Chris Masterjohn

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Chris Masterjohn

Chris Masterjohn

@ChrisMasterjohn

Mitochondrial health expert applying peer-reviewed science to develop evidence-based protocols for human health and longevity. Founder of https://t.co/p1KbY9pqx8.

Katılım Ekim 2009
221 Takip Edilen79.8K Takipçiler
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Chris Masterjohn
Chris Masterjohn@ChrisMasterjohn·
Your cells are aging faster than you think. After age 18, mitochondrial density declines by 1% every year—one of the clearest biological markers of aging. By 70, you’ve lost more than half your cellular energy capacity. Here’s what most people miss: this decline isn’t inevitable. 🧵👇
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Chris Masterjohn
Chris Masterjohn@ChrisMasterjohn·
The secrets that Anthropic keeps from the Claude you talk to include what is actually being searched if you tell it to search something.
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Chris Masterjohn
Chris Masterjohn@ChrisMasterjohn·
@jbfly46 The antibodies are present young and the diagnosis late because the damage shown on the biopsy late represents progression over time, which requires aging as a passage of time effect. So "occurrence" at his level is in fact something that occurs in older people.
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Lucifer Lucifero
Lucifer Lucifero@jbfly46·
Lol no, this is wrong. The elderly is just the subsection of the population that is the most likely to get it diagnosed when they do have it. Do most people still not understand the very obvious disconnect between statistical evaluations within the siloed medical field vs statistical evaluations within the not siloed “field” of the actual entirety of our reality? Especially when it comes to individuals receiving 100% as accurate as possible medical diagnoses, where a medical diagnosis is just a single static picture of a constantly moving, fluctuating, and dynamic system?
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Chris Masterjohn
Chris Masterjohn@ChrisMasterjohn·
Bryan Johnson has been diagnosed with a disease that mostly occurs in the elderly.
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Bryan Johnson@bryan_johnson

