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
1/6) A study published in Atherosclerosis found that 37% of individuals with “optimal” LDL (<70 mg/dL) still had measurable atherosclerosis.
That’s not a trivial number—but it does require nuance.
The first objection is familiar: a single LDL measurement may not reflect lifetime exposure.
Maybe these people lowered LDL later in life after years of higher levels?
But all participants were untreated—no lipid-lowering medications.
That makes it more likely that most had lifelong low LDL. Yet 37% still had atherosclerosis on CAC or carotid ultrasound.
🔗 Link to details at the end
PMID: 29751286
2/6) To be fair, this was modestly lower than the overall prevalence in the cohort (49%).
But a 12% relative difference, while not nothing, is a surprisingly small payoff compared to improving factors like blood sugar control or insulin sensitivity.
The punchline: across two diverse, untreated cohorts, having “optimal” LDL did not prevent atherosclerosis.
Not even close.
3/6) This is not to say LDL or ApoB don’t matter at all for anyone—it’s to say they’re only a small part of the puzzle. Yet LDL and ApoB dominate the cardio conversation, while risk factors related to global metabolic dysfunction—are consistently marginalized.
1/6) Today’s video on statins (linked below) dives into several key studies you need to understand, along with some provocative demonstrations that will definitely stick in your brain.
But in this short thread, let’s quickly review a few major takeaways...
2/6) Take Away 1: Across the board—whether you're looking at the 4S trial or more recent datasets involving cardiac imaging—a consistent pattern emerges:
People with good metabolic health and/or a zero-calcium score may see minimal benefit from statin therapy or LDL reduction.
Now, of course, there are nuances.
But broadly speaking, if your coronary artery calcium (CAC) score is zero, there's little to no reduction in cardiovascular events from lowering LDL.
3/6) And even if there is a tiny marginal benefit on subclinical progression at a population level (being generous)... does it outweigh the risks?
Statins are often treated as benign. They are not.
Side effects include—and go beyond—muscle pain:
↑ Insulin resistance
↓ GLP-1 levels (Shown, Atorvastatin vs Control)
↑ Risk of diabetes
Potential long-term muscle loss
Variable brain effects
This isn’t to say statins don’t have a place. It’s to say: the risk-benefit analysis must include actual risks.
Have High Lp(a)? You Need to See Today's Video covering a new 2025 study on Lp(a) and waist-to-hip ratio
1/5) Here's a quick breakdown...
The goal of this new study was to determine whether a measure of adiposity—waist-to-hip ratio—modifies the relationship between Lp(a) and cardiovascular disease risk.
2/5) To explore this, researchers analyzed data from 4,652 participants in the Multi-Ethnic Study of Atherosclerosis (MESA), following them over a median of 17.4 years.
The study stratified individuals based on Lp(a) levels defined as >50 mg/dL and investigated how this risk interacted with waist-to-hip ratio as a marker of central adiposity and visceral fat
*Lp(a) (nmol/L) = Lp(a) (mg/dL) x 2.15
3/5) And—remarkably—in individuals with a ↓ waist-to-hip ratio, Lp(a) levels were not significantly associated with increased cardiovascular risk…
New Study: Person Study Finds Statin Use Associated Decline in Muscle Mass
1/6) A colleague of mine—a medical doctor—texted me recently: “I’m stopping my statin.”
The new paper referenced concludes: “Continuous statin use is associated with a decline in muscle function and mass over time (25% decline in grip strength and 73% decline in appendicular lean mass compared to never- users).”
Let’s discuss. (links in 5/6 and 6/6)
2/6) We’ll break this up by discussing the cross-sectional (single time point) and longitudinal (over time) results.
Cross-sectional analysis: In the fully adjusted model, adjusting for age, sex, education, smoking, BMI, activity score, diet quality score, high blood pressure, diabetes, and so on, statin use was associated with lower grip strength and lower appendicular lean mass.
3/6) Longitudinal Analysis: Statin Use Associated with Steeper Muscle Decline
Echoing the prior analysis, continuous statin use was significantly associated with accelerated declining grip strength and lean mass.
*Nuance note: For those with keen eyes, we discuss the y-intercept in the full letter
TL;DR: Statins use is linked to fasting muscular decline.
2/8) As a quick recap, I recently did a self-experiment that can be summarized in just two words: Sardine Diet. After a couple weeks on this extremely high omega-3 diet, I became conspicuously cold-resistant.
This was weird.
And I wanted to understand what might be happening. So, I dug into the literature.
3/8) Here's what could be happening...
Metabolically active brown fat can convert omega-3 fatty acids into a hormone called 12-HEPE.
12-HEPE stimulates thermogenesis in brown fat and ramps up glucose uptake into muscle as well.
This ultimately promotes heat production, cold adaptation, and energy expenditure.
(1/8) Alzheimer’s disease is personal for me. In my early 20s, I discovered I carry the ApoE4/4 genotype—placing me at the highest genetic risk. I was terrified. But over time, that fear shifted to a realization:
👉A genetic predisposition is a vulnerability, not a destiny.
👉 Our choices shape our health trajectory more than our genes ever could.
Today, I want to share a piece of that puzzle: The Omega-3 Paradox.
👉The Signal: Data clearly shows eating fatty fish lowers Alzheimer’s rates and boosts cognitive longevity.
👉The Failure: Yet, large clinical trials using Omega-3 supplements often fail to protect the brain.
👉The Question: Why?
One answer lies in a specific delivery mechanism most people—and many researchers—overlook.
Here is the science of getting Omega-3s into the brain. 🧵👇
(2/8) So, why do supplements often miss the mark? The answer is likely the form in which the Omega-3s are packaged.
When you eat seafood, you ingest Omega-3s in diverse forms, including phospholipids. However, most supplements on the shelf provide them in other forms, like triglycerides.
The Form Matters…
(3/8) The Form of Omega-3 Matters.
Think of it like this: Consuming DHA as a free fatty acid triglyceride is like mailing a letter with no address. It enters your system, but it doesn't know where to go. It rarely reaches the brain.
But if you have phospholipid-bound DHA? That’s like sending a letter via express courier, straight to the correct neuron. More specifically, the “express courier” form is called Lyso-DHA.
This specific form has special access to the brain through a transporter called MFSD2A.
Without the phospholipid "address," the DHA gets lost in transit.