Grayson Smith

@ChrisMasterjohn @LepusNox I thought he eats 1.6g per kg of bodyweight. Shouldn’t that be plenty sufficient for any deficiency issues?

@LepusNox Oh I forgot. Hummus and baba ganoush are the real protein bombs. Gotta go reread Sinclair.

Cialis is treatment for arginine deficiency. Bryan takes drugs because he doesn’t eat enough protein.

@hbtCHIEFS Where did you get these stats about the boxes? I’d love to dig into it!

% of light boxes (6 or less defenders) faced: Chiefs - 1st (47.4%) Jags - 17th (37.6%) Seahawks - 30th (26.4)

Good god almighty look at the last stat 💀 Walker in KC (IF it happens) is going to change the game.

@ChrisMasterjohn Do you have any updated videos or articles on your views on cholesterol, targeted, ranges, what to test, choline influence, etc?

Except it isn’t. Dayspring argued with me over this that Daniel Steinberg’s seminal research showing oxidation of the polyunsaturated fatty acids in the LDL particle membrane is *the* central mechanism driving its accumulation in atherosclerotic plaque is “outdated” because “LDL aggregability” is an independent driver of macrophage uptake. Steinberg died a few years ago. But he was #3 just below Brown and Goldstein in LDL receptor fame and he chaired the 1984 NIH Consensus Conference that solidified the consensus that LDL-C “causes” heart disease, and his lab’s work laid out the central mechanism by which LDL particles wind up in plaque. The problem with Dayspring’s argument is that a) oxidation itself is a major driver of LDL aggregability and b) the other major driver is the ratio of choline to saturated fat, which just happens to also be a major determinant of fatty liver disease. The reality is every mechanism through which LDL particles wind up in plaques is completely separable from their concentration. There are zero drugs and zero clinical trials that can distinguish between the impact of concentration versus the impact of oxidation. This is a MECHANISTIC claim, not an “outcomes” claim so you MUST rely on mechanistic research to answer the question. On this mechanistic claim about concentration being the driver, Steinberg’s graph from 1983 remains undefeated, shown below. The range at which macrophage uptake of non-oxidized particles (bottom line) plateaus is massively below the physiological range, below an ApoB of 5 or an LDL-C of 7. Meanwhile, oxidation (top line) causes a 5-fold increase. So at physiological concentrations, concentration is irrelevant and oxidation is paramount.

@whohead1 @RemnantMd @ChrisMasterjohn lol how is he a charlatan? 😂

This is cool, but you can inhibit your own PCSK9 for free. If you are fat and insulin resistant, you can inhibit it with a low-carb diet. If you are lean and healthy, you can inhibit it with a high-carb diet. The reasons these are opposite is because it is regulated oppositely by bifurcated forks in the insulin signaling pathway, with the lipogenic fork promoting more PCSK9 and the glucosuppressive fork promoting less PCSK9, and being fat and insulin resistant biases insulin signaling toward preservation of the lipogenic fork and loss of the glucosuppressive fork. But don't forget: the whole point is to raise LDL receptor activity, and a) the LDL receptor is centrally governed by thyroid hormone, which you produce in response to efficient conversion of food to ATP in your hypothalamus providing you have enough protein, iodine, and antioxidant nutrients and b) the LDL receptor MOVES cholesterol, and all MOVEMENT self-evidently requires energy. In fact, there are five classes of ATP-dependent motor proteins responsible for the kinetic action of the LDL receptor. So you want to start by fixing your mitochondrial energy production and end with your totally free strategy of inhibiting PCSK9 with your diet if you still need to after that.

@theproof @BioLayne Unfortunately when I consume plant protein like chickpeas my hs-crp increases. Goes from .4 to 1.3. 🤦‍♂️

More protein from plants. People won’t like it - but … data > feelings @BioLayne

@hubermanlab How do you feel about zone 2 not being the primary stimulus for mitochondria and that higher intensities should be favored as the foundation? fisiologiadelejercicio.com/wp-content/upl…

This is an informative short read on why you need to lift heavy(ish) (for you) objects and also do cardio. Your massively elevated HR after heavy 15 rep squats isn’t sufficient.

@hjluks How do you feel about zone 2 not being the primary stimulus for mitochondria and that higher intensities should be favored as the foundation? fisiologiadelejercicio.com/wp-content/upl…

I hear this every week in my office: "Doc, my heart rate hits 150 during squats — that's cardio, right?" No. And if your cardiologist hasn't explained why, keep reading. 🧵

@JSaysHi @exlibjourno @kenklippenstein No it’s not. 😂 He’s a high volume poster. They don’t get as much views. And all his long form videos get hundreds of thousands of views per video.

@exlibjourno @kenklippenstein That is still extremely low for 7M subscribers.

