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Nick Norwitz

@nicknorwitz

Jul 24

5 Facts to Know About Fructose vs Fruit

1. Fructose isn’t just “empty calories,” but a biochemically active molecule that can negatively impact your liver and mitochondria. But does that mean fruit is bad? No. (🔗 in 5/5)

2. The small intestine acts as a “fructose filter,” where moderate-dose fructose is bioconverted and “detoxed” before it reaches the portal vein heading to the liver. This system can handle a handful of blueberries but gets saturated and overwhelmed if you smash a large bowl of cereal and a tall glass of OJ.

3. Fruits are a large and heterogeneous group of foods that interact with a large and heterogeneous group of humans. Saying fruit is “healthy” or “unhealthy” is like judging all books in a library by one chapter of the first book you read—it oversimplifies something rich, varied, and context-dependent. (GIF just because it's hilarious)

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Nick Norwitz

@nicknorwitz

Jul 23

The Ketogenic Diet and the End of OCD Suffering
(🔗to full letter in 5/6)

1/6) Patient: “I used to tell myself in the depths of OCD, ‘The only way out is death,’ as a kind of mantra to put things into perspective. I’m happy to say I found another way. It would make me really happy if others knew about ketosis as a way to end their suffering.”

This dramatic quote, drawn from a new medical case series, describes one patient’s experience whereby they completely resolved their symptoms of debilitating obsessive-compulsive disorder (OCD) with a ketogenic diet. People with OCD can suffer terribly, sometimes to the point that death may appear a reasonable therapeutic, as was the case with this patient.

In today’s Newsletter, we discuss the case series at hand and why you should care, whether or not you or a loved one suffer with OCD. This is important for everyone to hear.

2/6) Patient A: Early Onset, Harvard Student

Patient 1 was a 22-year-old student at Harvard College, who first started exhibiting symptoms of OCD at 18 months. What began as consistent object alignment evolved into cleaning his friends’ toys, excessive handwashing, balanced twirling (if he spun twice clockwise, he’d need to spin twice counterclockwise to “balance things out”), balanced hugging and kissing, and exclusively symmetrical works of art. He was formally diagnosed with OCD at age 4.

The path that led this young boy to a ketogenic diet, like many others, was unexpected. Noting concerns about his weight, his parents supported him in removing grains from his diet, “unexpectedly noticing a dramatic reduction in his OCD symptoms.” Intensifying his dietary regimen towards a ketogenic diet at age 15 resulted in a “complete cessation of ritualistic behaviors” within two weeks.

Also, of note—and a key element in any ‘case experiment’—reintroduction of the independent variable (dietary carbohydrates sufficient to knock him out of ketosis) results in a change in the dependent variable (OCD symptoms). Indeed, excursions from the ketogenic diet consistently result in a return of symptoms for this patient (and for the others, as we will see). For instance, once while on vacation he indulged in a carbohydrate-rich meal. Shortly thereafter, he was found in his hotel room, late at night, organizing shampoo and conditioner bottles into neat rows.

Patient Perspective:
“The ketogenic diet was transformative for resolving my OCD, mood disorders, and focus issues. Without making the changes to my diet that I did, I would not have had the mental wherewithal to perform well enough in high school to get into Harvard, much less college.”

3/6) Patient B: Trauma-Triggered OCD

The second patient in this case series was a 35-year-old woman who developed symptoms of OCD at age 16 following a mass shooting near her school. The trauma triggered the development of overwhelming intrusive thoughts characterized by fear of loss. The obsessions were so severe she began to isolate herself from friends and family, ran away from home, and tried to harm her own head in a desperate attempt to alleviate the intrusive thoughts. She was formally diagnosed with OCD at age 20.

Again, the patient adopted a ketogenic diet serendipitously.

Again, the patient noted massive symptom improvements within two weeks.

Again, “[r]eintroducing high-carbohydrate foods triggers symptom recurrence, which she describes as feeling like ‘swimming in a lake as a thunderstorm approaches.’”
Patient Perspective:

“I used to tell myself in the depths of OCD, ‘The only way out is death,’ as a kind of mantra to put things into perspective. I’m happy to say I found another way. It would make me really happy if others knew about ketosis as a way to end their suffering.”

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Nick Norwitz

@nicknorwitz

Jul 20

The NEW Microbial Molecule Linking Diabetes and Heart Disease (🔗 in 7/7)

1/7) What if one molecule, made by the bacteria in your gut, could quietly sabotage your blood sugar and clog your arteries?