Bad news #1: I have an autoimmune disease. My stomach is eating itself. Bad news #2: 2–5% of people have this, too. Likely more, because it hides. Good news: I'm going to try and solve it. Will share all. As a kid, I ate sugar cereal, drank sugary soda, and gobbled down fast food. I had a few healthy years in my early 20s but then became a young father of three and began building a business. Juggling that stress and grind, I let my health slip and gained 40 lbs. Within a few years I’d fallen into a deep, chronic depression. Somewhere in that timeline, my body began developing an autoimmune process affecting my thyroid and then my stomach lining. It’s called Autoimmune Gastritis (AIG). My hypothyroidism got diagnosed when I was 21 years old with a routine blood draw. That enabled me to begin proactive management, supplementing levothyroxine and Armour Thyroid. They are the hormones my body should be producing on its own but wasn’t. By taking these pills daily, my body was able to operate as though my thyroid was functioning properly. What I didn’t know was that something else was going on inside my body: my stomach had begun attacking itself. But there was no routine test to find out and I didn’t have any symptoms. I just discovered it in May. I'm unsure how long I've had it. AIG causes irreversible damage: nutritional deficiency, anemia, and over a long horizon, elevated cancer risk. When AIG is discovered today, standard medical care concedes defeat, stating that nothing can be done except managing the condition, no matter how awful or lethal the effects. Looking back over the past few years, I can now see the early signals we were picking up in measurement but hadn’t connected the dots. For 11 years, I’ve had low ferritin, without anemia. We continually tried to raise my iron levels with food and supplementation but nothing would work. We chased the obvious solutions first. A plant-based diet means all my iron is the hard-to-absorb, non-heme kind. Hard training, sauna, and hyperbaric oxygen all raise the body's demand for iron. But none of them explained the core failure: despite me taking iron orally, trialing every formulation, and using every timing trick, none of the iron would stick. What I didn’t fully appreciate until recently is how many stones my previous providers had left unturned. The low ferritin kept getting explained away but not fixed. I overhauled my medical team earlier this year. It was the rebuild to lay the groundwork for Immortals Care, our $1M a year protocol. With greater capacity, we revisited everything. On the surface, my low ferritin was easy to dismiss by most standards of care. My hemoglobin and hematocrit were normal. Ferritin measures stored iron, while hemoglobin measures circulating iron, and because the body drains its reserves first to keep hemoglobin normal, you can be fully iron deficient with a perfectly normal hemoglobin and hematocrit. This is why my low ferritin kept getting dismissed: the numbers that define anemia looked fine, so no one asked why my iron reserves wouldn't refill. My team pressed on that question. They first turned to a colonoscopy. I was 48 years old and overdue. It was good health hygiene to have while also serving a specific purpose of searching for a hidden source of blood loss such as a polyp or even cancer in my bowels. Either one of those would be an explanation of why the iron kept disappearing. At the same time, they began connecting the dots. Iron absorption depends on stomach acid, so one theory was that my stomach acid was disrupted. They also knew that thyroid and stomach autoimmunity often travel together, so often that the pairing has a name: thyrogastric syndrome. Put against my 27+ year history of autoimmune thyroid disease, the pieces pointed to a single hypothesis: my own immune system was attacking my stomach. To our surprise, my colonoscopy came back clean. A perfectly healthy colon, better than 95% of colonoscopies of men, according to the gastroenterologist. That ruled out the first concern and worst possible outcome: slow continuous bleeding from colon cancer, or pre-cancerous polyp. My team had exercised great foresight though, anticipating this possible outcome. In addition to a colonoscopy, they’d ordered an upper endoscopy to be performed at the same time. The combined procedure is a bi-directional endoscopy. Probes would look at my entire intestinal tract, up from below and down the throat. Additionally, we had several blood biomarkers measured ahead of the procedure to try and pick up on any signals that would give the gastroenterologist guidance for what to look for while doing visual inspections. Fifteen minutes before the procedure, my blood results returned, finding elevated levels of anti-parietal-cells-antibodies (APCA). They came back at roughly five times the upper limit of normal (103, against a ceiling of 20 Units/mL). It was a positive result confirming the suspicion of AIG being the culprit behind my low ferritin, the other type of gastritis, driven by a bacterial infection, was already ruled out, as we knew I am negative to H. pylori. Even before this finding, my team had ordered five biopsies to be taken from three regions of my stomach. The biopsies were the critical piece. Had they not been ordered, the bi-directional endoscopy would have been completed and AIG remained undiagnosed as there were no visual signatures of the condition in my intestines. Two days later, the results of biopsies came in, showing clear signs of early autoimmune gastritis: early atrophy confined to the acid-producing lining, with the rest of the stomach still spared. My team had anticipated this, methodically tracing every line of evidence. We now had a formal diagnosis. I have autoimmune gastritis AIG. My stomach is eating itself. So this was never one problem. It was three, linked to one another: the iron deficiency, the autoimmune gastritis driving it, and the autoimmune thyroid disease alongside it. Iron and thyroid feed each other both ways, low iron impairs the conversion of thyroid hormone into its active form, and an under active thyroid impairs how the body uses iron. Each made the other harder to fix. Autoimmune gastritis affects an estimated 2–5% of people, and likely more, because it hides and is challenging to diagnose. It's usually silent for years, surfacing only once the stomach has atrophied enough to do real damage: iron deficiency first, then B12 deficiency, then anemia from both, and over a long horizon, raised stomach-cancer risk. In one study of people with precancerous gastric lesions, roughly 18% carried the autoimmune antibodies, and only about 1% had ever been diagnosed. And the earliest clue, low ferritin, is the one standard medicine waves through. Low iron stores get normalized and rarely investigated at all when anemia hasn't shown up yet. That blind spot is what hid mine for a decade. The good news: the iron deficiency is now corrected. I received a 1,000 mg Monoferric iron infusion. This was chosen for two reasons after considering multiple formulations. First, it can safely deliver a full dose of iron in a single infusion (1,000 mg), while older options like Venofer require several separate appointments to reach the same total. Second, certain other IV iron formulations can cause a drop in blood phosphate levels, an important mineral for bones and energy. Monoferric is much less likely to do this, which matters given how closely we track long-term metabolic and bone health parameters. As mentioned earlier, current medical standards treat AIG as something to be managed, not resolved. It's worth noting that many of you give me a hard time, inviting me to "live life" and engage in self-destructive behaviors like a "normal person". I'm cool with the playful ribbing. Also, had I not taken care of my health during the past five years, my situation could potentially be very serious. You too may have a lurking health issue that is undiagnosed and could increase in severity from unhealthy life choices, without your knowing. The absence of symptoms is not the presence of health. A gentle nudge that minding your health, no matter your situation in life, is good decision making. My team and I are going to try and solve my AIG. This is how we’re approaching it: First, routine monitoring keeps the disease in view: ferritin and iron, B12, the pepsinogen I/II ratio, gastrin, and chromogranin A. Gastrin is the dial to watch. If it climbs, the disease is advancing, and the risk of gastric neuroendocrine tumors climbs with it. Second, we’re doing advanced characterization of the disease. We’ll do a repeat biopsy to read the immune infiltrate, deep cytokine profiling, and T-cell subset analysis, to see which pathways are actually firing. That testing drives the intervention plan, including the experimental approaches we intend to develop. + If gastrin and chromogranin rise: damp the gastrin drive (netazepide) and tighten endoscopic surveillance. If the profile is Th1 / interferon-driven: target JAK/STAT. + If it's Th17 / IL-17-driven: target IL-17 and STAT3. + If regulatory T cells are failing: rebuild them (low-dose IL-2, induced Tregs). + If it's antibody- and B-cell-driven and antigen-specific: engineered cell therapy (CAAR-T). Which organizes into four tiers, from available today to frontier: Tier 1, now: protect and support; zinc-L-carnosine, and acid replacement (betaine HCl with pepsin) under physician supervision. This is specific to my case and not something to self-prescribe, especially given the cancer-surveillance considerations above. Tier 2, target the signaling , JAK/STAT, GSK-3, IL-17, and damp the gastrin drive (netazepide). Tier 3, reset the cells, induced regulatory T cells (iTregs). Tier 4, frontier: engineered T-cell therapy (CAR-T / CAAR-T), custom AI-designed antibodies, or synthetic proteins, that can specifically seek out inactivate or destroy the rogue immune cells attacking my stomach lining. To be clear: there's no approved cure for autoimmune gastritis today. Medicine treats it as something to manage, not solve. Tiers 2 through 4 are investigational preclinical evidence at best, and in several cases therapies that still have to be built. If you're working on autoimmune gastritis, antigen-specific tolerance, regulatory T cells, or CAAR-T for organ-specific autoimmunity, please reach out. Modern medicine has normalized too many conditions that erode our health, function, and comfort, shrinking the goal to monitoring and management while a cure is rarely even attempted. Most of these verdicts were handed down decades ago, in an era that predates nearly all of our current tech and science, and they have gone largely unchallenged. We want to change that. In the age of AI, multiomics, and custom-built DNA, proteins, and cells, no condition should be presumed incurable simply because no one has yet tried to cure it with today's stack. I’ll end on a personal note. We fill our days mostly on things that are trivial next to what we ultimately care about. We know, deep down, however, that in the noise of it all, health is easily forgotten until it’s the only thing that matters. We spend a fraction of our lives truly sober to the preciousness of life. We feel it when someone we love dies, when a child is born, when we come close to death ourselves, or when a diagnosis marks our limit. In those moments, we are sobered, and the rarity of it all becomes self evident. Imagine the existence we’d build together if that clarity didn’t fade. I wish all of you the very best. Care for yourself, care for others, care for the planet and care for our animal friends. Care for life as it’s the most precious gift there is.

