Nick Norwitz MD PhD Profile picture
Dec 31, 2022 12 tweets 6 min read Read on X
My YouTube w @KenDBerryMD on #Entomophagy has gotten 🔥 responses!

Should I back off? Probs

But instead, I CHALLENGE YOU 🫵 to put aside emotions & watch 1 of these videos

11 m:
45 m:

1/ NOW for 🧵 on 5 MYTHS about eating Bugs!
A DISCLAIMER

I am NOT trying to take your meat
I am NOT saying meat is unhealthy
I am NOT trying to force you to eat bugs
I am NOT trying to force you to eat bugs
I am NOT trying to force you to eat bugs

I AM asking you to set aside emotion and have an open mind

Begin...
2/ MYTH #1) People only eat bugs if they need to

Entomophagy is a cultural practice

The "eww" factor is entirely psychological

Many cultures eat bugs as delicacies, EVEN when meat is also part of the diet

Norms change. Take🦞a large bug that used to be considered slave food
3/MYTH #2) Bugs aren't as nutritious as other animal foods

👉Cricket & meal worm have similar amounts of protein to beef (~20g/100g)

👉Protein in bioavailable

👉All essential amino acids

👉Rich in micronutrients, e.g. cricket has 2.5X or more iron than beef
4/ MYTH #3) Chitin in bug exoskeletons is toxic

Most human express chitinase (CHIA gene) to break down chitin

Gut microbes can produce chitinase enzyme too

Even if not all digested, it's a fiber. You poop it out, like the cellulose in a stalk of celery
5/ MYTH #4) Bugs all have anti-nutrients and toxins that are bad for you

Many bugs are low in anti-nutrients

True, there can be concerns, e.g. Thiaminase in African silkworm, exposure to mycotoxins, allergies, etc.

However... (con't)
6/ One could make a similar argument for any food

Eating improperly prepared pork has the risk of tines egg ingestion, with development of neurocysticercosis, holes in the brain, and seizures

Getting bitten by a lone star tick, and you can have a meat allergy
7/ The point here is that one shouldn't argue that a food group is bad because practices relating to the food need to be improved or people have individual sensitivities.

Do we need good safety regulations and sensible farming practices. Of course, but it's not the bug per se...
8/ MYTH #5 More bugs means less meat!

YES! THIS IS A MYTH! More bugs can actually mean more meat. Here's how...

We waste an absurd amount of food! 1.8 BILLION TONS per year, which simply generates waste and emissions

But what if this could be upcycled into animal feed?
9/ Meet the black soldier fly

They love eating decaying matter, grow insanely fast & produce high quality protein

They could not help get rid of our 1.8 Billion tons of wasted food and reduce emissions

& help treat undernutrition

& be used as high quality livestock feed
10/ In summary, I'm not trying to take your meat, or make you eat bugs

But I am asserting that it's essential we separate emotions from science

Otherwise, science is just another form of religion
11/ Now, if you have the courage, I encourage you to RT this thread in order to help normalize nuanced scientific discussion

@KenDBerryMD @DoctorTro @realDaveFeldman @AdrianSotoMota @ifixhearts @Cooking_it_Keto

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More from @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 Image
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.Image
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). Image
Read 6 tweets
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 referencesImage
Image
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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. Image
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.Image
Read 6 tweets
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
💪ProtocolsImage
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.Image
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
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.Image
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. Image
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+?Image
Read 9 tweets
Jan 2
Escape the Black Hole of Sugar Cravings

1/4) Why can some people say no to dessert, while others feel pulled toward sugar like it's a black hole?

It's NOT a failure of willpower.

🦷But before we start, tell me: do you have a sweet tooth? What's your dietary Achilles' heel?
2/4) Human data show that levels of a nutrient sensor, FFAR4, are reduced in diabetes, are negatively associated with fasting blood sugar, and are even linked to metabolic health in mendelian randomization studies. Image
Image
3/4) The researchers dissect a fascinating cascade whereby this nutrient sensor alters the microbiome to change GLP-1 and FGF-21 signaling to alter brain signaling and sugar cravings.

Sugar cravings aren't about willpower. THey're about metabolism. Image
Read 4 tweets
Dec 30, 2025
How Lp(a) Really Causes Heart Disease

1/9) New study finds that high Lp(a) increases the risk of death from CVD by as much as 230%.

Since Lp(a) is thought to be genetically determined, some people think if you have high Lp(a), you’re screwed.

🚨But I don’t think so... Image
Image
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2/9) The researchers studied 1,027 patients with advanced coronary artery disease who were undergoing cardiac surgery.

The conventional view is that Lp(a) and related molecules promote atherosclerosis by physically sticking to the artery wall, infiltrating it, and essentially “seeding” plaque.

But there’s more to the story…Image
3/9) The researchers found that patients with higher Lp(a) also had higher levels of a molecule called “superoxide” (O2×).

And no, despite the name, it’s not Superman of the molecular world. It’s not a hero—it’s a villain.

O2× is a reactive oxygen species. It fuels oxidative stress and inflammation—core pathologies that can drive atherosclerosis.
Read 9 tweets

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