New Scientist talks with Bryan Johnson:
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Blueprint is moving forward…
See full post here: https://x.com/bryan_johnson/status/1983196154490966322
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Good ideas
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With AI one can write so much yet say so little.
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On X Dr. Jack Schroder has a lengthy interesting critique of Bryan Johnson’s April 2025 labs.
Schroder vs. Johnson
Two points where I part ways.
First, LDL. Jack frames very low LDL as inherently problematic. My own LDL is lower than Bryan’s, intentionally so, and I’m comfortable with that given coronary risk context and outcome data from LDL-lowering trials. Observational associations between low LDL and adverse outcomes are heavily confounded and don’t translate cleanly to deliberate, monitored LDL reduction.
Second, IGF-1 and SHBG. Jack notes low IGF-1 and elevated SHBG and treats them as yellow flags. In my own case, E3 shifted both markers in the same direction as Bryan’s, without any obvious functional downside. These look like expected tradeoffs of certain longevity-leaning interventions rather than clear pathology.
Jack’s main concerns in the labs were:
• Low WBC and neutrophils
• Low platelets and globulin
• High SHBG
• Very low total cholesterol
• Low glutathione / GGT
• Low ferritin
• Low IGF-1
• Mild AST elevation←my ALT/AST are slightly better also, idkw
I’m not a doctor, and this stuff gets really confusing fast. But weighing the total picture, I still lean closer to Johnson’s interpretation than to the claim that these labs suggest hidden systemic breakdown.
(edit)
LatestJohnsonPost…Defensive?
He just now tweeted his HA1c results-super low. I don’t see how to jive this with the high blood glucose reading of 103 as I recall.
Also he’s rich, why wouldn’t he buy a high dollar hs-CRP? My poor boy $50 test gets down to 0.2. I think some labs have crp tests that go down to 0.10
(Last Edit)–The Mystery of the crushed A1c and spiked Glucose
I asked AI how you could have high blood glucose and super low A1c and got a list of possiblities, but #1 on the list???
Says AI:
If therapeutic phlebotomy / blood donation is in the mix and you’ve seen low ferritin plus hemoglobin shifts, then the A1c–glucose mismatch is no longer mysterious at all.
HbA1c is glycation over red blood cell lifespan (~120 days).
Phlebotomy:
- Removes older, highly glycated RBCs
- Forces marrow to make new, minimally glycated RBCs
- Shortens the average RBC age in circulation
Result:
- HbA1c drops, sometimes substantially
- Even if mean glucose does not drop proportionally
And the typical “tells” are:
Ferritin drifts low
Hemoglobin wobbles but stays “acceptable”
MCV may shift
RDW may increase slightly
A1c looks “elite”
This neatly explains the mystery, is it correct, IDK, but Johnson’s talked a lot about blood donations/transfusions and I seem to recall his ferritin was low and a few other slightly off blood markers
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I’ve never heard of Dr. Jack Schroder…
I agree with parting with him on on the LDL issue. Heart disease is the number one killer of men, so I lower LDL agressively… and I follow the best, long term studies available, like this one: The Coronary Plaque Progression Paradigm: Why Your "Low Risk" Score Might Be Lethal
IGF-1, I’m more mixed on this issue, low IGF-1 is generally associated with longevity but the biggest impact is when the organism (mammal or otherwise) is very young, so if you have low IGF-1 in the first 10% of your life, you’re likely to live much longer (and be much smaller), but after that the benefit seems to be quite minimal. And there are (in talking with people who use it) many benefits to GH in terms of how you feel. So this may be a bit of a “quality of life” vs. “length of life” trade off that many people would side with on the “quality of life”, because the impact on total lifespan (if you’re looking at IGF-1 or GH levels after middle age) is not much of a factor.
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Does anyone else believe Bryan is mistaken that science is to blame for hyperpalatable food?
I don’t think the foods that are enticing is Humanity’s first rodeo. Salt, sugar, and fat have been with us for a long time. Spices and processing as well.
