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Nick Norwitz MD PhD

@nicknorwitz

Oct 11

Cholesterol Confessions of an MD PhD Lean Mass Hyper-Responder. (link at the end)

1/7) I gave my cardiologist a heart attack. Well—not literally. But when a cardiologist sees an LDL cholesterol of 574 mg/dL, their eyes bug out like they’re a human-sized fruit fly.

And I understand why.

That number is higher than anything most doctors have seen in their entire careers. And it’s scary. It is.

It rivals levels found in “homozygous familial hypercholesterolemia,” a rare genetic disorder—occurring in ~1 in a million—that can cause fatal heart attacks in children as young as eight.

But I don’t have familial hypercholesterolemia.
Something very different is going on inside my body…

2/7) Today’s letter is an overdue ~3000-word essay on:
🩸My lipid levels
🩸Background on people like me
🩸Disclosure on my personal choices
🩸What I'm doing next
staycuriousmetabolism.substack.com/p/im-a-harvard…

Warning: It’s intense. And it’s only the beginning.

Caution: Please do not take this as medical advice or even the suggestion of such. Instead, my purpose is providing discloses it to reveal how I think, not what to think.

Note: The back half of the letter is currently only available for premium subscribers. For now, I’m reserving the most complex and intense details for a smaller, highly committed audience. Call it an intellectual stress test.

3/7) Still, at a high-level here in this thread, I want to reinforce a few points:

🚨First, people like me – lean mass hyper-responders (LMHR) on ketogenic diets – are unlike any other population ever studies with high LDL and ApoB.

🧬Our lipid levels are NOT the result of a congenital genetic lipid disorder (like familial hypercholesterolemia). And, generally, LMHR are in excellent metabolic health.

For these reasons, it’s in appropriate to extrapolate from the existing “preponderance of evidence” any certain claims with respect to cardiovascular risk to people like me.

Read 7 tweets

Nick Norwitz MD PhD

@nicknorwitz

Oct 7

🚨Low-Carb Gaslighting: How THIS Became “Keto” Science (link at the end)

1/8) What if you could live on a diet of Reese’s Peanut Butter Cups, lose body fat, and improve your health?
It sounds absurd—and it is.

But the absurdity of that thought experiment highlights a persistent misunderstanding about ketogenic and low-carb diets.

In today’s letter, I step through four shocking examples of low-carb and keto gaslighting—ultimately building to answer the question: why are these diets so grossly misunderstood.

@AKoutnik @janellison @realDaveFeldman @metcoalition @Metabolic_Mind @bschermd @TuitNutrition @BiggestComeback @BenBikmanPhD @thelowcarb_rd

2/8) Study 1: Skews the Truth with “Scores”

Take as our first example, recent study that was touted as “proof” online that low-carbohydrate diets don’t help—or can even exacerbate—diabetes.

At first, the headlines seem compelling, if for no other reason than the American Diabetes Association “seal of approval.”

But what did the researchers actually measure? What did they call “low-carb?”

This was a nutritional epidemiology study based on food-frequency questionnaires. Participants self-reported their diets, and researchers divided them into quintiles (fifths) according to carbohydrate intake. They then assigned each group a “low-carbohydrate score” relative to the others.

3/8) Here’s the problem… The lowest-carb group across multiple cohorts was still eating ~40% of calories from carbohydrates.

That’s not low-carb—it’s about the same carb proportion you’d find in a Reese’s Peanut Butter Cup.

Read 8 tweets

Nick Norwitz MD PhD

@nicknorwitz

Oct 5

Food is Medicine. Why Are We Poisoning Patients?

1/4) This is a plate of food at the hospital.

They say a picture is worth a thousand words. But I’d argue the fact that a wealthy, advanced Western society feeds its sick like this says more than all the words in the English language.

So, we must ask: Why do we do this?

And, how do we dig ourselves out of this sticky situation?

2/4) Honestly, the “why” is simple can be summed up in a words: ignorance.

I don’t believe those trays of food are driven by malice. I think it’s a genuine lack of understanding about just how harmful meals like these can be—especially for the metabolically vulnerable.

We toss around and consume misleading terms “empty calories,” phrases that distort biological reality.

On this example, nutrients that calories – carbohydrates (fructose, glucose), fats (stearic acid, linoleic acid, butyric acid), etc. – aren’t just passive carriers of vitamins and minerals; they are active biological signals with direct effects on your metabolism, mitochondria, and immune system.

3/4) For example, the photos I mentioned earlier. Each was a meal given to patients with some form of glucose dysregulation during the COVID pandemic.

