Robbie Bourke

[Robbie Bourke @RobbieBourke]

Part 1/18:

The problem

Chronic wearing of sunglasses contributes to circadian disruption, and circadian disruption leads to disease.

The primary role of the eye is perception of light - which provides information - which regulates our physiology.

[Robbie Bourke @RobbieBourke]

@the_no_mind What book is this from?

[Rusty ⚡️: Solar Powered ☀️ @ze_rusty]

Most people carefully track what enters their mouth

Almost nobody tracks what enters their eyes

More important than your macro ratio.

Your sunlight-to-screen ratio.

Want better numbers?

Just go Outside

[Jake Tuura @jake_tuura]

Weakness precedes injury.

It’s actually a difficult claim to validate with research but I found a piece that did it.

Those who had a peak isometric force of 1.8x bodyweight (on a single-leg) went on to injury their calf or Achilles.

Those who had a peak isometric force of 1.92x bodyweight stayed healthy.

In elite sport, with the fear of Achilles ruptures, it’s wise to check the box here and test peak plantarflexor force.

https://t.co/FsYo1pM2I9

[Dr. Rhonda Patrick @foundmyfitness]

Strength training for 90-120 minutes per week is associated with up to a 30% lower risk of death from all causes, CVD, cancer, and neurologic disease.

That seems to be the upper limit - no additional benefit was observed above 120 minutes of strength training per week.

These benefits were independent of total aerobic activity, but combining strength training with ~5-15 hours of moderate-to-vigorous-intensity aerobic activity reduced all-cause mortality risk by 45%!

Clear message here is: "do both."

[Chris Bishop @DrChrisBishop]

📄 New paper now online ahead of print in @NSCA’s #SCJ.

🔑 It challenges the notion of S&C being aligned purely to “athletic performance” and how the evidence base for injury risk and over-arching health is arguably greater.

🔗 Link to full text here: https://t.co/9VLNTv4TiK.

[Dan Howells @HowellsDan]

A brilliant session with @Jessepgreen this last week meant we got to go deep on COD analysis and exercise prescription with @1080motion

If you'd like access to the full recording, comment '1080' and I'll send you a link to gain access!

[Matt Gates @MattGates_XPE]

Wow, that is a bound. One of the first things we teach on the ground and on the shredmill. Not sure we’ve never had someone end up looking like this though.

[⚡️ The Blue Light Diet ⚡️ @BlueLightDiet]

My dermatologist bever told me this. She says its the sun causing my skin problems.

But skin damage could be from blue lit screens, blue spiked artificial LED lighting and the windows in my car and house artificially increasing the amount of blue light they let through...

Is my dermatologist stupid or unaware of what really causes skin damage?

[Thomas P Seager, PhD @seagertp]

Brown fat is an essential organ, which is why babies are born with so much of it. But because adults spend their lives in thermal comfort, over 95% of Americans >45 years old have zero detectable brown fat.

This is a clip from when @MaxGulhaneMD hosted me on his Regenerative Health podcast.

[MitohormesisClub @MitohormesisAct]

🚨 Your Liver’s Fat-Burning Switch Just Got Upgraded 🔆👑

No consistent morning sunrise = your liver struggles to burn fat.

Here’s what the latest science actually says:

2021 Discovery
Your liver has a built-in “day/night timer” for burning fat.

A protein called HRD1 acts like a smart brake:

• During the day (when you eat) → HRD1 is high → turns fat burning OFF

• At night (when you fast) → HRD1 drops → turns fat burning ON

This keeps everything perfectly timed.
2026 New Discovery

Scientists found HRD1 does even more. It also controls special “molecular post-it notes” (called m6A) on your fat-burning instructions.

This fine-tunes how well and how long your liver can burn stored fat.

Together, these two papers show your liver doesn’t burn fat randomly — it follows a solar-powered schedule.

The Big Takeaway

Morning sunlight is what sets this entire timer correctly.

No consistent sunrise (or too much artificial light at night) = the timer gets messed up → fat burning becomes weak and poorly timed → weight gain, low energy, fatty liver risk.

Simple Fix:

See the sunrise every morning + eat within daylight hours.

Free gift 🎁 → no sunglasses. Bare as much as possible. Earth barefeet. Make sure no stray voltage area. Dirty electricity
Free gift 🎁 → consume breakfast after 40mins of sunrise. High quality fatty protein BASED.

Your body already knows what to do when it gets the right light signal.

Science keeps proving it: Light is the original fat-burning medicine. 🌅

Who’s committing to morning sun this week? Drop a 🔥 below.

