Thanks! Interesting perspective. I’ll have to see if our lab can do the sTfR blood test since this sounds a lot more accurate for iron status than ferritin.
My normal lab offers it, but I’ve never ordered it. I’ve done TIBC to get at Transferrin saturation.
My lab also adds the following on sTfR:
“Useful in measuring the concentration of soluble transferrin receptor in blood When body cells are low in iron, the body produces more transferrin receptor. Serum soluble transferrin receptor increases in iron deficiency and is usually unaffected by chronic disease states. In general, to increase sensitivity and specificity, the measurement of serum soluble transferrin receptor should be performed in combination with other tests of iron status, including ferritin, TIBC, and serum iron”
Does anyone know, why Metformin and AKG cancel each other out? Both should increase autophagy, right?
Many thanks!
taking the same as you expect i take 6mg sirolimius weekly and I also take astaxanthin & fish oil + aged garlic.
[quote=“shc, post:5, topic:734”]
@shc “SGLT-2 inhibitors – when I am eating sugary, carby, or heavy meals. I avoid this soon after a rapamycin dose because I don’t want to be susceptible to UTI.”
Can you elaborate on why you would be more susceptible to a UTI, please?
I know Brian Kennedy commented that Berberine and Ca-AKG cancel each other out, if I remember it well. Are there studies that point out that Metformin cancels out the benefits of Ca-AKG also? Sorry if this has been mentioned.
I know it is often argued Rapa is an immune modulator rather than that it suppresses the immune system. However, certainly after taking a higher dose of Rapa it may have some immunosuppressive effects temporarily. In combination with increased urinary glucose secretion because of the use of a SGLT2-inhibitor, this could make one potentially more prone to UTI’s in the days after taking Rapa.
Compared with control cells, the presence of metformin dramatically lowered the molecular 13C carbon labeling (MCL) of the cellular TCA cycle intermediates citrate, α‐ketoglutarate , succinate, fumarate, and malate, as well as the MCL of the TCA cycle intermediate‐derived amino acids glutamate, glutamine, and aspartate.”
Maybe we have to understand how Metformin and Berberine work within the TCA cycle in order to understand how alpha-ketoglutarate cancels out their effect.
I think it is smart to take each of these, after the other one is cleared from the system.
Indeed. Thus far I’ve only waited 4-7 hours after taking Ca-Akg before taking any other supplement/drug because of this potential interaction. But admittedly I had no clue whether that may be sufficient at all, and it may very well not be the case.
Thanks for sharing. Yes you may be right. Admittedly I’m swamped currently but definitely something I’d want to look into a bit more the upcoming period.
Posted on the age reveral forum:
Longevity Science Singapore Conference & Opening of NUHS Centre for Healthy Longevity | PM Session
Didn’t know where to post this. But there is a section about Metformin - talk by Dr. Nir Barzilai starting at 1:33:09.
Professor James Kirkland’s, on senolytics, starts at 42:20.
The first speaker, Professor Thomas Rando 16:30 talks about Stem Cells and Ageing.
Dr. Barzilai’s scorecard comparing SGLT-2 inhibitors, Metformin, Rapamycin/rapalogues, Acarbose, ACEi/ARB (losartan, lisinopril), D+Q, Aspirin, Methylene blue, NAC at 1:43:28
SGLT-2 12
Metformin 11
Rapamycin 9
Acarbose 9
ACEi/ARB 8
D+Q 6
Aspirin 6
Methylene blue 6
NAC 4
Kirkland’s speech is mind blowing. Senescence spreads throughout your body? So senescent cells are like a disease. If you implant a mouse with senescent cells, it becomes frail and dies early. Wow. This changes my world view! Thanks for sharing.
Admittedly I have not watched the video yet, but do they discuss whether it is the result of the SASP that cellular senescence is accompanied by - as I had thought to have read previously.
I think they are targetting senescent cells that generate SASP, so yes. You should watch the video. Start with Kirkland’s part.
I like it at 1:27. Discussing aging clocks. She said it was especially helpful for people who are over motivated. She used example of someone who was so interested in longevity that he was taking all of the interventions. He was aging faster than his chronological age!
That is something that I worry about. I had two biological age tests done. One analyzed blood (Aging.ai) and I was 19 years younger. Then I did a saliva epigenetic test and I was 19 years older. So, I have come to realize I am as old as spit, but young at heart.
Honestly, I don’t know which to beleive. The only thing I had been taking at the time of these tests was Metformin and NMN.
What I am trying to do (with some success) is to reverse senescence. That is because I think senescence spreads through IL-10 through the Janus Kinase NF kappa B and SLC25A1 and therefore causes other cells to go senescent.
What is interesting about this process is that is explains why senescence tends to be patchy. What I am finding, for example, is that senescence and the failure to differentiate causes hair loss to be patchy as the IL-10 (I think that is the cytosine) does not go that far. Interestingly I am getting a slow reversal of hair loss (very slow) in the patchy sort of way that it went in the first instance.
@zazim That does sound disconcerting. Did she also discuss what type of interventions this person that seemed to age faster than his chronological age took? Or whether they had also measured his ‘biological age’ before he started these interventions - perhaps he had already a biological age higher than his chronological age before he started the interventions.
And yes I should definitely watch the video @strider, you are right. Unfortunately I’m rather tight on time currently.
I’ve also for years tried to target the Nf Kappa B pathway. What is your personal approach in trying to target these pathways, if I could ask? Thanks!