Hypermetabolism: An Unexpected Driver of Biological Aging

[area51puy]

Hypermetabolism: An Unexpected Driver of Biological Aging

The solution could be linked to mitochondria, the energy-providing organelles in cells. This concept is not novel, but until now, there was a lack of direct evidence in human cells. A recent study published in Communications Biology and led by researchers from Columbia University has uncovered th

scitechdaily.com

Mitochondrial defects caused by rare genetic mutations cause human cells to increase their metabolism. Though that helps short-term survival, it comes at a high cost: a dramatic increase in the rate at which the cells age. Hypermetabolism also may be a key reason why most cells deteriorate as everyone gets older.
The solution could be linked to mitochondria, the energy-providing organelles in cells. This concept is not novel, but until now, there was a lack of direct evidence in human cells.

A recent study published in Communications Biology and led by researchers from Columbia University has uncovered that human cells with impaired mitochondria respond by going into overdrive and using more energy. This process, known as hypermetabolism, allows the cells to temporarily survive, but it also accelerates their aging rate significantly.

 

[Izzybelle]

Chiming in here, although I'm not a biologist and I may be way off, but this sounds counter to Ray's views.

Statements like this:

“But exercise is known to increase the efficiency of an organism. An individual who runs, for example, uses less energy to sustain basic bodily processes than someone who is not physically active.”

This makes me think of when I was a runner, and the doctor once joked that my heart rate showed that I was "barely alive." In those days I thought it was a good thing.

And:

"Improving organismal efficiency, which would lower energy use in the cells and improve fatigue and other symptoms, may partially explain the health benefits of exercise in patients with mitochondrial diseases and otherwise healthy people."

Doesn't Ray say that the cells need to be energized, and that problems arise when there is not enough energy?

"The key idea was that energy and structure are interdependent, at every level." -Ray Peat

So in Ray's view wouldn't these mitochondrial defects be due to a lack of energy, and not the other way around? The mitochondria seem to be wasting energy, and it seems that they are theorizing that you need to deplete the energy in the mitochondira, instead of providing more energy so that the mitochondria has enough energy to function properly. Novice interpretation on my part, maybe someone more knowledgeable can chime in. Sure wish Ray was still around to comment....

 

[CLASH]

"OxPhos defects cause hypermetabolism and reduce lifespan in cells and in patients with mitochondrial diseases"

^Title of paper

Its not about increasing ATP generation, its about isssues with oxidative phosphorylation leading to an increased upregulation in metabolic flux. This is essentially a hypermetabolism, yet low ATP state. See quote below:

"Genetically or pharmacologically disrupting OxPhos approximately doubles cellular energy expenditure. This cell-autonomous state of hypermetabolism occurs despite near-normal OxPhos coupling efficiency, excluding uncoupling as a general mechanism. Instead, hypermetabolism is associated with mitochondrial DNA instability, activation of the integrated stress response (ISR), and increased extracellular secretion of age-related cytokines and metabokines including GDF15. In parallel, OxPhos defects accelerate telomere erosion and epigenetic aging per cell division, consistent with evidence that excess energy expenditure accelerates biological aging."

 

[Momma]

“Hypermetabolism” if running on cortisol. Sure. Yes.

 

[Slaweknysa]

that explains it:

The “cancer metabolism” drives aging in humans – To Extract Knowledge from Matter

 

[Izzybelle]

that explains it:

The “cancer metabolism” drives aging in humans – To Extract Knowledge from Matter

Thank-you @Slaweknysa and @haidut .