Kola Adetu
Mitohormesis Timer
Your Ultimate Quantised Health Coach

Head to my bio for 1 on 1 consultation. You don’t have wander alone in the dark

#MorningSun #FatBurning #LiverHealth #CircadianHealth #SimpleScience​​​​​​​​​​​​​​​​​​​​​​​​​​​​​​​​​​​​​​​​​​​​​​​​​​
#CircadianHealth #QuantumBiology #HRD1 #PPARα #m6A #MorningSun #FatBurning #LiverHealth #ScienceThread

[Louisa Nicola @louisanicola_]

Your ability to burn fat is not determined by willpower.

The limiting factor is your mitochondria. The study found that individuals with greater mitochondrial abundance achieved significantly higher peak fat oxidation, independent of aerobic fitness. Fat metabolism is not a motivation problem. It is a cellular infrastructure problem.

The biology of performance begins long before the workout starts.

[Thomas P Seager, PhD @seagertp]

Biophotons are the sunshine your mitochondria make inside your body.

You already know that during cold thermogenesis mitochondria in brown fat cells produce far infrared (FIR) light called heat. Well, they also produce other wavelengths -- including ultraviolet (UV).

It's the UV light of cold thermogenesis that boosted the blood serum levels of Vitamin D in a cohort of Polish women with multiple sclerosis undergoing a whole-body cryotherapy regimen under the supervision of researchers at the University of Krakow.

Your body is such a beautiful, complex system. It knows how to make its own sunshine during the winter, when it's dark and cold outside... as long as you're willing to give it the cold it needs to do it.

[Zaid K. Dahhaj @zaidkdahhaj]

I have some questions for modern dermatology

1. UV-B drives Vitamin D3 production, which has documented anti-tumor activity in melanocytes. Why is the molecule that suppresses tumor growth blocked by SPF 50 to the tune of 98%?

2. Why do you recommend Vitamin D supplementation, when VITAL, the largest randomized trial of its kind, showed that it had zero beneficial impact on lowering all cause mortality, whereas sun seeking behavior shows a dose dependent relationship with lowering all cause mortality?

3. Darker skin means more melanin and dramatically lower melanoma rates. Why isn’t the clinical recommendation to upregulate melanogenesis through structured circadian aligned sun exposure?

4. In situ melanoma grows faster than invasive melanoma. Mortality falls while incidence climbs. Are you detecting disease or expanding a diagnostic category?

5. Nine dermatopathologists reviewed biopsy specimens from 20 years prior and reclassified lesions originally called benign as melanoma.  If the same tissue can be called benign in one decade and malignant in the next, what exactly is the diagnostic standard being used?

6. Expert skin pathologists frequently disagree when distinguishing harmless moles from early cancer, and there is no single criteria that can confirm melanoma without doubt.  Why is a diagnosis with no definitive criteria generating a public health panic about a rising epidemic?

7. The proportion of Medicare patients biopsied annually nearly doubled between 2004 and 2017, and melanoma incidence in people over 65 doubled over the same period.  How is that a coincidence and not a direct measurement of billing behavior?

8. Dermatologists have a financial incentive to perform biopsies.  Which other disease epidemics are built on diagnostic procedures that directly revenue the diagnosing physician?

9. NRF2 is circadian controlled and governs DNA repair enzyme expression in skin cells. Circadian disruption suppresses it. Why is this absent from every melanoma etiology model?

10. DNA repair peaks at specific circadian phases. Shift workers show measurably impaired repair. Why is UV damage modeled as dose-dependent when the repair side is time-dependent?

11. Circadian disruption flattens cortisol, which degrades NK cell surveillance. Why is melanoma never framed as a failure of immune clearance rather than purely an initiation event?

12. Sunscreen use has risen over the same 40 years melanoma incidence has risen. If it blocks the causal agent, why does the intervention track with the outcome?

13. Sunscreen blocks UV-B more than UV-A. UV-B makes vitamin D. UV-A penetrates deeper and generates ROS without triggering vitamin D synthesis. What is the net biological effect of that ratio shift, plus systemic absorption of endocrine-disrupting compounds?

14. Highest sunscreen compliance populations are not lowest melanoma rate populations. Where is the dose response relationship?

15. The melanoma prevention model was built on sunburn studies of outdoor workers, then applied wholesale to a cancer that appears in places sunlight never reaches. Who signed off on that transfer?

16. Melanoma in situ is 50 times more common now than it was in 1975.  A 50x increase in a non-invasive lesion that cannot metastasize, over 50 years of rising sunscreen use. What causal model explains that?

17. An estimated 89% of white men and 85% of white women diagnosed with in situ melanoma are likely overdiagnosed.  The institution calls in situ melanoma Stage 0 cancer and treats accordingly. What is the harm calculus of treating a lesion with a 85-89% chance of never becoming dangerous?