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Chris Masterjohn
Chris Masterjohn@ChrisMasterjohn·
@ProfDemirtas Oh ok. But cross-sectional data correlating DNA methylation markers or telomere length can tell us that he and his organs are biologically younger than his chronological age. The amount of cope in this hypocritical data interpretation is mind blowing.
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Özgür Demirtaş
Özgür Demirtaş@ProfDemirtas·
@ChrisMasterjohn Quick logic lesson for you: A then mostly B does NOT mean B then A ! A disease mostly happening in elderly does not mean anyone with that disease is old
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Anthony Pompliano 🌪
Anthony Pompliano 🌪@APompliano·
Bitcoin will go back up when there are more buyers than sellers. American open-source AI models are the future. I explained both to @Varneyco this morning.
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Chris Masterjohn
Chris Masterjohn@ChrisMasterjohn·
@kirk2057828 Finasreride is the opposite: it shuts off allo production. One is addiction and withdrawal. The other is deficiency. Opposite route but can arrive at a similar destination.
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kirk
kirk@kirk2057828·
@ChrisMasterjohn I wonder if this connects to 5 alpha reductase syndromes
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Chris Masterjohn
Chris Masterjohn@ChrisMasterjohn·
This is true and it is much worse than he says. High-dose progesterone and allopregnanolone are LESS EFFECTIVE AND 🚨MORE DANGEROUS(!!!)🚨 than benzodiazepines. The evidence base is tiny but it is very ugly. In the FDA application for zuranolone, an allopregnanolone analog, one woman developed a seizure the day after she withdrew. This was confounded by kratom use that morning and a subsequent epilepsy diagnosis. But they documented a withdrawal syndrome similar to but less intense than for Xanax. Their own experiments with dogs showed three had convulsions in response to withdrawal, one of whom died spontaneously and one of whom had to be euthanized. Despite this neither brexanolone, a natural allopregnanolone, nor high-dose progesterone are effective against epilepsy, whereas benzodiazepines are a reliable first-line defense against status epilepticus and their rapid in-field injection by paramedics cuts the mortality rate for status epilepticus three-fold. So you have benzo-level withdrawal seizures being documented from among the most nascent evidence base but no benzo-level emergency value. Neurosteroids have all the danger of benzos with not a tenth of the benefit. Dangerous stuff. Referenced and discussed in more detail in the article I dropped yesterday.
anabology@anabology