The majority of the lifting was human ingenuity, cleverness, and trial-and-error over thousands of years.
Science did help make things cheaper and last longer. But the vast majority of impact it would be a stretch to claim it’s because of applied science. It’s more like chefs being chefs I think.
But scientists sounds more evil and more unnatural than chefs. There’s really no secret ingredients that makes us love hyperpalatable food. It’s base stuff!
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When the Odyssey was written by Homer I am most certain there was some unhealthy food addicts.
Butter: 2500 BC
Salt: 6000 BC
Bread: 12000 BC
Sugar: 4000 BC
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Gemini appears to have ignored your question and you get the sycophancy answer.
Feature Natural Food (e.g., Apple) Food Science Formulation (e.g., Apple Pie) Primary Driver Single palatability vector (Sugar) Combined vectors (Fat + Sugar + Sodium) Brake Mechanism Fiber, Water, Chewing resistance “Pre-chewed” texture, Fiber removed Brain Response Satiety signaling intact Dopamine reinforcement loop (Craving) Occurrence Evolutionarily common Does not exist in nature
The example of apple pie has origins from 14th century England.
The hamburger is meat, cheese, fat, salt, and bread, all are old ingredients and the combination likewise. The sauces are probably derived from old french aristocratic cooking.
So isn’t your example proving my point?
Science might improve a tasting experience on the margin, but the heavy lifting which is the vast majority of the rewarding experience was combination of base ingredients by chefs.
Not from science! Fat, sugar, and salt is thousands of years old and likewise has been used for so long. How difficult do people think it is to combine these three ingredients? Just taste it and add different amounts, it took one guy 5000 years ago to do it in a few afternoons, then reinvented over and over thinking “we are the modern guys!”
The scroll decoded from 2000 years ago:
The general subject of the text is pleasure, which, properly understood, is the highest good in Epicurean philosophy. In these two snippets from two consecutive columns of the scroll, the author is concerned with whether and how the availability of goods, such as food, can affect the pleasure which they provide.
Do things that are available in lesser quantities afford more pleasure than those available in abundance? Our author thinks not: “as too in the case of food, we do not right away believe things that are scarce to be absolutely more pleasant than those which are abundant.” However, is it easier for us naturally to do without things that are plentiful? “Such questions will be considered frequently.”
Since this is the end of a scroll, this phrasing may suggest that more is coming in subsequent books of the same work. At the beginning of the first text, a certain Xenophantus is mentioned, perhaps the same man — presumably a musician — also mentioned by Philodemus in his work On Music.
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I think both things are correct.
We’ve had enticing foods for a long time, but the food labs of the big companies have amped it up exponentially … and aside from the chemical makeup of the food, it’s also the easiest choice… there is no baking involved… no pricey speciality bakery you need to go to… you just pick up a package of the cheapest food available … and available everywhere.
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Perhaps, but not with minimized fiber, in an optimized way, mass produced with low cost HFCS (High Fructose Corn Syrup), (via the heavily government subsidized corn industry) and distributed to every store in a country at low prices for universal adoption.
It’s a matter of scale and frequency. People may have occasionally gotten a dish with optimized sugar, salt, fat etc. in a single meal, but now they can do it all the time, at low cost, conveniently at every cornerstore, fast food restaurant and grocery store in the country.
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It’s convenient that this is really a criticism about human development and industry, e.g paved roads and energy, as this decreased costs to mass produce pies developed by chefs (and at the margin improved by food scientists). So the cause is non-specific and general, and there’s no one really to blame. The solution might be specific and targeted though, like GLP-1+GIP+ etc agonists.
Lift all industrial boats and then sink the ones we don’t like, maybe, else you blame what improves life in other ways.
