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Nick Norwitz

@nicknorwitz

Sep 11

Stress Makes Sugar (Literally!) - New Study Blew my Mind...(🔗 at the end)

1/8) Groundbreaking research just published in @Nature shows that stress can trigger brain circuits with a direct hotline to the liver to make new sugar.

🚨TL; DR Stress can Make Sugar, even independent of eating carbs.

This newly discovered brain-liver axis bypasses the usual hormonal regulators of blood sugar—like cortisol, adrenaline, insulin—and instead sends a direct signal that forces the liver to make and dump sugar into the bloodstream.

Let’s break it down…

2/8) Let me start with an analogy: Imagine if I told you that I could instantly communicate with a friend on the other side of the world. You wouldn’t be shocked—you know I have access to email and a phone. But if I clarified, “No, I’ve invented telepathy,” and could somehow prove it to you, is it fair to say you’d be impressed? That’s analogous to distinction we’re dealing with here: an entirely new and direct line of communication between the brain and liver to influence blood sugar.

3/8) First, researchers first confirmed what we already know: different stressors—physical restraint, social stress, etc.—increase blood sugar and activated a particular region in the brain, the medial amygdala (MeA) that is associated with a stress response. That wasn’t shocking and is already a well-documented phenomenon in humans and animals.

The stressors also elevated the usual hormonal suspects like cortisol.

If the story stopped here, we might be tempted to conclude that stress hormones raise blood sugar. End of story. The end. Goodbye.

But that’s not the full picture. Not even close…

*Image Note: FOS is a label for early neuron activity. More green dots under the stress condition (bottom middle panel on the left) reveal more neuron activity as compared to the control (un-stressed) condition. This is quantified on the right. Stress increases neuron activity in both the anterior (front) and posterior (back) portions of the medial amygdala.

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Nick Norwitz

@nicknorwitz

Sep 8

Four Subtypes of Diabetes: Groundbreaking Research Out of Stanford (🔗in 7/8 and 8/8)

1/8) Overview:
👉New technologies reveal four subtypes of diabetes
👉Knowing your ‘flavor’ of diabetes (or prediabetes) can guide lifestyle and medical treatment
👉Combining bio-monitoring with big data and machine learning will bring forth a revolution in diabetes care and personalized medicine

*I’m releasing this letter early because the data it covers was conducted by one of my scientific heroes, Stanford’s Professor Michael Snyder @SnyderShot, who happens to be the guest on today’s @hubermanlab podcast episode.

*In fact, Professor Snyder is the only person I’ve pestered Andrew to have on his show, although I suspect the conversation would have happened anyway.

*My two-part interview with Professor Snyder, where we dig into some of his specific studies (Sub-phenotypes of diabetes, personalized medicine, and the famous two peaks of aging) will release part one later this week.

But first, let’s dig into these data!

2/8) The most common form of diabetes — Type 2, often associated with obesity and adult onset — isn’t one disease. It’s actually four different underlying pathologies, showing up in different proportions in different people.

Here’s a metaphor that might help: Imagine a dish made from bread, vegetables, and cheese. The general ingredients stay the same — but their ratios define what you’re eating.

Pile on the vegetables, go easy on the bread, toss in some protein — and you’ve got a Caesar salad with croutons. Flip the script: make bread the base, add a smear of sauce and some melted cheese — and now you’ve got a pizza.

Now imagine if we called both dishes the same thing. That’s what we’ve been doing with Type 2 diabetes.

3/8) First question: Why have we lumped different biological patterns under one umbrella?

The short answer: tools. In medicine, our understanding is often shaped — and limited — by what we’re able to measure.

For diabetes, it’s been easiest to classify people based on average blood sugar levels (for example, an HbA1c >5.7% indicates prediabetes, and >6.5% indicates diabetes) or based on their blood glucose levels at a singular timepoint on an oral glucose tolerance test (OGTT).

