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More from @nicknorwitz

Nick Norwitz MD PhD

@nicknorwitz

Jan 13

“You are going to die young.”

1/8) The first time I heard those six words, they were jarring. I was 23.

The insult that provoked that perceived threat was a single number on a lab report: my LDL cholesterol (LDL-C).

After I started a ketogenic diet (June 1, 2019), my LDL-C more than tripled from 95 mg/dl to 321 mg/dl.

Link at the end...

2/8) The logic was straightforward:

If I allowed my LDL-C levels to remain in the stratosphere, I would inevitably develop cardiovascular disease and die of a heart attack—young.

The question is this: Does LDL—or more accurately, ApoB—kill?

It sounds like an easy question. But it isn’t.

3/8) Now, there is controversy about the relationship of ApoB to All-Cause Mortality (ACM), or death by any cause.

Some people note that there’s a J-shaped relationship between ApoB and ACM and read into this that lower ApoB might not necessarily be better.

Read 8 tweets

Nick Norwitz MD PhD

@nicknorwitz

Jan 10

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.

Read 10 tweets

Nick Norwitz MD PhD

@nicknorwitz

Jan 8

Can TUDCA Really Slow Atherosclerosis? 🫀

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).

Read 6 tweets

Nick Norwitz MD PhD

@nicknorwitz

Jan 6

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.

Read 6 tweets

Nick Norwitz MD PhD

@nicknorwitz

Jan 5

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.

Read 11 tweets

Nick Norwitz MD PhD

@nicknorwitz

Jan 3

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+?

Read 9 tweets

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More from @nicknorwitz

Nick Norwitz MD PhD

Nick Norwitz MD PhD

Nick Norwitz MD PhD

Nick Norwitz MD PhD

Nick Norwitz MD PhD

Nick Norwitz MD PhD

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