It’s probably a bit of both. A person can definitely make plenty of hyper palatable foods from scratch combining only basic things like flour, butter, sugar etc. and certainly chefs are experts at it. Our modern food environment has perfected doing this on a mass scale cheaply so now rich or poor we can easily consume the magical combination of salt, sugar and fat that gives us a dopamine hit all day everyday if we don’t know better. I thought this podcast was interesting in pointing out the connection of UPF’s with the tobacco industry.
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And he makes the cover of Time magazine.
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Good to see him say this about LDL since a lot of people who pay attention to him get bombarded with “LDL is good” bad info.
https://x.com/bryan_johnson/status/2008362857847812387?s=46
“Definitely do not stop statins, and preventative LDL-cholesterole lowering therapies in general, based on these arguments, as they clearly misrepresent the facts.
The AMORIS study only showed that extremely low total cholesterol was negatively associated with the chance of becoming a centenarian (reaching 100 years of age) (observational association; not causal, and low total cholesterol can also reflect underlying illness in older adults).
Total cholesterol is different from LDL. Statins specifically lower LDL in the blood by increasing LDL receptor expression in the liver.
The points made here perpetuate a common misconception, often propagated by health influencers, which is mixing up the beneficial functions of a molecule (nearly all naturally occurring biological molecules have legitimate functions in cells, tissues, and organs) with the level of these molecules in the blood, abnormally high levels do not mean a particular molecule is doing its job better, for a simple example, think of glucose, it fuels the brain, too much would not cause your brain to function more, the contrary as it causes metabolic disease, diabetes, and even increases cognitive decline risk.
Cholesterol, and even LDL, have their legitimate functions, but these functions do not improve when the molecules are abnormally high in the blood. In fact, elevated LDL in the blood is often an outcome of defective liver uptake, frequently due to metabolic disease, and in rarer cases, solely due to genetics (familial hypercholesterolemia).
LDL is causally linked to cardiovascular disease, and lowering it reduces heart attack risks in patients with existing plaque. Mendelian randomization studies also show that lifelong exposure to lower LDL levels reduces coronary artery disease risk; a 38.7 mg/dL reduction correlates to over a 55% reduction in coronary artery disease risk. Moreover, loss-of-function mutations in PCSK9 lead to a 28% reduction in LDL and correlate to an 88% reduction in coronary heart disease.
The genetic variants with lower cholesterol share a similar mechanism with statin or PCSK9 treatments, in that they mainly lower LDL by increasing liver clearance.
The U-shaped relationship between LDL-cholesterol levels and all-cause mortality at a population level is likely driven by reverse rather than actual causation, since many aging and chronic disease drivers, including inflammation, malnutrition, cancer, and liver disease, can all contribute to lowered levels of lipoprotein.
Contrary to the observational data, a large meta-analysis showed that more intensive statin regimens and further reductions in LDL cholesterol produced further reductions in heart disease events and death risk. 20% reduction in coronary heart disease death and 10% reduction in all-cause mortality per 1 mmol/L (38.7 mg/dL) LDL-C reduction across trials.
With that said, you might want to reconsider statins in the following cases:
A severely lowered LDL coupled with partially increased blood glucose can be a sign of cholesterol “overmedication.” The same mechanism that leads to increased clearance by liver uptake also works to increase LDL uptake by pancreatic islet cells. Preclinical evidence shows that overmedication to lower blood LDL can lead to disrupted pancreatic islet functions and insulin secretion, and increased blood glucose (In humans, statins are associated with a modest increase in diabetes risk overall; this is not reliably diagnosed by “LDL too low,” and risk is most evident in predisposed individuals).
Consider swapping to PCSK9 inhibitors. This is a well-established injectable (once every month or every two weeks) class of biologics (recombinant monoclonal antibodies targeting PCSK9 and preventing its effect in degrading the LDL receptors in the liver). PCSK9 inhibitors have shown added protective effects in lowering cardiovascular disease risk even in patients already on statins. They also have a speculative anti-aging mechanism since circulating PCSK9 has been shown to increase with aging. While they can also plausibly interfere with the pancreatic islets and cause similar disruption seen with statins, there is no evidence yet to date of PCSK9 inhibitors increasing diabetes risk, such as evidence exists for statins (major outcomes trials have not shown a significant increase in new-onset diabetes over ~2–3 years of follow-up).
