Yes, I’d concur with you…new albumins, not dilution.
Secondly, why wouldn’t donation create a full new generation of the proteome? After zillions of blood donations, surely there’d be findings of metabolic dysfunction if only certain elements of the proteome?
“Increase in albumin”? Isn’t this about the quality of the albumin vs qty? But no, I’ve only tested albumin 3x in 5 yrs, no trending.
I see what you’re saying. The old albumin replaced by the new giving higher quality, not quantity.
Makes you now really wonder if frequent/ regular blood donations should be an integral part of the health/ longevity regimen for a whole multitude of reasons.
It seems most likely that its both actually. To remove old hazardous stuff in the blood cannot simulate adding young blood factors and adding young blood factors alone cannot simulate clearing away junk.
Yes, I’ve always intuitively believed this, and my research kept coming up with so many beneficial benefits. Conceptually, I’ve been most attracted to interventions that impact every cell in the body…diet, exercise, blood donation. Pharma is often a narrow singular pathway, although Rapamycin targets a central longevity nutrient sensor pathway, so is perhaps unique (and supported by a plethora of longevity studies)
Blood donation and blood donor mortality after adjustment for a healthy donor effect
“We observed an inverse relationship between donation frequency and mortality. Analyses adjusted only for demographic characteristics showed a 18.6% reduction in mortality per additional annual donation (95% confidence interval [CI], 16.8%-20.4%). After additional adjustment for the internal healthy donor effect, each additional annual donation was associated with a 7.5% decreased mortality risk 7.5%”
I donate 9x/year +/- for over 5 yrs…extrapolate the MRR (mortality rate ratio) curve?!
“According to several studies, blood donation is associated with better health outcomes. A 33–
88% lower risk of cardiovascular disease (CVD) has been reported in donors versus non-donors. Repeated blood donations reduce blood viscosity, thereby potentially lowering blood pressure and the risk of plaque rupture. It is also known that with a 500ml whole blood donation, up to 250mg of heme iron is lost. This iron loss, which may reduce oxidative stress and the availability of iron for malignant cells, may have a protective effect against insulin resistance and atherosclerosis, and may as well protect against cancer.”
Data mining of human plasma proteins generates a multitude of highly predictive aging clocks that reflect different aspects of aging
hmm. The body will gravitate to a homeostasis in albumin qty (proteome) needed. Like most of the human systems, things are tightly regulated. In the mouse study, they were extremely careful to replace exactly the quantity for this reason. Of course, there are certain diseases that cause high or low albumin, but these are not phlebotomy induced.
Secondly, they’d never let you donate very 7 weeks if there was an issue with increasing/decreasing albumin levels.
So to summarize, blood donations lower iron and blood viscosity as well as rejuvenating the proteome, of which albumin is probably the most important factor. There may be more benefits that we don’t know about.
Of interest also is the role of rapamycin in this. Hematopoietic stem cells are a necessary part of this replacement and studies have shown that HSC’s are rejuvenated by rapamycin. Can’t leave that out of the picture or stem cells may not be able to keep up.
There are other benefits without a doubt. Let me dig up my archive and share.
But what if donations are a hormetic stressor that supports blood stem cell rejuvenation? I assume bone marrow is signalled/marshalled to support in phlebotomy. HSC anti-senescence (preventing exhaustion)?
From the paper reference, Rapamycin prevents enlargement of HSC. Blood donation will trigger new small stem cells from bone marrow, thus allowing Rapamycin to act in its HSC therapeutic modality keeping NEW stem cells from enlarging.
In the lifespan.io article it mentions (as I think everyone knows):
Over the currently normal human lifetime, they decrease in quality through the accumulation of damage, as seen in the other Hallmarks of Aging, and, eventually, the pool of stem cells runs out.
Given the Hayflick limit, shouldn’t increasing blood donations also result in increased stem cell turn over, and thus moving towards exhausting the pool of stem cells?
Duly noted Hayflick limit, although it’s only a theory.
“What gives more hope is that no one has actually proved that the Hayflick limit actually limits the lifespan of an organism. Correlation is not causation. For instance, despite having a very small Hayflick limit, mouse cells typically divide indefinitely when grown in standard laboratory conditions. They behave as if they have no Hayflick limit at all when grown in the concentration of oxygen that they experience in the living animal (3-5% versus 20%). They [make enough telomerase] an enzyme that replaces degraded telomeres with new ones. So it might be that currently the Hayflick “limit” is more the Hayflick “clock”, giving readout of the age of the cell rather than driving the cell to death.
The same site reference:
“the pool of stem cells can regenerate itself”
They only reference exhaustion = SASP (senescence)
I am betting donation is a fundamental rejuvenation intervention, preventing senescence in HSC, like Rapamycin…up to some limit of course.
BUT…will monitor closely my CBC for derailment?
@rivasp12 Is CBC a good tracker of this stem pool dyanmic/derangement?
So you have significant telomere attrition of 30 base pairs per year in your stem cells leading to genome instability and mutations. These mutated stem cells are the predominant forms after age 70. Not good.
Maybe a combination of rapamycin for stem cell rejuvenation and Centella Asiatica for telomere maintenance as well as a sweet spot for blood donations would be smart.
“Mechanistic investigations reveal that young sEVs stimulate PGC-1α expression in vitro and in vivo through their miRNA cargoes, thereby improving mitochondrial functions and mitigating mitochondrial deficits in aged tissues. Overall, this study demonstrates that young sEVs reverse degenerative changes and age-related dysfunction, at least in part, by stimulating PGC-1α expression and enhancing mitochondrial energy metabolism.”