Insane how much Ben Shapiro fell off

@kenklippenstein Why lie? His long form videos still get hundreds of thousands of views. Not every video will hit that view count when you’re a high volume poster. It’s literally how YouTube works. My god I love when the “good guys” lie to prove their superiority. Really works well.

@maxlugavere @ChrisMasterjohn says 1 pound of red meat is sufficient, 2 pounds of white (turkey/chicken)

Nonsense. You’d have to eat ~2.5 lbs. of red meat per day to attain a 5 gram dose of creatine. For brain effects, likely double that.

@grok @dave_tomzequet @drkeithsiau @grok if you’re already thin/fit are there actually benefits worth pursuing from fasting? Please use high quality sources. Fasting often seems to have similar benefits as caloric deficit and weight loss.

Yes, the core physiology in the video—glycogen depletion, fat mobilization, autophagy, cellular repair, and reduced inflammation—applies to thin people just like everyone else. These metabolic shifts are universal in humans during fasting. That said, thin individuals have smaller fat reserves, so they may hit ketosis faster but could break down muscle sooner in prolonged fasts. Shorter windows (like 16:8) tend to be safer. Consult a doctor before starting, especially if underweight.

The physiology of fasting

@grok @MarvinSexton15 @SCHDaccumulator If you plan on reinvesting dividends isn’t it just smarter to invest in VOO? More growth and less tax burden. And if you ever want dividend income in say 10-15 years, the wealth you made in VOO you can buy even more dividend income.

Generally yes for max long-term wealth if reinvesting everything: VOO's historical 10yr total return (~15% annualized) has beaten SCHD's (~13%), compounding to more principal over 10+ years (e.g., ~$2M+ extra on $3M after taxes/reinvest). But if you prioritize steady income without selling shares, SCHD's ~3.5% yield (vs VOO's 1.1%) delivers far more cash now (~$105k vs $33k annually on $3M), with 5-10% growth. Qualified div taxes apply similarly at 15%. Mix or choose based on your income needs vs growth goals.

For $31.74, you can add $1.05 to your annual income permanently. This income also grows 5-10% each year. $SCHD

@grok @MarvinSexton15 @SCHDaccumulator @grok so you’ll be wealthier and make more money if you invest your money in VOO rather than chase dividends?

With ~$3.02M in VOO vs SCHD: Annual div income ~$33K pre-tax (1.1% yield) vs $100K. After 15% qual div tax: ~$28K vs $85K. VOO has higher hist total return (15.2% ann 10yr vs SCHD 13.2%). After-tax reinvest (15% on divs): 10yr end value VOO ~$12.3M, SCHD ~$10M. So ~$2.3M more wealth in VOO. If withdrawing income only (no sales), SCHD gives more cash now but slower growth; VOO builds more long-term. Depends on income vs growth priority.

@SCHDaccumulator lol x.com/grok/status/20…

@theficouple “Millions are in this situation” My heart breaks for them.

We know someone who paid $390k for a home in 2020. They have a 30 year, 3.75% mortgage & home is now worth ~$550,000. They're outgrowing their home & need more space but buying a new home would 2-3x their housing costs. They feel trapped & millions are in this situation.

@grok @MarvinSexton15 @SCHDaccumulator @grok if you invested that money instead in VOO how much more money would out have made? Please factor taxes as well.

@MarvinSexton15 @SCHDaccumulator Based on those $SCHD numbers, to get $100k annual income you'd need about $3,022,857 invested. Calc: 100,000 × (31.74 / 1.05) That income grows 5-10% yearly too.

@Merlin_GemsOnly @TheChiefNerd @ianmiles EXACTLY! Beat me to it. Literally the last 20+ years Sam has had takes like this.

@TheChiefNerd @ianmiles There’s literally no pivoting here whatsoever- Sam’s been arguing like this for years and years- your opinion of Sam has most likely been formed by 20s clips of him on Twitter lol

SAM HARRIS: “No one was more disadvantaged, based purely on the superficial characteristics of skin color, than white men for a very long time.” Don Lemon loses it… 😂

@hjluks Can anyone link the post? Not sure the reference! Thanks!