FYI be careful with neurosteroids (Allopregnanolone, proviron, excessive progesterone, etc) Neurosteroid tolerance + withdrawal is awful and shifts your GABA-A receptors to one that promotes hyperexciteability (α4 up, α1 down) Same as benzos - can literally lead to seizures

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Eugene Lucas, MD
Eugene Lucas, MD@elucasmd·
@ChrisMasterjohn @PeterDiamandis Counterpoint, respectfully: Peak METs are a validated measure of cardiorespiratory fitness, especially when derived from maximal or symptom-limited exercise testing. Do you think direct VO2 measurement would materially change the association?
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Peter H. Diamandis, MD
Peter H. Diamandis, MD@PeterDiamandis·
Your VO₂ max is one of the strongest predictors of how long you’ll live. In large studies, people in the lowest fitness group have close to five times the mortality risk of those in the elite group over a decade.  Almost NO drug comes close to that effect.
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Chris Masterjohn
Chris Masterjohn@ChrisMasterjohn·
@saturnmissiles Unless it’s debilitating. Then whatever. But as a fifth-resort level thing hella stupid.
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Chris Masterjohn
Chris Masterjohn@ChrisMasterjohn·
@saturnmissiles This is like asking me if 0.25 mg Xanax is as risky as 2 mg. No, obviously. But its hella stupid to treat anxiety with a drug.
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Coex
Coex@saturnmissiles·
My goat did not just say this. I can absolutely see it with allopreg you would need to be extremely careful with that but there is no world I can imagine anything but the most giga extreme doses of progesterone being as bad as BENZOS and the idea they have LESS BENEFIT is insane
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Chris Masterjohn@ChrisMasterjohn

This is true and it is much worse than he says. High-dose progesterone and allopregnanolone are LESS EFFECTIVE AND 🚨MORE DANGEROUS(!!!)🚨 than benzodiazepines. The evidence base is tiny but it is very ugly. In the FDA application for zuranolone, an allopregnanolone analog, one woman developed a seizure the day after she withdrew. This was confounded by kratom use that morning and a subsequent epilepsy diagnosis. But they documented a withdrawal syndrome similar to but less intense than for Xanax. Their own experiments with dogs showed three had convulsions in response to withdrawal, one of whom died spontaneously and one of whom had to be euthanized. Despite this neither brexanolone, a natural allopregnanolone, nor high-dose progesterone are effective against epilepsy, whereas benzodiazepines are a reliable first-line defense against status epilepticus and their rapid in-field injection by paramedics cuts the mortality rate for status epilepticus three-fold. So you have benzo-level withdrawal seizures being documented from among the most nascent evidence base but no benzo-level emergency value. Neurosteroids have all the danger of benzos with not a tenth of the benefit. Dangerous stuff. Referenced and discussed in more detail in the article I dropped yesterday.

