• Due to excessive bot signups along with nefarious actors we are limiting forum registration. Keep checking back for the register link to appear. Please do not send emails or have someone post to the forum asking for a signup link. Until the current climate changes we do not see a change of this policy. To join the forum you must have a compelling reason. Letting us know what skills/knowledge you will bring to the community along with the intent of your stay here will help in getting you approved.

Aging is an energy deficiency problem, taking cardiolipin may reverse it

haidut

Member
Joined
Mar 18, 2013
Messages
18,915
Location
USA / Europe
Yet another study demonstrating that "aging" is nothing but a phenotype characterizing an organism with declining energy production. Since most of the cellular energy is produced in the mitochondria, another way of stating the same is that aging (and any specific disease for that matter) is a mitochondrial dysfunction problem. Conversely, reversing that energy/mitochondrial deficiency may reverse the aging/sickness. The study below corroborates the latter hypothesis, by demonstrating that aging is characterized a decline in the communication between mitochondria and the lysosomes, driven by decline in cardiolipin inside the mitochondria. As discussed before, cardiolipin is a crucial mitochondrial protein responsible for the function of the last enzyme of OXPHOS, known as cytochrome C oxidase. Multiple studies across many animal species have already demonstrated that cardiolipin content not only declines with aging but also changes in composition so that its lipid component shifts in composition from saturated fat to PUFA, and that feeding fully saturated fats to aging organisms restores their mitochondrial function back to normal. Well, in this case, the study used direct supplementation with (saturated) cardiolipin, but the effects were the same - reversal of aging and significant extension of (maximum) lifespan.

NFYB-1 regulates mitochondrial function and longevity via lysosomal prosaposin - Nature Metabolism
Subcellular chatter regulates longevity

"...From their research, the scientists found a nuclear protein called NFYB-1 that switches on and off genes affecting mitochondrial activity, and which itself goes down during ageing. In mutant worms lacking this protein, mitochondria don’t work as well and worms don’t live as long. Unexpectedly, the scientists discovered that NFYB-1 steers the activity of mitochondria through another part of the cell called the lysosome, a place where basic molecules are broken down and recycled as nutrients. “We think the lysosome talks with the mitochondria through special fats called cardiolipins and ceramides, which are essential to mitochondrial activity,” says Max Planck Director, Adam Antebi, whose laboratory spearheaded the study. Remarkably, simply feeding the NFYB-1 mutant worms cardiolipin restored mitochondrial function and worm health in these strains. Because cardiolipins and ceramides are also essential for human mitochondria, this may mean human health and ageing can be improved by understanding on how such molecules facilitate communication between different parts of the cell. This work has been recently published in Nature Metabolism."
 

rei

Member
Joined
Aug 6, 2017
Messages
1,607
it's astonishing these kinds of studies even get published. Maybe we have a change in ages at hands.
 

Risingfire

Member
Joined
May 10, 2016
Messages
728
I'm going to finish my bottle of Mitolipin tonight and expect to look 5 years younger tomorrow morning!
 

Xref

Member
Joined
Apr 9, 2020
Messages
19
"Multi-omics analysis reveals that NFYB-1 is a potent repressor of lysosomal prosaposin, a regulator of glycosphingolipid metabolism. Limiting prosaposin expression unexpectedly restores cardiolipin production, mitochondrial function and longevity in the nfyb-1 background."
 

whollygod

New Member
Joined
Mar 21, 2018
Messages
4

Could someone interpret this for the below average lay person with a curious mind nonetheless?

Abstract​

Mitochondria can depolarize and trigger cell death through the opening of the mitochondrial permeability transition pore (MPTP). We recently showed that an increase in the long chain n3 polyunsaturated fatty acids (PUFA) docosahexaenoic acid (DHA; 22:6n3) and depletion of the n6 PUFA arachidonic acid (ARA; 20:4n6) in mitochondrial membranes is associated with a greater Ca2+ load required to induce MPTP opening. Here we manipulated mitochondrial phospholipid composition by supplementing the diet with DHA, ARA or combined DHA+ARA in rats for 10 weeks. There were no effects on cardiac function, or respiration of isolated mitochondria. Analysis of mitochondrial phospholipids showed DHA supplementation increased DHA and displaced ARA in mitochondrial membranes, while supplementation with ARA or DHA+ARA increased ARA and depleted linoleic acid (18:2n6). Phospholipid analysis revealed a similar pattern, particularly in cardiolipin. Tetralinoleoyl cardiolipin was depleted by 80% with ARA or DHA+ARA supplementation, with linoleic acid side chains replaced by ARA. Both the DHA and ARA groups had delayed Ca2+-induced MPTP opening, but the DHA+ARA group was similar to the control diet. In conclusion, alterations in mitochondria membrane phospholipid fatty acid composition caused by dietary DHA or ARA was associated with a greater cumulative Ca2+ load required to induced MPTP opening. Further, high levels of tetralinoleoyl cardiolipin were not essential for normal mitochondrial function if replaced with very-long chain n3 or n6 PUFAs.
 

Blaze

Member
Joined
Apr 25, 2020
Messages
444
Yet another study demonstrating that "aging" is nothing but a phenotype characterizing an organism with declining energy production. Since most of the cellular energy is produced in the mitochondria, another way of stating the same is that aging (and any specific disease for that matter) is a mitochondrial dysfunction problem. Conversely, reversing that energy/mitochondrial deficiency may reverse the aging/sickness. The study below corroborates the latter hypothesis, by demonstrating that aging is characterized a decline in the communication between mitochondria and the lysosomes, driven by decline in cardiolipin inside the mitochondria. As discussed before, cardiolipin is a crucial mitochondrial protein responsible for the function of the last enzyme of OXPHOS, known as cytochrome C oxidase. Multiple studies across many animal species have already demonstrated that cardiolipin content not only declines with aging but also changes in composition so that its lipid component shifts in composition from saturated fat to PUFA, and that feeding fully saturated fats to aging organisms restores their mitochondrial function back to normal. Well, in this case, the study used direct supplementation with (saturated) cardiolipin, but the effects were the same - reversal of aging and significant extension of (maximum) lifespan.

NFYB-1 regulates mitochondrial function and longevity via lysosomal prosaposin - Nature Metabolism
Subcellular chatter regulates longevity

"...From their research, the scientists found a nuclear protein called NFYB-1 that switches on and off genes affecting mitochondrial activity, and which itself goes down during ageing. In mutant worms lacking this protein, mitochondria don’t work as well and worms don’t live as long. Unexpectedly, the scientists discovered that NFYB-1 steers the activity of mitochondria through another part of the cell called the lysosome, a place where basic molecules are broken down and recycled as nutrients. “We think the lysosome talks with the mitochondria through special fats called cardiolipins and ceramides, which are essential to mitochondrial activity,” says Max Planck Director, Adam Antebi, whose laboratory spearheaded the study. Remarkably, simply feeding the NFYB-1 mutant worms cardiolipin restored mitochondrial function and worm health in these strains. Because cardiolipins and ceramides are also essential for human mitochondria, this may mean human health and ageing can be improved by understanding on how such molecules facilitate communication between different parts of the cell. This work has been recently published in Nature Metabolism."
The research I have read on oral supplementation treatment for membrane lipid replacement is intriguing. The consensus is that it seems to require a combo of glycerolphospholipids and fructooligosaccharides to work at all properly and make it through the digestive process. Any suggestions for a commercially available product that you think would be beneficial? Do you have anything like that in your boutique supplement store lineup?
 
Last edited:

Mauritio

Member
Joined
Feb 26, 2018
Messages
4,337

Similar threads

Top