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Nick Norwitz MD PhD

@nicknorwitz

Nov 2

Creatine Mini-Masterclass
💪How is Really Work?
💪How Do You Maximize Benefits?
🔗 in 8/8

1/8) Creatine is one of the most extensively studied performance-enhancing supplements in the world of exercise science and nutrition.

For examples, a recent meta-analysis of RCTs examined the effects of full-body resistance training programs, with and without creatine supplementation.
The key findings:

💪Compared to resistance training alone, creatine supplementation significantly increased lean body mass by 2.5 lbs (1.14 kg).

💪Creatine also led to reductions in body fat percentage by 0.88% and total fat mass by 1.6 lbs (0.73 kg).

And yet, despite its popularity, few people truly understand how it works or what its full range of effects might be.

So... what is Creatine and How Does It Work?

2/8) Creatine is a naturally occurring compound made up of three amino acids: arginine, glycine, and methionine. Your body produces it in small amounts, and you also get some from food—especially meat and fish.

Creatine is primarily stored in muscle tissue, where it plays a critical role in cellular energy metabolism. Its main function? Helping to rapidly regenerate a molecule called ATP—the primary energy currency of your cells.

3/8) Phosphocreatine for Rapid Energy

When you engage in intense physical activity—sprinting, lifting weights, or even just climbing stairs—your muscles burn through ATP in a few seconds. Once ATP is used, it becomes ADP (adenosine diphosphate), and the cell needs a way to quickly replenish its ATP stores.
That’s where phosphocreatine comes in.

Phosphocreatine is simply creatine bonded to a phosphate group. This phosphate can be rapidly donated to ADP to regenerate ATP—restoring your energy supply nearly instantly. Even glycolysis is slow by comparison.

By supplementing with creatine, you increase your phosphocreatine stores, effectively boosting your energy buffering system. This leads to greater performance in high-intensity, short-duration efforts and quicker recovery between bursts of activity.

But that’s just the creatine biochemistry 101. I know you can handle more…

Read 8 tweets

Nick Norwitz MD PhD

@nicknorwitz

Nov 1

How to Hack the Black Hole of Sugar Cravings

(1/7) Why does one person politely decline dessert while another feels irresistibly pulled toward it, as if by a "gustatory black hole?" 🍰

It's NOT a failure of willpower. It's metabolic wiring.

A fascinating paper just published in Nature Microbiology uncovers a precise gut-to-brain pathway that modulates our biological preference for sugar.

2/7) Before we get to the rest of the thread, a quick reminder. This is DAY 1 of the Nuance November Promotion at 👉 StayCuriousMetabolism.com

Link to this letter: staycuriousmetabolism.substack.com/p/the-metaboli…

Now, ONWARD!

3/7) The story's main character is a gut receptor called FFAR4 (Free Fatty Acid Receptor 4).

Researchers found that FFAR4 levels are consistently reduced in human patients with diabetes and elevated fasting blood sugar.

Going deeper, they find that genetic differences in the FFAR4 gene are directly linked to increased sugar preferences in humans.

Read 7 tweets

Nick Norwitz MD PhD

@nicknorwitz

Oct 28

Measuring Insulin Resistance: Your Potato-to-Grape Ratio?! 🥔🍇 (link at the end)

1/5) Your potato-to-grape ratio might predict your insulin resistance.

A 2025 study from @Stanford Snyder Lab (@SnyderShot) published in @NatureMedicine is challenging one-size-fits-all nutrition, and the findings on personalized blood sugar spikes are fascinating.

2/5) Researchers studied 55 individuals, giving them seven standardized 50g carb test meals (white rice, bread, potatoes, pasta, beans, berries, and grapes).

They tracked everyone's individual glycemic response to each meal using CGMs.

One striking finding?

🚨Quoting the paper: "for each individual, different meals produced the highest glycemic response."

Someone might spike most from bread, another from grapes, someone else from potatoes.

But the patterns weren't random.

3/5) The researchers identified a metric they call the "potato-to-grape ratio" (PG-ratio).