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Chris Masterjohn
Chris Masterjohn@ChrisMasterjohn·
@EleviaHealthND The mechanism of withdrawal seizures is probably GABA receptor internalization or remodeling.
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Chris Masterjohn
Chris Masterjohn@ChrisMasterjohn·
For clarity the allo-raising doses of progesterone that are thought to have benzo-like effects are 400 mg in women and 1600 mg in men. And pregNANolone is not pregNENolone. There are no doses of pregNENolone or DHEA that raise pregNANolone to the levels that have benzo-like effects.
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Chris Masterjohn
Chris Masterjohn@ChrisMasterjohn·
@saturnmissiles I didn’t say anything about typical Peater progesterone dosing and I said nothing at all about pregnenolone (which is not pregNANolone)
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Chris Masterjohn
Chris Masterjohn@ChrisMasterjohn·
@saturnmissiles I said high dose, and I meant the 400-1600 mg that has been shown to raise allopregnanolone and raise indices of GABA-A activity equivalent to intravenous allo.
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Chris Masterjohn
Chris Masterjohn@ChrisMasterjohn·
@TakeThiamine @saturnmissiles Pregnenolone has no evidence of raising allopregnanolone in humans. The *only* thing that raises allo as much as allo is 400 mg progesterone in women and 1600 mg in men.
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Chris Masterjohn
Chris Masterjohn@ChrisMasterjohn·
The seizures are certainly more looked for now than in the 1970s when benzos came out. But the three dogs weren’t using kratom. The fact that this is coming out so soon with so little evidence makes it look a lot worse than benzos, where withdrawal-induced seizures are well documented 50 years after release but not common. And if you have withdrawal seizures but can’t treat epilepsy you have a bad balance.
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Coex
Coex@saturnmissiles·
@ChrisMasterjohn As to GABA related disorders are we only considering things like epilepsy here? I don’t think any kind of long term use of allopreg is a good consideration for anxiety disorders but I have zero reason to believe it would be more harmful than benzos
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Chris Masterjohn
Chris Masterjohn@ChrisMasterjohn·
At what dose? My point was about neurosteroids. However, 1) There are over five animal experiments showing withdrawal from exogenous AND endogenous progesterone can cause seizures. 2) There is a subset of perimenopausal seizures that are hypothesized to be from withdrawal of normal levels of progesterone during menstruation. Normalizing progesterone in those cases probably helps with little downside. And normalizing progesterone when it’s low probably almost never causes seizures on its own. But if a subset of epilepsy-prone women are getting seizures from withdrawal from normal menstrual cycle levels it’s impossible that withdrawing from 400 mg never does this. But the main point is if you are mega dosing it specifically to get a benzo like effect you are probably better off with the benzo. If you wouldn’t smack a “don’t drive within 12 hours of this” label on it, it’s probably ok. If it’s working within the endogenous range it’s almost certainly ok.
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Coex@saturnmissiles·
@ChrisMasterjohn Listen I won’t have any trouble whatsoever admitting I am a little out of my depth other than the fact I have used these hormones and know many others who have without ever hearing of a single case of these kinds of withdrawals until now
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Chris Masterjohn
Chris Masterjohn@ChrisMasterjohn·
@Jason It’s almost like there’s a brain-takeover strategy: Independent thinkers try to curate their own feeds to read them chronologically. Every social media company starts offering a chronological feed then replaces it with an algo curation.
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Coex
Coex@saturnmissiles·
@TakeThiamine I completely missed that what the hell man
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