participants.

And it's also worth noting that those with lower microbiome diversity tended to be the inflammatory responders, raising the 🤔hypothesis🤔 that there might be protocols by which one could train-up a microbiome such that it responds with a healthier anti-inflammatory response to fiber...

It’s possible.

But the fact remains that some people have a pro-inflammatory response to fiber that could have negative health consequences and contribute to or exacerbate chronic disease.

3/6) Fiber & Microbiome Diversity🥬🤔

One point that is often raised is that fiber depletion or elimination will decrease microbiome diversity, a presumed marker of good health. This is fair speculation at a population level. However, there are deeper nuances.

First, microbes in the gut can feed off more than just fiber and eating a low-fiber diet doesn’t necessarily lead to decreased diversity.

For example, in one impressively comprehensive case study, a man who had been on a carnivore diet for 4 years had his microbiome compared to that of omnivores and, reading from the study, “[T]he comparison showed surprising results. The carnivore’s gut microbiome did not stand out regarding α- and β-diversity, indicating that it did not lack richness or diversity when compared to its omnivore counterparts.”

And “Our study indicates that adherence to a carnivorous diet does not cause detrimental changes in the gut microbiome. Instead, it suggests that the effects on the gut microbiome are due to the combined influences of dietary regime and lifestyle, rather than meat consumption alone. Further research is needed to identify which components of the carnivore diet could act as prebiotics in the absence of plant-derived prebiotics and maintain gut health over time.”

Granted, this is a case study. But even an N = 1 it’s sufficient to make the point that even complete fiber elimination for 4 years doesn’t starve off the microbiome.

Read 6 tweets

Nick Norwitz

@nicknorwitz

Apr 13

What if all *autoimmune diseases* were stemming from the same source, from a seed planted 2 Billion years ago that’s just beginning to flower? 🔥🤔🧵

1/6) That might sound wild—but it’s actually the central thesis of a perspectives paper published in @Nature, which proposes that many autoimmune diseases may be driven by the failure of a relationship that began 2 billion years ago: the one between your body and your mitochondria.

For me, this idea carries personal weight since I suffered from debilitating inflammatory bowel disease, which went into remission on a ketogenic diet.

I’ve seen others similarly put IBD, lupus, multiple sclerosis, and rheumatoid arthritis into remission with lifestyle change.

And I desperately want to know how it works.

But enough chit chat, the paper is entitled: “A break in mitochondrial endosymbiosis as a basis for inflammatory diseases.” (PMID: 38326590).

This thread will explain it in simple terms, but with nuance. 🧵👇

(link to more at the end)

Potentially of interest to:
@ChrisPalmerMD #BrainEnergy
@thegarybrecka @joerogan - Discussed Autoimmune Disease on Epi #2304. I agree with Gary, "God [metaphorically or literally speaking, depending on your beliefs], didn't make a mistake." And THIS might be what we are missing
@hubermanlab @R_Mohr @bryan_johnson because of relationship to circadian rhythms
@MitoPsychoBio because #mitochondria
@AdrianSotoMota @drmarkhyman @MatthewNehsMD @drericwestman @JEverettLearned @AKoutnik @lowcarbGP because I know they will
And Ht/ @davidludwigmd who passed me the paper that inspired this thread, newsletter & upcoming video
#autoimmunity #inflammation #mitochondria #metabolichealth #metabolism

2/6) What is "Mitochondrial Endosymbiosis?"

About 2 billion years ago, a cell consumed another, smaller bacteria-like cell (technically it was an Asgard archaeon). That second, smaller cell didn’t get digested and pooped out, but integrated into the larger one.

This is what’s meant by “endosymbiosis.”

And, you guessed it, that smaller cell was the precursor to our very own mitochondria, the engine and the powerhouse of most of the cells in your body and the center of your metabolism.

But your mitochondria are far more than just little engines.

They are also informational hubs and communication stations, signaling all over your body to cue and coordinate near infinite pathways and processes.

And how mitochondria do this derives, at least in part, from their foreign origins. Truly, mitochondria retain many of the signatures of their foreign origins that mark them much like bacteria or viruses and apart from other components of “you.”

The authors write, “we can also consider mitochondria as a pseudobacterium ‘bricked in’ behind the mitochondrial outer membrane.”

3/6) A Break in Endosymbiosis Triggers Autoimmunity

And your body’s immune system is great at recognizing the “other” – foreign invaders.

Mitochondria, for the most part, are shielded within cells and so don’t get targeted and attacked. However, the body can selectively release mitochondrial components or mitochondria-derived signaling molecules to trigger certain events.

In the authors’ words, “[T]he endosymbiotic origin of mitochondria marks them apart from the rest of the cell in a way that can be co-opted to produce key messages pertaining to cell fate.”

For example, in response to cell stress, mitochondria can release proteins from the intermembrane space, like cytochrome C, to trigger a form of organized cell death called apoptosis. Mitochondria also retain their very own mitochondrial DNA (mtDNA), separate from the DNA in your cells’ nuclei.

And the release of this DNA can also trigger immune reactions. In some cases, the inner portion of mitochondria can swell, and components can literally herniate out (illustrated below) of the mitochondria, pushing components including mtDNA, and triggering an immune/inflammatory reaction.

Read 6 tweets

Share this page!

Enter URL or ID to Unroll

Nick Norwitz

Try unrolling a thread yourself!

More from @nicknorwitz

Nick Norwitz

Nick Norwitz

Nick Norwitz

Nick Norwitz

Nick Norwitz

Nick Norwitz

Did Thread Reader help you today?

Don't want to be a Premium member but still want to support us?

Send Email!