18. Melanoma diagnoses are six times higher than 40 years ago while mortality has remained broadly stable.  Every genuine epidemic, infectious or otherwise, produces a mortality signal. Where is the mortality signal that justifies calling this an epidemic?

Any answers would be great!

[no.mind @the_no_mind]

This is Clint Ober.

He spent 30 years grounding electrical systems in the cable industry.

Then he asked one question medicine never asked:

What happens when the human body is no longer connected to earth?

The answer is 40+ studies & a mechanism behind chronic inflammation: 🧵

[MitohormesisClub @MitohormesisAct]

When leptin signalling [the quantum energy accountant] is not registering at hypothalamus, you become food guru on steroids, you become a supplement dealer and you become a lean meaning running machine. Too insane to sit down and read circadian medicine 101

You can get jacked BUT visceral fat only obey circadian and photonic medicine

[Zaid K. Dahhaj @zaidkdahhaj]

For the most part, there is only one human chronotype, and it rises with the sun and sleeps relatively shortly after nightfall

People’s minds have been hijacked through marketing to believe that a chronotype is a personality trait. That they’re a “bear” or a “dolphin”

This is New Age pseudoscientific bullshit

A chronotype is simply the timing of when your body naturally wants to sleep and wake, based on how it’s currently synced to light and darkness. It’s the time of day your body clocks are set to under current environmental conditions

The key words to remember are “under current environmental conditions” as we discuss artificial light and circadian disruption

Studies on hunter-gatherer populations with no artificial light show sleep timing clustering within about a 2 hour window across all individuals

2 hours

The 4 to 6 hour spread we see in modern populations is not a matter of genetic expression. A “night owl” doesn’t exist. That is the result of circadian disruption

The genetic variation in chronotype is real but modest, and it lives almost entirely in a handful of clock genes

The core ones are PER1, PER2, PER3, CLOCK, and CRY1. These genes encode the proteins that drive the transcription-translation feedback loop sitting at the heart of every cell’s 24 hour oscillator. Small mutations or polymorphisms in these genes can slightly lengthen or shorten the intrinsic period of that loop, which in turn shifts the phase of the whole system earlier or later

The most studied example is a mutation in CRY1 that extends the intrinsic clock period to around 24.5 hours instead of the normal 24.2. That half hour difference compounds over days and pulls sleep timing progressively later

People carrying this variant have what clinicians call Familial Delayed Sleep Phase Disorder. It’s heritable, it’s real, and it genuinely resists behavioral correction. But, people need to understand that this is a disorder. It sits at the extreme tail of the distribution

PER3 has a well documented length polymorphism, meaning some people carry a longer version of the gene and some carry a shorter one. The longer variant correlates with earlier sleep timing and stronger homeostatic sleep pressure, meaning those people feel the cognitive consequences of sleep deprivation harder and faster. The shorter variant correlates loosely with later sleep timing and slightly more resilience to sleep loss. This is probably the most relevant polymorphism for what people casually call chronotype

The CLOCK gene has a variant associated with evening preference and is also linked to higher rates of mood disorders and metabolic dysfunction, which itself tells you something important, that evening shifted genetics carry health costs, which suggests the ancestral optimal is morning anchored

Now here’s what ties it all together from a circadian standpoint:

These variants do NOT change what your circadian clocks responds to. Light still entrains every genotype. The variants just shift the default period slightly, so a genuinely late running clock needs a stronger morning light signal to land at the same phase as a neutral genotype. Same prescription, but higher dose

Most people claiming a genetic chronotype have never tested that under ancestral circadian aligned light conditions

Hunter-gatherer populations carry the same genetic diversity as industrialized ones, but show dramatically narrower sleep timing variance. The genes are there, but the environment just stops amplifying them

[Louisa Nicola @louisanicola_]

Most people think exercise benefits the brain because it increases blood flow.

That is only part of the story.

Every workout triggers a cascade of biological signals from muscle, heart, liver, adipose tissue, and immune organs. These molecules travel throughout the body, influencing inflammation, energy metabolism, neuroplasticity, and cellular repair.

The result is not simply a healthier body.

It is a brain that processes information more efficiently, adapts more effectively, and resists degeneration for longer.

Your cognitive performance is not determined by the brain alone.

It is the product of constant communication between every major organ system in the body.

Exercise strengthens the entire network.

[no.mind @the_no_mind]

A banana in January in New York floods your mitochondria with deuterium.

Your body has no tools to handle it.

Dr. Laszlo Boros — former professor of pediatrics at the UCLA School of Medicine & pioneer of deutonomics — explains why seasonal & local eating isn't just a dietary preference.

