Metformin May extend life?
- Thread starter JackSteel
- Start date
seems like some Doctors are already using it for this purpose
https://antiaging-systems.com/articles/116-metformin-as-a-safe-effective-weight-loss-drug
TotalPackage
Member
I've been using it for a couple years because of that reason. 2000 mg a day!
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TotalPackage
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There is speculation on the mitochondria, I just make sure I take enough l citrulline to counter that.
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JackSteel
Banned
Is it a bad affect? What does citrulline do?
Citrulline is an amino acid precursor to L-arginine which improves circulation and lowers BP.
E
Endure
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What about Berberine?
JackSteel
Banned
Why would that effect mitochondria though?
TotalPackage
Member
Sorry I'm just now getting back on this guys...........for me I love what I read about the benefits of Metformin..........so I take 2000 mg a day. The newer studies do show Metformin can have an adverse effect on Mitochondria. Mitochondria and ATP are simialar...........energy stores in the cells. L Citrulline can help with this through it's NO (Nitric Oxide) function...........also Creatine can help too with ATP. A lot here to consider.......for me I'm borderline pre-diabetic.........TRT and Metformin has helped keep my A1c in the 5.4 to 5.6 range. When you have time google "The many wonders of Metformin", "Metformin's effect on Mitochondria" "L Cittruline and Mitochondria", "Creatine and ATP".
E
Endure
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^ Have you tried Berberine for comparison? Just curious as many claim the same benefits minus some of the metformin sides.
TotalPackage
Member
I have not. From what I read berberine has some nice benefits and is very interesting. The only thing for me is the half-life of berberine and having to take it twice a day. That kind of does not go well for my schedule.
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JackSteel
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Thanks for the post man. I saw a documentary on YouTube recently mentioning it and I can’t remember the title. Pretty fascinating!
TotalPackage
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Yeah man! I don't have time to browse through here like I used to. I miss scrolling through and seeing posts and commenting.
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TotalPackage
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So you definitely need to be supplementing with l-citrulline, and creatine when taking metformin!
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Good stuff brother! Keep sharing THIS kind of knowledge with the rest of us "ignorant folk"!!!
TotalPackage
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One more post on this..........this seems to be the most comprehensive independent review I've seen on Metformin's effect on Mitochondria. Seems the effects are dose dependent, meaning mega dosing versus therapeutic dosing (500 to 2000mg).
Seems there are a lot of flaws and assumptions in the studies suggesting that Metformin's effect on Mitochondria.
However, the hypothesis that metformin accumulates in mitochondria contradicts several observations.
First of all, the accumulation of numerous positive charges in the matrix compensated by proton extrusion by the respiratory chain, should lead to a collapse of mitochondrial membrane potential associated with an increase in delta pH. However, note that metformin did not depolarize isolated mitochondria (8).
Secondly, assuming that the total mitochondrial volume represents approximately 20% of hepatocytes, a 1,000-fold accumulation of metformin inside mitochondria would represent an approximately 200-fold accumulation of metformin in liver (without accounting for accumulation in the cytosol). Such an accumulation is 2 orders of magnitude higher than that measured by several groups (32, 35, 42, 43).
Thirdly, a large mitochondrial accumulation is not compatible with the low volume of distribution of metformin and its short half-live (see above).
Fourthly, using radioactive [14C] metformin, the radioactivity was not found to accumulate in liver mitochondria of rats treated orally with metformin (45) and no radioactivity was measured inside mitochondria when Xenopus laevis oocytes were exposed to concentrations of metformin that led to Complex I inhibition (6). Importantly, Complex I remained inhibited after mitochondrial isolation. Although this result does not definitively exclude a possible accumulation of metformin in mitochondria as a cause of Complex I inhibition (accumulated metformin may diffuse during the isolation procedure), it rules out the hypothesis that the inhibition of Complex I by metformin requires metformin inside mitochondria.
In summary, unlike the less hydrophilic biguanides (46), the accumulation of metformin inside the mitochondria is not supported by direct measurements, is not consistent with the pharmacokinetic data, and would require a transporter that has not yet been discovered.
Seems there are a lot of flaws and assumptions in the studies suggesting that Metformin's effect on Mitochondria.
However, the hypothesis that metformin accumulates in mitochondria contradicts several observations.
First of all, the accumulation of numerous positive charges in the matrix compensated by proton extrusion by the respiratory chain, should lead to a collapse of mitochondrial membrane potential associated with an increase in delta pH. However, note that metformin did not depolarize isolated mitochondria (8).
Secondly, assuming that the total mitochondrial volume represents approximately 20% of hepatocytes, a 1,000-fold accumulation of metformin inside mitochondria would represent an approximately 200-fold accumulation of metformin in liver (without accounting for accumulation in the cytosol). Such an accumulation is 2 orders of magnitude higher than that measured by several groups (32, 35, 42, 43).
Thirdly, a large mitochondrial accumulation is not compatible with the low volume of distribution of metformin and its short half-live (see above).
Fourthly, using radioactive [14C] metformin, the radioactivity was not found to accumulate in liver mitochondria of rats treated orally with metformin (45) and no radioactivity was measured inside mitochondria when Xenopus laevis oocytes were exposed to concentrations of metformin that led to Complex I inhibition (6). Importantly, Complex I remained inhibited after mitochondrial isolation. Although this result does not definitively exclude a possible accumulation of metformin in mitochondria as a cause of Complex I inhibition (accumulated metformin may diffuse during the isolation procedure), it rules out the hypothesis that the inhibition of Complex I by metformin requires metformin inside mitochondria.
In summary, unlike the less hydrophilic biguanides (46), the accumulation of metformin inside the mitochondria is not supported by direct measurements, is not consistent with the pharmacokinetic data, and would require a transporter that has not yet been discovered.
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