Btw, what some of these mushrooms look like.
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Green peas also appear to be a good food source of spermidine, and less calorically dense than aged cheddar cheese. I’d love to get all my spermidine from cheese, but my waist line would not approve haha
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Unless you are vegan, 10g of aged cheddar is only about 50 calories, but delivers approx 20 mg Spermidine.
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Closer than you might think…calories wise
100 grams cheddar…400 calories
100 grams green peas…200 calories
Of course, cost wise 1 year old cheddar is about 6X the peas
Calorie for calorie…broccoli and cauliflower best bet for spermidine.
I have been using the product that RapAdmin mentioned, yes I ordered it from Germany. Was not able to locate this product in the US
Has 5mg per scoop / 1mg per gram
MAC, could you please provide a link/reference for the levels of spermidine in aged cheddar cheese? Thank you!
I believe MAC was off by a decimal point. Cheddar has 2 mg per 10 grams, not 20. Still not insignificant as the average daily intake of spermidine in USA is estimated to be about 10 mg/day.
If you go to this thread. I posted a document that shows amounts in foods. There is a list of the top 10 foods and amounts.
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Here are a few. Correction, 10g aged cheddar would be 2mg. Aged cheddar is 200 mg Spermidine/kg aged cheddar.
Natto is really the super Spermidine food. At about 340 mg/kg natto, a typical 50 g serving would deliver about 17mg.
I eat a serving of Natto, approx 50g and about 25g of 10 yr old cheddar daily, so total Spermidine before other food intake, approx 20-25mg/day.
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If the average intake of Spermidine of a modern country is 10mg … then (considering what the average person usually buys at grocery) a good daily dose would probably be 20+ mg at least
The real question, is it possible to even hit close to optimal with food sources that usually would either be too hard to eat enough of or contain some other component that would be suboptimal at a high amount.
Sidenote : Regularly cooked soybeans seem to contain as much spermidine per weight as natto, so it should work similarly as a dietary source.
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hmmm…looking at food/spermidine content table, I doubt very much anyone in the modern world is getting anywhere near 10mg Spermidine just from food intake.
Yes, regular soybeans due contain a relatively high level of Spermidine. Fermentation into Natto raises it approx 40% higher, and perhaps(?) more importantly, enriches with several other super nutrients.
https://www.scirp.org/journal/paperinformation.aspx?paperid=107932
The Japanese eat at lot Natto, and Cretans/Sardinians eat a lot of aged cheese. I’ll roll the dice and add these foods daily to my hacks in lieu of other dietary choices.
Unfortunately, spermidine supplementation may not work. Rich Miller PhD (director of the ITP) gave large doses to mice over 6 months and found no increases above baseline in serum or various tissue/organ levels of spermidine. Based on this fact, they didn’t even bother to proceed further with doing a study. Maybe the picture will be different in humans, but in mice at least, it appears that spermidine is very tightly regulated. See my post about the new interview with RM on Live Longer World.
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Unfortunately, none of this stuff ……natto or spermidine or otherwise….might work. There is a fair amount of work on humans and several large population studies indicate significant increases in lifespan attributed to increased spermidine intake from foods I am not sure if I saw bloodwork trials but think so. I believe the spermidine intake shows up in blood as spearmint, another polyamine with related activity.
Who knows? But I believe it is Ill considered to discard a possibility based on a single top of the line screening when so much other information says otherwise.
You have to remember that wild type mice only die of cancer.
Humans die of dozens of diseases, cancer is just one of. Everything we eat, drink, the supplements and drugs we take, the air we breathe, amount of sun exposure, sleep, our lifestyle choices and interventions, and of course our unique genes, alters literally millions of pathways.
A single molecule might not prevent cancer in wild mice, but have a meaningful impact on humans in other longevity enhancing pathways.
As an example, studies on transgenic mice that are bred/engineered to express human Alzheimer risk genes because wild type mice do NOT ever die of Alzheimer disease! Billions have been spent on experimental drugs given to these mutant transgenic mice for hope in clinical translation…all models have failed to translate to understanding root cause Alzheimer’s in humans. Many big Pharma companies have abandoned the space due to failure and complexity.
The best way to measure true longevity extension in humans is “all cause mortality”. For a person to live longer, he/she must push out all chronic disease, not just a single mortality pathway.
Excitingly, Rapamycin has been shown to increase lifespan in wild type mice, improve other unique human disease transgenic mice models (CVD, neurodegenerative), and extend other mammalian models. It’s one of the most robust and safe (in humans) speculative longevity small molecules we have. Until something better comes along, many of us are adding it to the intervention stack.
Let’s hope it translates to humans, but we are sorely lacking good human trials. Off patent, so very hard to fund.
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Right, I was talking about spermidine not rapamycin. Rapamycin has held up extremely well (and repeatedly) in the ITP trials. Spermidine supplementation didn’t even budge the tissue levels in the mice, so the ITP researchers didn’t even bother to proceed with the study. I see this as a caution for spermidine that it may not work as a supplement, but not the last word by any means.
Theres no study, if hes making a point to talk about it and then conveniently using the no results as a reason for there not being a study this is just a rumor, a rumor from a PHD is still just a rumor. How large is a “large dose” … spend 6 months giving spermidine to mice then not even publish the results as a study (even no rise in tissues is a result). The whole premise sounds fishy.
Im not even currently taking any spermidine.
His NIH-funded lab studies are the gold standard for drug/supplement longevity research in mice and form the basis for much of the evidence that rapamycin increases life span in mammals. I’d recommend listening to the Peter Attia podcast with Rich Miller if you want to know his background and creds. I guess you can speculate that Rich Miller hates spermidine for some reason and wants to cover up its supposed anti-aging properties, but that doesn’t seem likely to me.
Being right about rapamycin extending lifespan isnt exactly a high bar, if he was wrong all the time he wouldn’t be where he is. The amount of studies showing spermidine to either resolving a negative aging pathology or extending median lifespan are enough to call Rich Millers assertion into question.
Polyamines are shown to be readily absorbed by the body.
Now if he saw no rise its possible that:
1 Some step in the measurements or implementation was wrong
2 Having influx of spermidine results in body having to produce less, this may have benefits despite the levels remaining similar.
Actually the “why” of someone going off mistaken assumption and maybe even doubling down on it doesnt matter, you and I both know he doesnt have to hate spermidine.
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Actually after doing a quick research review, you make some good points. I didn’t know there were so many published studies showing benefits in mice with oral spermidine supplementation (although it appeared to make type I diabetes worse, even then it was still absorbed and doing something). Like you said, maybe Miller’s lab was either having some kind of measurement error with spermidine in tissues/serum, or maybe it’s the polyamine flux that’s more important than absolute levels of spermidine at any given point in time. It’s a shame he didn’t proceed with the study, but I bet he’ll go back to it if more and more evidence from other labs points to a benefit.
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Yea thats fair , I believe perhaps he’s more focused on bigger drug-like regulators of macronutrients. Aging is such a complex issue that sometimes even the relatively minor pieces add up.
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