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Nick Norwitz

@nicknorwitz

Sep 6

Can Visceral Fat Cause Depression? (🔗at the end)

1/7) New data reveals how molecular packages called extracellular vesicles (EVs) can travel from visceral fat in the abdominal cavity, through the bloodstream, and into the brain, where they alter the function of specific brain areas and promote depression.

This is no joke. It's (literally) mind-bending science. Let's dig in...

2/7) First, some human context: depression and obesity are highly 'co-morbid'—meaning they often occur together.

Individuals with obesity are twice as likely to experience depression as those with a healthy weight.

Moreover, those diagnosed with depression are similarly at (58%) higher risk of developing obesity down the line, in part due to the adverse effects of certain antidepressant medications.

This can establish a vicious cycle between obesity and depression—a descending spiral with social, psychological, pharmacological, and metabolic components.

But one big question remains unanswered: How does fat tissue contribute to depression?

This is a very difficult question to answer in humans. You can’t perform controlled trials, and the social baggage of living with obesity introduces many psychosocial confounders. So, we turn to animal models.

We return to the human story in the letter—but first, let’s get murine and mechanistic.

3/7) Visceral Fat Transplant Causes Depression in Animals

In this study, researchers first demonstrated that a high-fat, high-sugar diet designed to cause obesity in mice also induced depression-like behaviors.

...But here’s where things get interesting: to test the hypothesis that visceral fat was responsible for the depression-like behavior, researchers transplanted visceral fat from the obese mice into normal, healthy mice.

Compared to a control group that received fat from lean mice, the mice that received visceral fat from obese donors similarly exhibited depression-like behavior. This suggests that transplantation of visceral fat alone is sufficient to cause depression.

But how?

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Nick Norwitz

@nicknorwitz

Sep 1

Causality is Overrated” – A Respectful Rebuttal to Dr @PeterAttiaMD cc @hubermanlab (🔗at the end)

This thread is about one word: causality.

1/8) People are obsessed with it. But first, let me identify the causal stimulus for this nibble: the quotes Huberman podcast clip @HLPClips (posted yesterday on X) in which Peter Attia expounds upon his “obsession” with causality.

To quote Peter: “Causality is an obsession of mine. Most of the day, on some level, I sit around thinking about causality.”

In this thread I’m going to make the case, respectfully, that Peter misses a big-picture point. This isn’t to ‘mic drop’ or puts points up on some imagined. This is not to end a discussion – it’s to reopen one that is desperately needed.

cc @realDaveFeldman @AdrianSotoMota

2/8) The first three minutes of the clip are devoted to lung cancer, where Peter uses the Socratic method with Andrew to examine the causal relationship between smoking and lung cancer. He ultimately lands on the point:

“If you believe smoking is causally related to lung cancer, then smoking cessation reduces the probability of lung cancer. That is a logical equivalency. There can be no debate about that.”

He then pivots, replacing smoking with ApoB and lung cancer with atherosclerosis, stating: “There is no ambiguity that ApoB is causally related to atherosclerosis.”

Peter even goes so far as to argue that not treating elevated ApoB—even if the a person’s overall major adverse cardiovascular event score is low—is “as idiotic” as permitting someone to smoke.

But here’s where I think Peter is wrong because causality is not the same as importance.

3/8) 🚨Again, here’s the point: Causality is not the logical equivalency of importance, nor does the presence of a causal stimulus necessitate a causal intervention.🚨

To illustrate, let’s return to Peter’s analogy: “If you believe [X] is causally related to [Y], then [X] cessation reduces the probability of [Y].”

Now swap smoking and lung cancer for oxygen and fire: “If you believe oxygen is causally related to fire, then oxygen cessation reduces the probability of fire.”

Technically true. But that does that mean I should deplete my environment of oxygen to prevent spontaneous combustion?

What Peter knows—but underemphasizes—is that causality does not imply sufficiency. And often, targeting a “causal” factor has consequences far beyond reducing the risk of the primary undesired outcome.

