last week, Johnson revealed that he has a chronic autoimmune condition, called autoimmune gastritis. The disease causes “irreversible damage” to the lining of the stomach, he said, and often develops silently and asymptomatically over the course of years. He was diagnosed in May, he wrote, after years of persistently low ferritin, a protein that stores iron inside cells, that his team struggled to explain.
I’m curious, what interventions led to this? Or it was written in his genes?
I understand that it started 11 years ago… probably before interventions. Bryan Johnson on X: "I had low iron for 11 years. Yes, even when I ate meat, my ferritin was low and averaged 38 ng/mL. I’ve finally boosted it back to healthy levels. You can see my protocol below. On the surface, my low ferritin was easy to dismiss by most standards of care. Most doctors miss https://t.co/lgsvoiqbJk" / X
I am the opposite… my ferritin level is always above the max level by 20%. No I do not have hemachromatosis. My level was more than 3x the normal levels initially. When I started C15 supplement, and my liver recovered, it dropped to 1.2x the normal level. I consume a lot of red meat. He should probably eat some red meat.
It’s most likely not even connected to red meat. As an example, I don’t eat red meat or any meat for decades and my iron levels are always normal. He has many specialists working for him and they don’t know the reasons. I’m glad we cannot blame rapamycin for that. He wasn’t on it 11 years ago. At least one thing can be excluded.
He says his ferritin was “always low and averaged 38 ng/mL” and he “finally boosted it to healthy levels”.
Well, that’s a matter of opinion. Average of 38 ng/mL is not particularly low, and well above the cutoff low range of 30 ng/mL by LabCorp. Low would be mine, at 20 ng/mL and it was flagged as “Low” by LabCorp. Even that is a matter of opinion, as some MDs (e.g. Dr. Greger is one), “low” doesn’t start until it’s below 15 ng/mL - so by that standard my 20 is not low either. FWIW, I don’t experience any negative side effects from my “20” that I can tell, nor is it reflected in any other serum biomarkers as a negative (hemoglobin etc.). And a ferritin of 38 is not a diagnostic level of any disease that I am aware of.
That said, it’s possible that my “20” is suboptimal. I have therefore elected to raise it to at least 30 ng/mL (with lactoferrin supplementation to start with). However, I don’t feel any need to go much higher than 30 - most literature I’ve seen does not clearly make a convincing case for any level beyond that. My reasoning is simple - raising my level to 30 is unlikely to be risky, while possibly providing a small additional cushion of safety.
possibly, as an example, I can take 50,000 IU of Vitamin D3 and it will not raise my D3 level by much. But if I opt for the active form of D3, just 20mcg will raise my D3 level through the roof. Basically my kidneys can convert the regular D3 to the active form properly.
Yes, I agree and it doesn’t look like low to me too. My son’s ferritin is 9 - it’s very low - and so far nobody could come up with a reason for that even after many different tests.
There is an argument that dopamine metabolism in the brain would like ferritin at 50-70.
This confuses me.
There is cholecalciferol ie D3. Then cacifediol 25OHD the storage form and calcitriol 1,25 dihydroxy VD which is actually the active form.
Normal total serum quantities of calcitriol would be under 1mcg.
I used to take cholecalciferol 50,000 IU… now I take 20mcg of cacifediol. My blood work is in the 150… which is better than the 77 before. I am speculating that my kidneys are not converting them properly.
Type A gastritis is autoimmune gastritis, which has a prevalence rate of up to 2% (H. pylori is linked to type B). Since Bryan also has hypothyroidism, he is already at a high risk for it. So it’s not strange at all that he got diagnosed with type A.
Of the 320 atrophic body autoimmune gastritis patients, 171 (53.4%) had an associated autoimmune disorder. Autoimmune thyroiditis was the most common concurrent disease, diagnosed in 116 patients (36.2%).
D3 → 25OHD is in the liiver
25OHD → 1,25(OH)₂D is in the kidneys.
Your issue if any is in the liver. There is an issue which is that people generally have a limit as to how much D3 can be converted to 25OHD in a day.
There are some charts on conversion that are quite interesting.
I am using my weekly 25OHD measurements to compare the effects of taking D3 fasting and non-fasting and also the balance with 25OHD itself (dedrogyl).
I am currently aiming for at least 200 nmolL (80 US units).
Bryan Johnson, the “longevity guru,” has spent more than $2 million on a quest to stay young. This week, he disclosed that he has an autoimmune disease that causes the stomach to eat itself. As a practicing physician who helps patients live longer, believe me when I say: you absolutely don’t need extreme measures to live a healthy life. Here’s what actually works.
As a doctor, I read the announcement from a specific vantage point. I study longevity science and work as a hospital-based physician, which means I spend part of my week working on how to give people more years and the other part at the bedside when the years run out. Johnson’s diagnosis itself is manageable and well-studied. What interests me is the story Johnson told about how he got it, because the science tells a different one.
Autoimmune gastritis (AIG) is a chronic, progressive disease in which the immune system attacks the stomach cells that make acid. “‘My stomach is eating itself,’ is not exactly accurate,” Dr. Supriya Rao, a board-certified gastroenterologist and assistant professor at Tufts University School of Medicine, told Outside. What actually happens is slower and more specific—the immune system attacks the stomach lining, shutting down acid production and the intrinsic factor needed to absorb B12. The lining thins over time, in a process called atrophy, and can turn into intestinal-type tissue that no longer works like stomach cells.
Read the full story:
This stimulated me to look up what links there are between this particular autoimmune disease and mRNA splicing/ageing etc. It appears that there is a general link between autoimmune diseases and splicing issues although there is not direct evidence for this disease, but it does appear to be a disease of aging in the sense that it gets worse and more prevalent as people get older.
Interesting thing that he rejected Rapamycin, which lowers the burden of hyperactive immune system. And put a lot of efforts as far as i know to modify his immune system with immunomodulators. At the end he got autoimmune condition.
Maybe its a coincidence. But for me it looks like + 1 score to the scorebook of Rapamycin. Better stick with it.
And one more joke to say
Here in Russia medics have a proverb
“There are no healthy people, only under-examined ones.”
This situation is a perfect example of this. If even him, the really most examined person in the world, missed an autoimmune disease… What can we, puny mere mortals, can expect?