If your HDL is too low, you need to pursue strategies to increase it, including exercise, healthy diets rich in MUFA and Omega-3 fats and fibers, avoiding added sugar and refined carbs, and abstaining (or seriously cutting down) on alcohol.
If you are experiencing muscle ache and discomfort with statins, this is also a strong reason to switch. While the more acute form of muscle degeneration is very rare and would have been detected earlier as you began your statin therapy, lower-grade muscle aches are common in statin users. Changing to PCSK9 inhibitors, or other medications like ezetimibe (a cholesterol absorption blocker), can also help.
Personally, I am currently on Repatha, a PCSK9 inhibitor, as I replaced statins after noticing they slightly increased my blood glucose.”
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Update via email:
How I’m doing:
New protocols for 2025:
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- sauna (link)
- magic mushrooms as a longevity therapy (link)
- metformin cycling (link)
- pulsed electromagnetic field (PEMF) therapy (link)
- intermittent hypoxia-hyperoxia therapy (IHHT) (link)
Graveyard protocols for 2025:
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- SLU-PP-332: caused sleep disturbances (link)
- plasmalogens: didn’t do much for my biomarkers (link)
- methylene blue: made me less tolerant of IHHT, a potentially more beneficial protocol (link)
Our biggest discovery of 2025:
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- I hit a metabolic reset switch with the psilocybin (magic mushrooms) therapy. This is a first-in-world observation in humans. More below, and a deep dive coming soon.
—————
Big breakthroughs:
#1… Magic mushrooms as a longevity therapy
We are testing 3 doses of magic mushrooms over 3 months. I’ve taken 2 doses, and we have already seen surprising results (watch).
The biggest breakthrough so far: Psilocybin may be a metabolic reset button for the brain. My blood sugar control improved from the top 2% of the population to 0.2%, better than 99.75% of 18-25-year-olds. I’ll share more data from our mushroom experiment in future emails, including more about our first in-human observations.
We think psilocybin is a longevity therapy.
#2… Skin age reversal of 9 years
I effectively froze my skin aging over the past 5 years.
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- skincare: Blueprint cleanser, serum, and moisturizer
- diet and supplementation: Blueprint collagen peptides, flavonols, polyphenols (extra virgin olive oil), and antioxidant supplementation. My diet, which focuses on plant protein, fiber, and polyphenols, is also geared toward eliminating inflammation, oxidative stress, and glycation. All sources of skin damage.
- smart UV exposure: protect your skin when the UV index is high (10am - 4pm)
- skin-focused therapies: 1927-nm laser, 1550-nm laser, and Sofwave every 6 months
- whole-body therapies: daily red/nir light panels, hyperbaric oxygen therapy (HBOT), and dry sauna
#3… Sauna as a top longevity therapy
I started dry sauna in early 2025… and it turned out to be one of the most effective therapies I’ve done. I now do 20 min of sauna daily at 200°F (93°C). Clinical evidence for the temperature target in dry sauna is between 175°F and 212°F (79-100°C).
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- 15 sessions of sauna dramatically reduced environmental toxins in my body
- my vascular function improved by a 10-year reduction in age
- sauna coincided with my fertility markers being at an all-time high (when I iced the boys)
#4… Eliminated 85% of microplastics from my ejaculate
Microplastics can invade organs, cross the blood-brain barrier, and wreak havoc with your hormones, fertility, and immune system. To reduce them, I tried to remove as much plastic from my life as possible.
Also, surprisingly, this year we discovered that sauna reduced microplastics in my blood and ejaculate by ~85%.
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I’d love to read more about his experience with IHHT. For those interested we’re discussing IHT and IHTT here: Oxygen, hypoxia and hyperoxia