It's a fundamental requirement for mitochondrial function.

Three independent mechanisms explain why.

1) Sunlight and photon pressure:

Tropical fruits are naturally high in deuterium — the heavy isotope of hydrogen that causes ATP synthase nanomotors inside your mitochondria to stutter and break.

In equatorial regions, high-intensity red and infrared sunlight penetrates the body and decreases the viscosity of water inside mitochondria — allowing the nanomotors to keep spinning despite the deuterium load.

Eat that same banana in a dark New York winter — without the corresponding sunlight — and your mitochondria receive the heavy fuel without the light needed to process it.

The nanomotors stall.

2) Microbiome desynchronization:

Your gut microbiome is your primary deuterium filter.

Here's the mechanism most people miss:

Bacteria actively collect deuterium to fuel their own division.

They run their nanomotors in reverse — pumping clean protons out while trapping heavy deuterons inside their cells.

As they ferment your food, they strip out the deuterium and release deuterium-depleted metabolites — short-chain fatty acids and ketone bodies — back into your gut for clean energy production.

The trapped deuterium gets excreted in your stool.

But this filtering mechanism only works when your microbiome is adapted to the food you're eating.

Bacteria are highly specialized.

They only efficiently metabolize a narrow range of substrates.

When you eat a consistent local diet — your microbiome develops a stable tailored population that knows exactly how to extract deuterium from those specific local foods.

When you introduce an imported tropical fruit in winter — your gut bacteria are caught off guard.

They haven't adapted to this foreign substrate.

They can't ferment it efficiently.

They can't trap the deuterium fast enough.

It slips past the gut's mucosal barrier directly into your circulation — and into your mitochondria.

3) Nanomotor stutter and metabolic crowding:

Inside your mitochondria are ATP synthase nanomotors — spinning at up to ~9,000 rotations per minute to pump protons and produce energy.

A deuteron is twice as large and twice as heavy as a normal proton.

When it enters these fast-spinning motors — it acts like a medicine ball thrown into a precision engine.

It becomes stuck.

The nanomotors stutter and break.

The consequence is metabolic crowding.

With the motors destroyed, protons can no longer return to the mitochondrial matrix to mix with oxygen and form metabolic water.

Complete biological combustion stops.

Just like an engine choked with fuel but lacking a working exhaust — your mitochondria can no longer fully burn incoming carbohydrates, fats, and proteins into their natural end products of carbon dioxide and water.

The unburned fuel backs up and piles up inside your cells.

Your body stores it as visceral fat, excessive glycogen, or abnormal proteins.

This is metabolic crowding.

And it is the biochemical root of obesity, diabetes, and cancer.

Boros:

"When you walk into a department store and you see those shiny apples and watermelons from wherever they're from — it's really not your food. First of all, it doesn't grow there, especially not in that season. And when you eat it, you don't have the light exposure, the oxygen partial pressure, and you name it."

Eating locally and seasonally isn't a wellness trend.

It's what your mitochondria were built for.

[Zaid K. Dahhaj @zaidkdahhaj]

Bryan Johnson restricts UV-B exposure, parrots modern dermatology mindlessly, then takes 2,000 IUs of Vitamin D from an exogenous source

This is the idiotic, iatrogenic loop

Remove the source, sell the isolated downstream product back, ignore everything else the source

Does he know that there are 20+ metabolites of vitamin D produced from UV-B exposure?

Of course not

And the greatest irony here is that the supplementation literature undercuts him

VITAL, the largest randomized vitamin D trial, was broadly null for cardiovascular events and cancer incidence

If oral vitamin D reproduced the benefit of sun, those trials should have lit up, but they didn’t, which is the strongest available evidence that sunlight’s value is not reducible to serum 25(OH)D

He’s replacing a multiplexed circadian hormone with a single molecule and assuming equivalence

[Andy Galpin, PhD @DrAndyGalpin]

New Perform with Dr. Andy Galpin episode: How to Think Clearly in an Age of Distraction | Sam Harris

0:00 Introduction & Sam Harris
2:30 Intelligence, Smartness & Wisdom
16:13 Outsourcing Cognition: AI as Tool vs. Competitor
21:19 The Death of Boredom & the Inner Voice
30:07 Mindfulness & Three Paths to Mental Freedom
42:20 Overcoming Resistance to Meditation
1:01:25 Psychedelics vs. Meditation
1:09:01 Emotion, Reason & Handling Criticism
1:28:06 Process, Expertise & the Scientific Crisis
1:50:44 Restoring Trust in Institutions
2:02:29 Consciousness, AI & the Hard Problem
2:16:18 Uploading, Teleportation & the Revenge of the Humanities
2:25:14 Closing

Includes paid partnerships.