Meet “imidazole propionate” (ImP) a microbial molecule made by gut that is now metabolically linked to both diabetes and heart disease.

2/7) Let’s start with the most recent findings: a paper published in Nature just four days ago found that ImP was associated with atherosclerosis in two independent human cohorts (PESA and IGT) and was shown to cause atherosclerosis in an animal model.

Looking first at the human data: in both cohorts, higher ImP levels correlated with higher fasting glucose, increased markers of inflammation (such as hsCRP), more visceral fat, and lower HDL cholesterol—all signs of metabolic dysfunction.

What’s more, ImP levels directly correlated with the degree of atherosclerosis, as measured by vascular ultrasounds and coronary artery calcium (CAC) scores.

These are interesting associations. But—of course—we must ask: what came first, the chicken or the egg? In this case: the ImP or the metabolic dysfunction?

3/7) Unraveling the Evidence: Cause or Correlation?

To answer that question, we need animal models. So, the researchers injected mice with ImP or a control solution. They used two different mouse models to improve the generalizability of their findings. And, indeed, ImP caused atherosclerosis in both.

How? What is the causal mechanism?

ImP did not affect cholesterol levels. Instead, it caused an increase in the expression and activation of several inflammatory proteins and signaling pathways, including TNF-alpha cytokine signaling, NF-κB signaling, and expansion of pro-inflammatory Th17 immune cell populations.

In short: ImP heightened the inflammatory, atherogenic environment.

They also found—or more accurately, confirmed—that a key player in this pathway was the protein complex mTOR. I say “confirmed” because this link was first identified in a 2018 Cell paper, when researchers discovered that ImP is elevated in type 2 diabetes and causes insulin resistance.

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Nick Norwitz

@nicknorwitz

Jul 14

Omega-6/3 Ratio: What the Science Says about Mortality (🔗 in 5/6)

1/6) Perspective shapes everything. Sometimes, we can flip our viewpoint easily. But sometimes, the more informative lens takes effort to uncover. That’s what we’re going to do together in today’s newsletter — unpacking the story of Omega-3 and Omega-6 fats and why the ratio can be misleading.

As a brief primer: Omega-3 and Omega-6 fats are both essential nutrients — we need to consume them in our diets. However, the common belief is that, while both classes are essential, Omega-3s are “heart-healthy,” “brain-healthy,” and more is generally better for you.

Omega-6s, on the other hand, are considered easy to overconsume in modern diets, especially through processed foods and industrial seed oils. They can also be converted in the body into pro-inflammatory compounds.

What’s more, research consistently suggests that the balance between these fats matters. A lower Omega-6/3 ratio is associated with better health outcomes — including reduced cardiovascular risk and lower all-cause mortality.

So, it's understandable why many conclude: Eat more Omega-3s; Eat less Omega-6s; Improve your 6/3 ratio — and better health will follow. Sounds reasonable, right? Hold that thought.

And remember our theme: perspective. Because the full story of these fats is a more complex than the ratio alone might suggest.

2/6) In the study I want to review with you, researchers measured blood levels of Omega-6 and Omega-3 in 85,425 people and followed them for an average of 12.7 years. Over that period, 6,461 participants died of various causes. The researchers examined the association between fat levels and mortality — including the Omega-6/3 ratio.

They found that higher Omega-6/3 ratios were associated with a greater risk of death. Specifically, the highest quintile (median ratio of 14.8) exhibited a 26% increased risk of all-cause mortality relative to the lowest quintile (median ratio 5.9).

So once again, the conclusion seems clear: High Omega-6/3 ratio = bad. Lower ratio = good. Therefore, eat less Omega-6, more Omega-3, and you’ll optimize the ratio. Right? Well… not so fast…

3/6) Both Omega-6 and Omega-3 Associate with Better Outcomes

The researchers ran additional analyses — this time looking at Omega-6 and Omega-3 levels individually rather than as a ratio.

And the result? Both higher Omega-6 and higher Omega-3 levels were independently associated with lower all-cause mortality. In other words, more Omega-6 in the blood = better outcomes. More Omega-3 = better outcomes.

And the effects compounded!

The group with the highest Omega-3 and highest Omega-6 levels had the lowest mortality risk — a relative risk of just 0.48. That’s a 52% reduction in all-cause mortality.

