Turns out it's not my fault,I'm biologically lazy.
this post was submitted on 18 Mar 2026
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I'm not lazy, I just have advanced critical evaluation abilities coupled with a natural drive for efficiency resulting in a very high threshold for determining what is worth the effort of my considerable skills.
As I suggested in my comment in https://lemmy.world/c/nootropics, a remedy could be use of ATP boosters such as creatine.
Creatine, a naturally occurring compound known for its role in energy metabolism, has long been used as a dietary supplement to boost physical performance. It plays a key role in producing adenosine triphosphate (ATP), the main energy source for cells, which is critical for maintaining optimal cellular function...
Adenosine is the sleepy endogenous drug the body uses, that caffeine inhibits. Is Adenosine triphosphate a different drug then that the body uses? Is it on a feedback loop with adenosine?
I think a lot of depression, not all, is just due to our often shitty circumstances.
ATP is what cells use to power all of their processes
Oh thanks I have heard of ATP before I didn't make the connection from adenosine triphosphate I guess.
ATP bioenergetics and fatigue in young adults with and without major depression http://dx.doi.org/10.1038/s41398-026-03904-y
Abstract
Fatigue is a pervasive and difficult-to-treat symptom of major depressive disorder (MDD) that contributes to disability. Understanding this problem in its earlier stages will be critical for averting long-term negative outcomes. To investigate the molecular roots of fatigue in early-stage depression, the current work measured bioenergetic mechanisms, with a focus on adenosine triphosphate (ATP), in brain and blood cells in young adults with MDD versus healthy controls (HC). To measure ATP concentration and ATP production rate in the visual cortex, we utilized 31P magnetic resonance spectroscopy imaging with magnetization transfer (31P MRSI-MT) at 7 Tesla, with and without gamma-ATP resonance saturation. ATP level was also measured in peripheral blood mononuclear cells (PBMCs) at rest and after serial addition of mitochondrial inhibitors. Out of 25 participants (mean age 21.8 years), usable data were available for 18 participants for imaging (9 per group); 24 for PBMCs (13 HC; 11 MDD). The MDD group demonstrated higher ATP production rate in the visual cortex than HC, which correlated positively with Fatigue Severity Scale (FSS) scores. ATP concentrations in PBMCs were higher in MDD than HC, and also correlated with FSS scores. After mitochondrial uncoupling, PBMCs in the MDD group had a lower capacity for ATP production than HC. For the first time, we demonstrate an ATP biosignature of fatigue in young adults with MDD that is visible in both brain and peripheral blood. The findings suggest a compensatory mechanism that occurs early in the disease stage.