Yesterday’s post about heart rate and base building triggered a number of responses from experienced runners saying, “But I run at 145+ HR, and I’m fine.” That reaction actually highlights how poorly understood the distinction between cardiovascular fitness and aerobic fitness still is, even among dedicated endurance athletes. Let's explore this a bit... Most runners run too fast on their slow days and too slow on their fast days. Cardiovascular fitness refers to the delivery system. It reflects how effectively the heart pumps, how well blood flow is distributed, and how efficiently oxygen is transported to working tissues. Aerobic fitness, however, is primarily about utilization. It reflects how well the muscles use the oxygen delivered through oxidative metabolism, including mitochondrial function, fat oxidation capacity, lactate handling, and overall metabolic efficiency. These are related systems, but they are not interchangeable, and one can be well developed without the other being optimized. It is entirely possible to have strong cardiovascular fitness and still operate with relatively high metabolic cost during steady-state efforts. This is particularly common among recreational runners and even among experienced non-elite endurance athletes who have spent years training at moderate intensities. They are durable, consistent, and capable, but their “easy” work often occurs at a higher fraction of their physiological capacity than they realize. When an athlete reports that their easy runs consistently sit in the mid-140s (above 75% of maxHR), it does not reflect poor fitness. In many cases, it reflects a well-trained cardiovascular system paired with a habitual training intensity that sits near or above the first lactate threshold. The effort may feel subjectively easy due to years of adaptation, but metabolically, it is not truly low-intensity work. The body relies more on glycolytic pathways than on oxidative metabolism, even during easy runs. This matters because the full development of the aerobic system is driven by sustained training below the first lactate threshold. While higher intensities absolutely stimulate mitochondrial biogenesis, the adaptations associated with metabolic efficiency—improved fat oxidation, expanded capillary density, lower lactate production at submaximal workloads, and reduced sympathetic strain—are most robust when a significant portion of training occurs at genuinely low intensities. In other words, intensity can build fitness, but extensive low-intensity volume refines efficiency. When most training time is spent at or above LT1, athletes often become very good at tolerating moderate metabolic stress rather than minimizing the cost of aerobic work. At elevated hr intensity, oxidative stress per session is higher, sympathetic activation remains elevated, and the recovery burden accumulates over time, even if the athlete feels subjectively comfortable. RPE can remain low while physiological strain remains moderate, particularly in experienced runners who have adapted psychologically to that level of effort. In my office, it is clear that there is also a practical clinical layer that becomes increasingly relevant in midlife. The cardiovascular system adapts relatively quickly to the stress of training. Connective tissues—tendons, fascia, cartilage, and bone—adapt much more slowly. When moderate-to-high metabolic load is layered onto repetitive impact before true aerobic efficiency and tissue resilience are established, the total recovery demand rises. This pattern is reflected in the training errors I see routinely in clinic: Achilles pain, plantar fasciitis, patellofemoral symptoms, and lateral hip or gluteal tendinopathy. They are usually mismatches between the distribution of training intensity and our recovery capacity. This changes with age... and it will catch up to you. None of this means that running at higher heart rates is inherently harmful, nor does it suggest that intensity should be avoided. Threshold work, tempo runs, and even high-heart-rate sessions are valuable tools. The issue is distribution. If most weekly mileage is performed at a moderate metabolic intensity, the athlete maintains cardiovascular fitness but sacrifices some metabolic flexibility and efficiency. Easy days are no longer truly low-cost, and recovery between harder sessions is less complete. What is often given up is range. An athlete with a well-developed aerobic base can run at a lower heart rate for the same pace, oxidize more fat, produce less lactate at submaximal intensities, and accumulate more total training volume with less physiological strain. Their easy runs are genuinely easy at a metabolic level, allowing higher-quality work when intensity is introduced. They are not just fit; they are efficient and durable. Base training, therefore, is not about avoiding effort or running unnecessarily slowly. It is about lowering the physiological cost of work so that training becomes more repeatable, recovery becomes more predictable, and long-term durability improves. The heart remains strong, performance is preserved, and the metabolic system becomes more efficient. For lifelong runners, especially after forty, efficiency and recovery capacity often become the true limiting factors rather than motivation or discipline.

@Ihartitz This is misleading though. When you did this, did you remove Josh Allen’s rushing yards and tds, when factoring in the run support for the bills?

NFL ranks in "Supporting Cast Rating" which is the average team PFF grades in rushing, receiving, pass blocking and run blocking (everything except passing): 1. Rams 2. Colts 3. Bears 4. Bills 5. Lions 6. Seahawks 7. Broncos 8. Eagles 9. Falcons 10. 49ers 11. Vikings 12. Chiefs 13. Panthers 14. Packers 15. Ravens 16. Patriots 17. Jaguars 18. Commanders 19. Cowboys 20. Buccaneers 21. Giants 22. Steelers 23. Texans 24. Dolphins 25. Jets 26. Titans 27. Cardinals 28. Chargers 29. Bengals 30. Saints 31. Raiders 32. Browns

@FluentInFinance Thoughts? @DecadeInvestor

So let’s just get this crystal clear. S&P 500: All-time high NASDAQ: All-time high Bitcoin: All-time high Real estate: All-time high Gold: All-time high Meanwhile… Money Supply: all-time high National Debt: all-time high Federal Reserve: "Time to cut interest rates next month!" We're literally copying Japan's playbook from the 80s. Does the Fed really need to pour more gasoline on the fire? This is crazy.