So, higher circulating levels of both fats may be beneficial, but Omega-3 appears to have a stronger effect. When we analyze the ratio, it gives the impression that more Omega-6 in the body is worse; however, we are now starting to see how that story can be misleading.

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Nick Norwitz

@nicknorwitz

Jul 12

How Stress Steals Your Willpower – And How to Steal It Back (🔗in 4/4)

1/4) A new study, published in Nature, explores how chronic stress rewires the brain. It shows that stress shuts down flexible, goal-directed thinking and pushes us into rigid, automatic habits. Let’s break down how it works.

🧠DMS. - The Hub of Willpower🧠

The dorsomedial striatum (DMS) is a brain region that plays a central role in action–outcome learning and goal-directed behavior. For simplicity, think of the DMS as the brain’s hub for agency and willpower.

In fact, when DMS activity is suppressed, people tend to lose a sense of control — and fall into inflexible, often unhelpful, habits.

✌️Two Pathways: Learning vs. Habit.

The DMS sits at a crossroads of two pathways. The “Learning” pathway leads to flexible, thoughtful behavior, whereas the “Habit” pathway… well, that one is obvious.

🧠“Learning Pathway” The basolateral amygdala (BLA) activates the DMS, supporting action–outcome learning and goal-directed decision-making.

🧠 “Habit Pathway” - The central amygdala (CeA) sends inhibitory signals to the DMS, promoting automatic, rigid habit formation.

2/4) To summarize:

BLA → DMS = learning and flexibility. Think BL = Brain Learning.

CeA → DMS = habits and rigidity. Think Ce = Craving Enforcer.

😩Chronic Stress Turns the Dial Toward Habits😩

The researchers found that chronic stress weakens the Learning Pathway (BLA → DMS) and strengthens the Habit Pathway (CeA → DMS).

In their study, mice exposed to mild, unpredictable stressors — like a tilted cage, damp bedding, or mild foot shocks — started falling back on ingrained habits. They’d press a lever for food even after they were satiated, just because that’s what they were used to doing. Sound familiar?

3/4) The human equivalent is exactly what I’m sure you’ve experienced from time to time. I know I have. When we’re under chronic stress, that goal-oriented Learning Pathway (BLA → DMS) pathway gets dialed down — making it harder for us to connect our actions with their results. At the same time, stress activates the Habit Pathway (CeA → DMS) — this leads to repeating behaviors without thinking, even if they’re not helpful.
This all means less agency and more “Why did I just eat a tub of Chunk Monkey while watching Harry Potter until 1 am again?” moments.

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Nick Norwitz

@nicknorwitz

Jul 10

How Weighted Vests Trick Your Body into Losing Weight
(🔗 in 9/9)

1/9) Remarkable research is showing how mechanically loading your skeleton can toggle your brain to decrease hunger.

In today’s letter, I want to walk through three studies, including two human RCTs and a third study that blew me away!

2/9)👉Study #1 (RCT): Short-Term, Big Impact
In a proof-of-concept pilot trial, 72 participants with obesity were randomized to wear a weighted vest (11% body weight) or a non-weighted vest (1% body weight) eight hours per day for three weeks.

The study wearing the weighted vest resulted in statistically significant weight loss over just three weeks (1.61 kg). Furthermore, all of this weight loss was fat loss (-1.73 kg), with a +0.20 kg change in lean mass. Even for people with obesity, losing fat without losing (or maybe even gaining?) muscle over a short time period is impressive.

But this study was just three weeks. What happens if one were to wear a weighted vest for much longer?

3/9) Study #2 (RCT): Long-Term Weight Loss Defense

In another randomized controlled trial, participants were randomized to wear a weighted vest (~6 kg for 6.6 hours per day) for six months or to a control group. But this study came with two additional features.

First, during this six-month phase, both groups were placed on a strict, very low-calorie diet (1,100–1,300 Calories).

Second, all participants were then followed for an additional 18 months after the intervention ended. In other words, for 0–6 months people ate a very low-calorie diet with or without wearing a weighted vest; and then for 6–24 months people were left to live their lives freely without the weighted vest or a diet.

Both groups lost the same amount of weight during the initial six-month intervention, likely owing to the very restrictive nature of the diet. But what happened next was fascinating…

While the control group gained all their weight back, the weighted vest group only gained half the weight back.

In other words, weight regain was twice as much in the control group as compared to the weighted vest group after the intervention ended.

This suggests there was a ‘lingering’ metabolic effect of wearing the weighted vest. Weird? How? What’s going on?

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