Yes, if I remove oxygen, I’m less likely to burst into flames—but I’ll also suffocate.

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Nick Norwitz

@nicknorwitz

Aug 30

The Molecular Gym: How Your Heart Trains from the Inside Out (🔗in 4/4)

1/4) Every time you exercise, you're not just straining a muscle — you're triggering molecular rewiring in your heart.

The truth is your heart is not “just a pump” — your heart is an endocrine organ, a nucleus of signaling, and a complex communication network...

2/4) But let’s ‘warm-up’ with an intellectually light fact that I bet you didn’t know: Exercise remains the only known physiological stimulus that promotes the generation of new heart muscle cells.

Let’s double-click on this: of all the environmental stressors and physical inputs into our body, only exercise causes the growth and development of new heart muscle cells in adult mammals.

This matters because the adult heart is known for being notoriously resistant to regeneration. Yet with exercise, that rule is bent, if not broken.

3/4) This special and specific adaptation occurs as the result of the deployment of a complex suite of molecular programs.

These include the secretion of cell signaling molecules from other tissues, and from the heart itself (so-called “autocrine signaling”), that bind to receptors on heart cells and trigger intracellular cascades.

Additionally, exercise changes gene expression in the heart, alters regulatory RNAs (microRNA and long non-coding RNAs), and changes the molecular tags on proteins (post-translational modification) to toggle their function like a dimmer switch or the brightness function on your phone.

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Nick Norwitz

@nicknorwitz

Aug 28

Seed Oils: A Provocatively Reasonable Take
*In anticipation of a 3.5hr debate between me and @paulsaladinomd 👉🔗to full letter at the end

1/10) I’m fascinated by the seed oil debate for two reasons:
(1) The data are complex and often contradictory
(2) It’s surprisingly hard to get people to hear what I’m actually saying—rather than what they assume from a headline, thumbnail, or opening remark.

Sometimes those assumptions are shaped simply by the framework of the conversation, such as the debate partner sitting across from me.

But in today’s newsletter, I’m taking a different approach:
🔥I’ll start by outlining, in broad strokes, what I believe and what I do.
🔥Then we will walk through arguments commonly made against seed oils and evaluate each.
🔥Finally, we will end with a set of questions I want you to ask yourself to help you decide what makes the most sense for your own and how to better assess such claims and arguments made about health and nutrition.

All the references are hyperlinked in the letter linked in 10/10

2/10) At a High Level: My Stance on Seed Oils

In short, I believe seed oils—here defined as highly industrialized and processed oils extracted from plants using “harsh” chemical and heating methods—are unnecessary at best and harmful at worst.

I personally avoid sunflower, safflower, corn, and canola oil in my diet (with the sole exception of one brand of salt-and-vinegar pistachios containing a light dusting of sunflower oil—an indulgence I admit in the spirit of transparency).

My decision follows the “precautionary principle.”
We still don’t fully understand these industrialized seed oils, but the balance of probability suggests they’re more likely to be harmful than beneficial—at least compared to more natural fat sources such as extra-virgin olive oil, unprocessed nuts and seeds, and, yes, animal-based fats like ghee or tallow.

3/10) Now, some of you may be thinking, “Wow, Nick. Way to be anti-climactic.”

But please pause and consider how I said what I said as compared to what is often said.

🛑I am NOT claiming that seed oils are “toxic engine lubricants in a conspiracy by Big Food and the academic elite to keep you sick.” While that may sound like parody, many of you know it’s a fairly accurate summary of a common belief.

My stance is simpler: I’m curious and suspicious. The evidence on whether—and/or to what extent—seed oils are harmful is unclear, so all else being equal, I choose fats I believe are more likely to be health-positive.

Do you see the distinction?

With that in mind—and with full transparency about my own decisions—let’s take a clear-eyed look at the most common arguments against seed oils.

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