And, in fact, we know how high blood sugar alters immunity and increases risk of severe COVID or risk of death from COVID: Let me inject you with some knowledge:

💉Hyperglycemia (high blood sugar) causes mitochondrial dysfunction.
💉Unhealthy mitochondria increase the production of reactive oxygen species (ROS), leading to oxidative stress.
💉This results in the oxidation of fragile lipids (fats), a process called lipid peroxidation (LPO).
💉 LPO, in turn, leads to the degradation of STAT4, a protein that regulates gene expression and the differentiation of CD4+ T-cells—key players in antiviral immune defense.
💉This sequence ultimately leads to impaired immune response and higher morbidity and mortality in those with T2D and poor glycemic control.

In short: Chronically high blood sugar weakens your immune system at the cellular level.

Read 4 tweets

Nick Norwitz MD PhD

@nicknorwitz

Oct 4

The Gut Molecule Makes Blood Less “Clotty” (New Research) 🔗 in 8/8

1/8) Imagine your blood as a river, delivering life to every organ downstream. A heart attack is a dam—a single clot that blocks that river, starving your heart or brain until it begins to die.

A new paper in @NatureCVR (PMID: 40217125) has identified a key molecule from our gut that keeps this river flowing.

Stick with me. I’ll break down these data.

2/8) Researchers compared patients with coronary artery disease (CAD) to healthy controls and found a stark deficiency.

The CAD patients had significantly lower levels of a particular bile acid called Deoxycholic Acid (DCA).

They also had fewer of the specific gut microbes responsible for producing it, revealing a potential link between a missing microbe and a missing protective molecule.

3/8) What is the functional consequence of low DCA?
In plain English: their blood was clottier.

The study showed a direct inverse correlation between DCA levels and platelet aggregation.

The ultimate consequence?

In their four-year follow-up data, higher DCA levels were linked to a lower risk of heart attack, stroke, or death (adjusted hazard ratio = 0.43).

Read 8 tweets

Nick Norwitz MD PhD

@nicknorwitz

Oct 2

We Just Discovered a Fructose “Vaccine” — and It's at the Grocery Store (🔗 in 8/8)

1/8) When I read this new paper in Nature Metabolism (PMID: 38862620), I started with a smirk and ended with a sigh of relief. “FINALLY!” I thought. “A fiber paper that’s not fluff.”

I have a bone to pick with how fiber is discussed: hand-wavy "more is better" claims. It's like evangelizing "eating is fantastic" without differentiating salmon from a breadstick coma at the Olive Garden.

This paper is different. It shows how one specific fiber can immunize against fructose. Stick with me.

Authors note regrind 'vaccine.' Yes, that's called a hook. Congrats. Give you the definition of the word, it's "a biological preparation that provides active immunity to a particular infectious disease" ... and, honestly, I could easily argue that applies here.

2/8) First, some background. Metabolic dysfunction-associated Steatohepatitis (MASH)—fatty liver—is a serious risk, worsening cardiovascular health and increasing cancer risk. One dietary driver can be fructose, which uniquely enhances de novo lipogenesis: the synthesis of new fat in the liver.

Crucially, this can be uncoupled from weight gain. In controlled experiments, mice fed high-fructose corn syrup don't always gain weight, but they gain fat, lose lean mass, and develop a fatty liver.

The simple answer is "eat less fructose," but if that's all you wanted, you wouldn't be here.

3/8) So, let's ask a more interesting question: Can you immunize against fructose?

The researchers tested a fascinating, long-shot hypothesis using inulin—a prebiotic fiber. The twist? Inulin is a polymer made of fructose units. To test this, they fed mice several diets: (C) Chow (CF) Chow + Fructose (IF) Chow + Fructose + Inulin

Could a fructose-based fiber really protect against fructose itself?

Read 8 tweets

Nick Norwitz MD PhD

@nicknorwitz

Sep 30

Statins Harm Mitochondria (Human Trial)💊❤️‍🔥

1/5) Even at very low concentrations, and without symptoms, statins can impair mitochondrial function. (link at the end)

In this study, patients were treated with atorvastatin daily for eight weeks. The results included:
👉Decrease in mitochondrial respiratory capacity
👉Decreased skeletal muscle oxidative capacity
👉“Striking” inhibition of mitochondrial complex IV.

2/5) The researchers in this study noted that the statin therapy caused a 23% reduction in the rate constant of muscle recovery. To quote the authors, this “indicates a decrease in muscle oxidative capacity.”

In simpler terms, statins impaired a functional metric of muscles metabolism. How? …

3/5) Statin therapy progressively reduced mitochondrial function.

🚨Quoting directly from the study: “The magnitude at which mitochondrial respiratory capacity in skeletal muscles decreased in response to 8 weeks of high-intensity atorvastatin treatment was striking.”

Complex IV of the mitochondrial electron transport chain was most severely impacted. Even at very low concentrations — as little as 10 nm — atorvastatin inhibited complex IV activity by >50%.

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More from @nicknorwitz

Nick Norwitz MD PhD

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Nick Norwitz MD PhD

Nick Norwitz MD PhD

Nick Norwitz MD PhD

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