They found that people who were more insulin-resistant consistently spiked more strongly from potatoes relative to grapes as compared to insulin-sensitive individuals.

It suggests this simple PG-ratio could one day serve as a real-world biomarker for muscle insulin resistance. It’s a powerful example of how your unique physiology matters more than a generic glycemic index chart.

The nuance goes deeper…

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Nick Norwitz MD PhD

@nicknorwitz

Oct 16

Why Lp(a) May Not Be as Dangerous as You Think—If This One Metric Is Low (🔗 in 8/8)

1/8) A new study offers real hope for those with high Lp(a), a genetic risk for heart disease. While you can’t change your genes, the risk of high Lp(a) appears to be conditional on a modifiable factor: your waist-to-hip ratio.

2/8) For context, Lp(a) is a cardiovascular boogeyman. Unlike LDL, its unique apolipoprotein(a) tail makes it "sticky," more likely to promote blood clotting, and more atherogenic on a per-particle basis.

Your Lp(a) level is largely genetically determined, a fact that has been frustratingly difficult to address as few effective, proven therapies currently exist that lower Lp(a) and lower cardiovascular risk.

3/8) This new analysis used data from the landmark MESA study to understand this risk. It followed 4,652 people for a median of 17.4 years, tracking 'new cardiovascular disease-related events'—a composite including heart attack, fatal/nonfatal CHD, specific angina, stroke, and other atherosclerotic deaths.

Read 8 tweets

Nick Norwitz MD PhD

@nicknorwitz

Oct 15

1/6) How Fructose Hijacks the Liver to Fuel Cancer (Link in 6/6)

Quote: “In all cases, diets supplemented with high-fructose corn syrup resulted in faster tumor growth compared with control diets.”

This includes melanoma, breast, and cervical cancers. What’s going on is ‘sneakier’ than you might think? Let’s break it down 🧵👇

2/6) Cancer is a master hijacker. In this case, it co-opts the liver. When the liver gets fructose, it turns it into molecules that cancer cells repurpose into specific phosphatidylcholines—key building blocks for cell membranes.

Fructose → liver → raw materials for cancer’s construction project.

3/6) But this isn’t just about fructose—it’s about how molecules we eat aren’t passive.

And, it’s why I can’t stand the phrase “empty calories.”

That phrase implies calorie-containing molecules (e.g. fructose) are neutral unless they come with nutrients. But that’s empty thinking. Here’s why...

Read 6 tweets

Nick Norwitz MD PhD

@nicknorwitz

Oct 14

DON'T DRINK Again Until Your Read THIS 🍺🍷🧠

(1/8) Sleep Deprivation Mimics Drunkenness on a Molecular Level — Here’s What That Really Means (Link in 8/8)

A paper in PNAS that provides a stunningly deep dive into how a lack of sleep and alcohol hijack the brain through the exact same pathway.

Stick with me. I'll break down why society's acceptance of "burning the midnight oil" is so dangerous.

(2/8) When I first opened this paper, I was struck by a simple thought: we socially accept exhaustion but demonize drunkenness.

We praise the all-nighter but would be horrified if a surgeon showed up to the OR after a few drinks. The data in this paper reveals just how backward that thinking is.

It turns out that both states flip the very same master “dimmer switch” in the brain. This switch is governed by a key molecule called adenosine, and it explains why the cognitive impairment from sleep loss is so severe.

(3/8) So let me break down that dimmer switch.

Think of adenosine as your brain's 'sleep pressure' gauge. As your cells burn energy all day, adenosine is the metabolic exhaust—it slowly builds up, pushing you toward rest. Normally, sleep is the cleanup crew that clears it all out.

But when you pull an all-nighter, that cleanup crew never arrives.

Adenosine builds and builds, cranking down your brain's dimmer switch.

Here's the kicker: alcohol is like a master key that lets a stranger into the control room to do the exact same thing. Two different paths, one identical outcome of cognitive impairment.

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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

Nick Norwitz MD PhD

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